The genetic material of DNA viruses is either single-stranded (ss) or double-stranded (ds) deoxyribonucleic acid. Virus DNA genomes are variable in size, ranging from small with a size of 1 kilobase pairs (kbp) to large examples of several megabase pairs. DNA viruses use host cells for replication and subsequent infection. The first viral genes to be expressed, which are made by larger viruses, are called early genes. Genes encoding DNA polymerase and proteins incorporated in DNA replication often belong in this group. After DNA replication, viruses change the expression profile to the so-called late genes. Those genes are essential for the production of structural proteins used for coating the replicated DNA genome and forming new viral particles. At the end of the proliferation process, viral particles are released from the cell to infect new sites. In this article, the four main groups of DNA viruses significantly affecting swine are reviewed: porcine circoviruses, African swine fever virus, porcine parvoviruses, and pseudorabies virus. The genetic diversity inside a particular group and family classification, the structures of virus particles, the clinical syndromes, the course of infection, and recent progress in vaccine development as an effective means of protection against infections with swine DNA viruses are described.
Porcine circoviruses (PCVs)
Porcine circoviruses are the smallest autonomously replicating swine viruses containing circular single-stranded DNA (ssDNA) with a size of 1.76 kbp (73, 75). PCVs were first discovered by Tischer et al. (113) in 1974 when PCVs were mistaken for picornavirus-like particles in a contaminated PK-15 pig kidney cell line. Those circoviruses were non-pathogenic, and after they were classified into the Circoviridae family, their apparent harmlessness caused them to merit little attention so only a few articles concerning the topic were written until around 20 years later, when a new pathogenic type of porcine circovirus appeared called PCV2 (75). In 2015, PCV3 was discovered and associated with porcine dermatitis and nephropathy syndrome (PDNS) (90), and in 2019, a new type of PCV (type 4) was found in China (124).
Virus structure. PCV virions are small isometric particles with a diameter of 17 nm containing circular ssDNA which only contains three protein-coding genes (114). The virus particle of both PCV1 and PCV2 is composed of a single structural protein called the capsid protein (Cp), with a molecular mass of 30 kDa and which is responsible for spontaneous capsid formation (62) (Fig. 1).
Fig. 1
Structural characteristics of viruses of interest
PCV1. This was the first identified porcine circovirus. It was designated PCV PK-15 after its discovery and characterisation as a contaminant in the PK-15 porcine kidney cell line (113). Interestingly, it was also found in lymph nodes from piglets affected by a wasting syndrome in France (4, 60).
PCV2. In 1998, Meehan et al. (74) observed that monoclonal antibodies raised to circoviruses causing post-weaning multisystemic wasting syndrome (PMWS) were different from those raised to the PCV PK-15 isolate. They also published the first nucleotide sequences of the circoviruses associated with PMWS, which showed less than 80% identity with the PCV PK-15 isolate, and they thus provided evidence for a new pathogenic type of porcine circovirus, referred to as PCV2 (74). Based on the results of the phylogenetic study using the capsid protein gene region as a marker, PCV2 sequences were divided into two main groups: the first group, which subdivides into three clusters 1A to 1C, and the second group, which branches into five clusters 2A to 2E (40, 85). There is also another grouping method considering the geographic localisation of the virus, dividing PCV2 into PCV2a for the North American-like isolates (which also fall into the first capsid protein gene region-differentiated group of PCV2), and PCV2b for the European-like isolates (also in the second capsid protein group of PCV2) (86).
PCV3. This is a recently discovered type, and yet it has been detected and characterised in many countries throughout the world, including China (55), Italy (31), Brazil (115), and Sweden (121). PCV3 was first identified in 2015 in North Carolina (USA) in isolates from sows showing high mortality, low conception rates and typical signs of PDNS (90). Therefore, PCV3 was associated with PDNS and reproductive failure (90) and it has also been linked to congenital tumours in piglets as well after Chinese PDNS cases were investigated (21). This new type of PCV shares only a small percentage of homology in genomic DNA sequence with those of PCV1 and PCV2 (90). The homology between PCV3 and PCV2 found by sequencing in the rep gene sequence is 55% and in the cp gene only 37% (90). In China, PCV3 was divided into two groups (a and b) and five subgroups (a1–a3, b1, and b2) by a phylogenetic study using full-length sequences of PCV3 DNA (22). In a phylogenetic study conducted in Germany where only open reading frame (ORF) 2 (coding for the Cp protein) was used for grouping, the number of subgroups differed; group a was not divided but group b was, into three subgroups (22, 39). The difference is caused by the usage of whole-genome sequences in the Chinese study, while ORF2 was considered a critical phylogenetic marker in Germany (85).
PCV4. This type was only discovered in April 2019 (124). Type 4 contains 1.77 kbp long DNA and shares 67% homology with mink circovirus, which is the highest homology across circoviruses, and 43–52% homology with other porcine circoviruses (124). The size of two crucial genes was predicted at 891 nucleotides for the rep gene and 687 nucleotides for the cp gene (124). For the understanding of porcine circovirus’ pathogenicity and infection, further investigations will be necessary.
Clinical syndromes. Postweaning multisystemic wasting syndrome was first described in 1996 and a year later was associated with PCV2 (46). The precise definition of PMWS was proposed by Sorden in 2000 (109). For pigs to be diagnosed with PMWS, they must show all of the following conditions: firstly, clinical signs like wasting, weight loss or failure to thrive; secondly, histological lesions, which are signs of depletion of lymphoid tissues and organs, and inflammation of the lungs and lymphoid tissues in usual cases and less often the liver, kidneys, pancreas or intestine; and thirdly, PCV2 infection inside the lesions. The effect of PMWS on the host immune system is pronounced, causing virus-induced lymphocyte depletion. In the work of Mandrioli et al. (69), the presence of activated macrophages was described as an essential factor for the development of the syndrome. Although mainly CD4+ T-lymphocyte counts were decreased during the infection, a dramatic decline in CD8+ and CD4+/CD8+ T-lymphocyte and B-lymphocyte numbers was also observed, associated with the loss of lymphoid follicles (69). The reduced proliferation of lymphocytes thus results in a reduction of cytokines as positive growth factors, which can affect the further expression of major histocompatibility complex I antigens type I and II (MHC I and MHC II) and thus impair the immune response (72). Interestingly, apoptosis was not observed in lymphoid tissues that showed a decreased rate of virus proliferation (69). However, the work of Shibahara et al. (106) showed that apoptosis occurred only in B-lymphocytes and not in macrophages (106). This can be explained by the yet-unknown cause of the apoptosis in lymphoid tissues of PMWS in swine (69).
Another disease associated with porcine circoviruses is PDNS. Pigs affected by this syndrome are slightly febrile, depressed, and have ventrocaudal subcutaneous oedema (100). The incubation time of this disease is very short, and most swine die within three days. There are some similarities between PMWS and PDNS, such as lymphoid depletion and the presence of syncytial cells and others, suggesting that PCV2 may be responsible for this disease. Typically, this disease leads to skin lesions on the hind legs, however PCV2 has not been confirmed as the causative agent of this phenomenon (100).
Porcine respiratory disease complex (PRDC) is a disease that affects mainly 2–8-month-old pigs. PRDC is characterised by poor appetite, weight loss, or weak growth accompanied by clinical signs like anorexia, fever, cough and dyspnoea (19, 52, 86).
Development of vaccines. PCVs are highly resistant to conventional detergents and disinfectants, which makes decontamination problematic (4). To cope with the negative impacts on pig livestock, scientists have developed vaccines for combating these viruses. The first step in producing an efficient vaccine against pathogenic PCV2 is creating and characterising monoclonal antibodies against the pathogen. In 2001, McNeilly et al. (72) prepared and characterised monoclonal antibodies against six PCV2 isolates. One year later, Fenaux et al. (32) reported the first construction of a DNA clone containing an inserted infectious PCV2 genome and its subsequent use for in vivo transfection of pigs. The results from transfection testing showed that the cloned PCV2 genomic DNA could be used for future pathogenesis testing, replacing the virulent virus for greater safety (32). The same research group observed that not only PCV2 genomic DNA could enhance the production of specific monoclonal antibodies, but also that a DNA clone containing a capsid gene from PCV2 inserted into the backbone of PCV1 could achieve the same (34). This DNA clone was further tested as a live attenuated vaccine, which enhanced cell-mediated immune response and thus protected pigs against a pathogenic PCV2 challenge (33).
The first preparation which came onto the market (Circovac®, now produced by Ceva, France) successfully vaccinated sows and piglets older than three weeks (87). Interestingly, the two-dose vaccine was observed to enable the transfer of specific PCV2 antibodies from sow to offspring via colostrum (66). This type of vaccination was named dam vaccination. Another preparation used for immunisation of pregnant sows was a baculovirus-expressed PCV2 vaccine (Ingelvac CircoFLEX®, Boehringer Ingelheim, Germany). Only a single dose of the vaccine could develop neutralising antibodies against PCV2, but 10% of the piglets born to those vaccinated sows contracted in utero infection (67, 68). These studies also suggest that the timing of vaccination is crucial, selection of the life stage for administration depending on the desired result. For example, if a farm with sows wants to prevent in utero infection in the next generation, they will specify pre-breeding and post-farrowing vaccinations (66, 68). As another example, in the case of protecting piglets in the early stage of growth, the vaccination should be administered pre-farrowing, when colostrum contains more specific antibodies (66). The two vaccines described are currently used frequently for controlling PCV2 infection.
A useful way of combating PCV can also be the application of vaccines or drugs which could block the attachment of viral particles to host cells. Recently two studies have reported two different components which can accomplish that. Li et al. (63) found that epigallocatechin gallate from green tea can inhibit the infection of PCV by interfering with the capsid protein and thus inhibiting its binding to the host cells. Another option could be therapeutically neutralising antibodies. In the study of Huang et al. (49), a new neutralising monoclonal antibody was prepared capable of blocking the capsid protein attachment to PK15 cells. These findings can provide useful information for the development and synthesis of new vaccines and drugs against porcine circoviruses.
Recent approaches to vaccines mostly target the sole capsid protein (Cp), recognising it as the most important. This protein was either expressed in bacterial strains (Lactobacillus lactis) (116) or viruses (adenoviruses) (127) or used to produce PCV2 virus-like particles in insect cells in a baculoviral expression system (18, 70).
African swine fever virus (ASFV)
ASFV is a large DNA virus that is the sole member of the Asfivirus genus within the Asfarviridae family (64) affecting all species of swine and predominantly vectored by ticks from the Ornithodoros genus (37). ASFV causes a highly infectious disease called African swine fever (ASF). Even though ASF was first identified in 1921, its first occurrence had already been observed in 1910 in British East Africa (the Kenya Colony) as an infectious disease affecting domestic pigs (78).
Virus structure. ASFV is a large virus, of which the viral particle has icosahedral symmetry (Fig. 1). The size of ASFV derives from the trilayer viral envelope protecting the core that contains linear dsDNA. Each of the layers is composed of different structural proteins playing not only a protective role but also an infective one. A brief description of each envelope layer and the most important structural proteins follows.
Outer envelope. The outer layer is composed of the structural proteins p12 (pO61R), p22 (KP177R) and CD2v (EP402R) (3, 17, 98). The p12 protein (pO61R) is a late structural protein which attaches the viral particle to the host cell (3), and the p22 (KP177R) protein is an early structural protein which is localised on the outer envelope of the viral particle (17). CD2v is a more complex protein which plays different roles during ASFV infection. It is a transmembrane protein containing 402 amino acids showing a high degree of similarity to CD2, an adhesion receptor of T lymphocytes, particularly sharing the immunoglobulin Ig domain with 28–30 highly glycosylated sites (76, 99). This protein functions in the adsorption of red blood cells on the surface of infected host cells (13, 99) and was found to interact with an adaptor protein complex (AP-1) through the diLeu motif in the C-terminal domain (91). Adaptor protein complex 1 is a group of cytosolic heterotetramers which sort membrane proteins to endosomes by the formation of clathrin-coated vesicles using clathrin as a scaffold protein (80). In this way, CD2v helps ASFV to enter into the host cells.
Capsid envelope. The major capsid p72 protein (encoded by the viral B646L gene) is knowable by its assembly in the area of the inner core matrix and outer capsid layer of the viral particle (24). This assembly is mediated by a chaperone encoded by B602L and takes place on the membrane of the endoplasmic reticulum, where the process of envelopment is localised (24). Another crucial structural protein is p49 (B438L), which forms the icosahedral shape of the viral particles by localising in the vertices of the capsid (29).
Inner envelope. The inner envelope contains five structural proteins: the abundant transmembrane p17 (D117L); the late structural pE248R (E248R), j5R (H108R) and j18L (E199L); and p54 or j13L (E183L) (15, 96, 97, 111, 112). Their functions have also been characterised, and it was learned that j5R and j13L/p54 are involved in the assembly of viral particles in which j13L is accumulated on the endoplasmic reticulum membrane, and involved in recruiting viral membrane precursors (15, 98). Protein p17 is also involved in recruiting viral precursors (111). Although the function of pE248R is not precisely known, it has been ascertained that it is an actor in the early phase during virus entry into the host cell (97).
Core layer. The first step in forming the viral particle is protecting the genomic DNA with a core layer of proteins. This layer is composed of structural proteins, which originate from polyproteins pp62 (CP530R) and pp220 (CP2475L) (107, 108). Both polyproteins are processed by SUMO-like protease (S273R) yielding different structural proteins, which in the case of pp62 are p15 and p35 and in the case of pp220 are p14, p34, p37 and p150 (107, 108).
Genomic DNA. ASFV genome is 170 kbp long and contains 151 ORFs (20, 120). The genome contains multiple genes with different functions. There are genes involved in DNA replication, genes encoding enzymes and factors involved in transcription and processing, genes encoding structural proteins and proteins involved in the assembly of viral particles, genes encoding proteins involved in host defences, and last but not least, multigene families, which correspond to the 30% of the genome (29).
Genetic classification. Distinct ASFV genotypes were identified based on the p72 structural protein. Phylogenetic analysis of the C-terminal end of the p72 gene showed the presence of 22 different genotypes (I–XXII) (14). Recently two new genotypes were added, XXIII and XXIV (2, 94), of which XXIII shares a common ancestor with the genotypes IX and X (2). In Europe, two types of genotypes caused outbreaks: genotype I on Sardinia and genotype II in Eastern Europe (11).
Clinical syndromes. The clinical signs caused by ASFV infection include lesions, high fever, skin haemorrhages and neurological diseases (117). Although these clinical signs may be similar to those of other diseases like classical swine fever virus and porcine reproductive and respiratory syndrome, African swine fever is manifested by additional symptoms including depression, apathy, anorexia, vomiting, and red skin on the ears, abdomen and chest (117).
ASFV and host immune system. The primary target cells of ASFV include macrophages and monocytes (45). ASFV uses macropinocytosis and clathrin-mediated endocytosis as two different mechanisms to enter the host cells (47). When the virus enters the cell, the lower pH inside late endosomes causes the disruption of the outer envelope and capsid (47). Thus, the inner envelope is exposed and subsequently fused with the endosomal membrane to release the viral genome into the cytosol (6). This fusion is mediated by the pE248R transmembrane protein of the inner envelope (6). Cholesterol from the endosome is also essential for the ASFV genome release to the cytosol (26). The further transport of the genome is mediated by p54 protein, which interacts with the light chain of dynein until it reaches the perinuclear spot near the microtubular organizing centre (MTOC), where DNA replication and transcription take place (5). Interestingly, the ASFV genome replicates independently on the host cell (29). The next step of ASFV infection is forming viral factories. These are formed near the nucleus at the MTOC, where virus proteins and DNA are assembled to form new viral particles (41). The integrity of the microtubules is necessary for the formation of viral factories (41). The last step is the release of completed viral particles outside the cells. The pE120R virus protein helps in the microtubule-mediated transfer of viral particles from the viral factory to the plasma membrane (7). The protein is attached to the surface of intracellular virions by binding to the p72 major capsid protein, which helps to incorporate pE120R into the viral particle (7).
Evasion from the host immune system. ASFV contains multiple genes that inhibit the function of interferon type I (IFN I), which results in inhibition of the antiviral state in infected host cells (30). One study suggests that the MGF 360 and 505 multigene families are involved in evasion from the antiviral state, due to the sensitivity of the virus to IFN I when MGFs were deleted (42). The essential part of the escape from the host immune system includes inhibition of cell death by apoptosis. Here, many proteins from ASFV can disable the apoptosis mechanism of the host cell. One of these is a protein encoded by the A179L gene, which belongs to the B-cell lymphoma Bcl2 family (10). This family is characterised by an anti- or pro-apoptotic function depending on the type of homology region (BH1–BH4) and the protein interactions (56, 122). This protein is known for its interaction with proteins containing the BH3 domain (such as Bak and Bax) and resultant inactivation of them (10). Bak and Bax are primary gatekeepers, which upon activation by apoptosis inducers cause disruption of mitochondrial membranes, and the subsequent release of cytochrome c activates the caspase cascade resulting in apoptosis (56, 122). However, their inactivation by the A179L gene–encoded protein causes the inhibition of apoptosis in infected host cells. Another protein which can inactivate apoptosis is that encoded by the A224L gene. This protein belongs to the inhibitors of apoptosis protein family, which is recognised by the BIR motif, and uses tumour necrosis factor alpha (TNF-α) as a stimulus for inhibition of apoptosis (30). That inhibition by this protein is accomplished by inhibition of caspase 3 and activation of the NF-κB nuclear factor (30), which then activates the expression of cFLIP, an inactivated caspase 8 homologue that subsequently blocks caspase 8 activity (30). However, this protein is not essential for growth or viral virulence (81), which suggests that inhibition of apoptosis by TNF-α is not necessary for the replication of ASFV.
Development of vaccines. The development of vaccines for combating ASFV began in the 1960s (9). During those early years, multiple vaccines were developed, but none of them proved effective enough for commercial purposes. There are three main types of vaccines which were designed against ASFV: inactivated vaccines with a killed virus, live attenuated vaccines and subunit vaccines. Inactivated vaccine approaches were not successful at all; such vaccines could not enhance the immune response in pigs, even with the addition of different types of adjuvants (12).
Live attenuated vaccines (LAVs). These vaccines, containing viruses with deleted genes responsible for host invasion, infectivity or immune system inhibitors, were found to enhance cellular and humoral immunity and further protected pigs against the virulent virus type (102). There are three successful LAVs, which derive from the OURT88/3, NH/P68 and BA71ΔCD2v isolates (61, 77, 79). The OURT88/3 strain has been observed to enhance the production of CDβ8+ lymphocytes, the part of CD8+ lymphocytes confirming the importance of cellular immunity in the resistance to ASF (89). Interestingly, using the OURT88/3 isolate, it has been found that deletion of genes involved in virulence such as DP71L, DP96R and the IFN I interferon modulators MGF 360 and MGF530/505 weakened the infectivity of and conferred subsequent protection against the OURT88/1 virulent strain (1, 95). However, MGF360/505 and 9GL deletion in the ASFV Georgia 2007 isolate also reduced the virulence of the isolate but without affording protection against the parental virus (84). A similar result was observed using the Georgia isolate with the deletion of the thymidine kinase gene involved in the virulence of ASFV (104). It has also been noted that cross-protection provided by the non-virulent OURT88/3 isolate and virulent OURT88/1 isolate used in combination induced protection against two isolates, Benin 97/1 and genotype X Uganda 1965 (53). Interestingly, the mutant virus BA71ΔCD2v conferred protection to both parental BA71 and heterologous E75 virulent strains, which are two genotype I strains (77). Furthermore, pigs also survived a lethal challenge with the virulent Georgia 2007/1 genotype II strain (77). In the study of Sánchez-Córdon et al. (103), the immunisation technique was observed to be crucial for protection against ASFV: vaccination through the intranasal route was markedly more effective than the intramuscular route (103).
Subunit vaccines. Subunit vaccines use biomacromolecules for immunisation, such as DNA or protein antigens. DNA vaccines have one main disadvantage, which is their reduced immunogenicity in large animals. This fact was confirmed by failed immunisation with a DNA vaccine containing ASFV genes (8). The study of Argilaguet et al. (8) attempted the construction of a new DNA clone encoding ASFV genes fused with a fragment of an antibody specific to a swine leukocyte antigen II and yielded the observation that targeting antigens to the antigen-presenting cells induced an immune response in pigs. Unfortunately, protection against lethal challenge was not achieved (8). There was also protection by a DNA vaccine containing ASFV genes encoding p54, p30 and the HA extracellular domain fused to ubiquitin against challenge with the virulent E75 strain (57). Protein antigens are, however, more effective than DNA vaccines; even if they do not confer protection in all cases. For example, immunisation with baculovirus-expressed p30, p54, p72 and p22 ASFV antigens showed only a temporal delay in the onset of disease and reduced viremia (82). It has been observed that neutralising antibodies were raised to p54 and p72 antigens inhibiting virus attachment to the surface of the host cells (44). Neutralising antibodies specific to the p30 antigen, which is the most immunogenic among ASFV antigens, were found to inhibit virus internalisation (44, 92). Recently, new p30-specific monoclonal antibodies were prepared, and their binding epitopes were mapped (92). It was found that immunisation with either p30 or p54 recombinant antigen was not successful because pigs were not protected and eventually died. However, when the antigens were used together as a cocktail, immunisation was successful and pigs raised neutralising antibodies, which delayed the disease and even stopped the infection (43). The study of Ruiz-Gonzalvo et al. (101) conducted in 1996 showed that immunisation with recombinant CD2v antigen inhibited the haemagglutination, restricted the infection temporally and in some cases also conferred protection against lethal disease. A more recent study from 2016 reports a similar result, which was that serotype-specific CD2v or C-type lectin induced haemadsorption-inhibition serotype-specific protective immunity. This shows that these antigens could be used for future vaccine development (16).
Porcine parvovirus (PPV)
PPV (58, 65) is a small ssDNA icosahedral nonenveloped virus (Fig. 1) with 5 kbp-long genomic DNA, which belongs to the Parvoviridae family, Parvovirinae subfamily and Protoparvovirus genus. PPV was first isolated in 1965 as a cell-culture contaminant (71) and this first isolate is designated PPV1. From 1965 onwards, different genotypes were identified, and recorded as PPV2 to PPV7, which were further classified based on their different characterisation as a separate genus within the family Parvoviridae.
Genetic classification. PPV1 genotype is the first identified genotype that was classified as the Parvovirus genus (65). PPV2 and PPV3 were both sorted into the Tetraparvovirus genus (27). PPV2 was identified for the first time during a study of the hepatitis E virus in swine sera collected in Myanmar in 2001 (48). The PPV3 genotype is closely related to human parvovirus 4 (PARV4) and porcine hokovirus that was identified for the first time in Hong Kong in 2008 (59). PPV4, PPV5 and PPV6 were classified in the Copiparvovirus genus (83, 110). Even though PPV4 belongs to the Copiparvovirus genus, it is closely related to the Bocavirus genus, containing an additional ORF3 (23) as Bocavirus does. The PPV5 and PPV6 genotypes were first identified in 2013 and 2014 in the USA and China, respectively (83, 105, 118). The first occurrence of PPV6 in Europe was observed in Poland in 2017 (28). The last identified genotype was PPV7, which was found in the USA, China and Korea in 2016 and 2017 (88, 119).
Clinical syndromes. The pathogenicity of PPV1 is the best known among the genotypes. PPV1 causes a reproductive failure disease in pregnant sows with clinical signs called SMEDI, an acronym of stillbirth, mummification, embryonic death and infertility (54). The route of infection in gravidity can influence the pathogenesis of the virus. The study by Joo et al. (50) shows that the intramuscular route facilitated the transfer of the virus from the dam through placenta and caused infection of foetuses earlier than oral routes of infection. However, the natural PPV entry path is oral, and such infections occur only when dams are exposed in the first part of the middle trimester of gestation (50).
PPV and host immune system. Induction of a cellular immune response to infection with PPV was observed (58). More specifically, CD4+ CD8+ T-cells were found to proliferate, while the activity of cytotoxic T-lymphocytes (CTL) was weak during the infection, indicating the role of humoral activity (58). The invasion by PPV also causes cell death by apoptosis, probably as a result of reactive oxygen species formation, which activates the Bax apoptosis regulator and translocates it to near the mitochondrial membrane, triggering the subsequent release of cytochrome c and a caspase cascade (128). A recent study discovered that the NS1 PPV non-structural protein is responsible for the induction of apoptosis and thus involved in placental tissue damage and reproductive failure (125).
Development of vaccines. Vaccines designed against PPV infection are, in most cases, inactivated virus preparations based on PPV genotype 1 strains. It has been observed that inactivated vaccines can only prevent the disease but not the infection and virus shedding of PPV (35). In 2016, the study by Foerster et al. (35) showed that this applies both to homologous heterologous challenges with virulent PPV. Several approaches in vaccine development have been assessed. Vaccines based on genotype 1, including PPV-NADL2, PPV-IDT (MSV) and PPV-143a, and a vaccine based on the Stendal strain (51), are used for combating the disease caused by PPV1 (51, 123). It has been found that these vaccines were able to protect pigs against the disease but not against PPV-27a genotype 2 strain infection (51). PPV-27a was also used to prepare an inactivated vaccine, which likewise was only successful in providing protection from the disease and not from the infection and DNA replication (35). A vaccine against other genotype strains was not designed mainly due to inadequate information on the pathogenicity of these strains.
Pseudorabies Virus (PrV)
PrV is a large enveloped virus with a size of approximately 180 nm containing dsDNA (25). This virus was first described by Aujeszky in Hungary in 1902 as the agent of a disease, and although that disease was not related to rabies, its viral agent was named pseudorabies virus (the disease being termed Aujeszky’s disease). The virus symptoms had already been observed previously, however, in the USA in the 1800s (25).
Virus structure. The viral particle appears in diagram form in Fig. 1. It is composed of morphologically different layers including a capsid protecting the dsDNA in the centre of the particle and thus forming a nucleocapsid and a protein matrix known as a tegument coated by the outer envelope, which contains a lipid membrane with distinct glycoproteins (93). A description of all structural proteins and their genes is given in detail in the article by Pomeranz et al. (93).
Genetic classification. Originally called suid herpesvirus 1 or Aujeszky’s disease virus, PrV is classified into the Herpesviridae family and Alphaherpesvirinae subfamily containing a single serotype (36). A phylogenetic study based on sequences from the UL44 gene encoding glycoprotein C (gC) divides PrV into five genotypes (A–E), which are neither country- nor continent-specific, in large part as a consequence of swine imports (36).
Clinical syndromes. Aujeszky’s disease is typified by neurological and respiratory disorders resulting in weight loss, decreased growth and high mortality of piglets (93). Recently, it was found that the coinfection with PrV and PCV2 causes severe neurological and respiratory symptoms in pigs while damaging brain and lung tissue in piglets, resulting in higher mortality (126).
Development of vaccines. Two different vaccine types were developed for combating Aujeszky’s disease. Inactivated and live attenuated vaccines were explored and live vaccines transpired to show higher efficiency and be more genetically stable than inactivated vaccines (38). Furthermore, live attenuated vaccines were observed to exhibit no or minimal residual virulence, suggesting their safety (38). The development of live attenuated vaccines against PrV is reviewed in the article by Freuling et al. (38).
The main DNA viruses significantly affecting swine are divided into four groups: PCVs, ASFV, PPVs, and PrV. Both porcine circoviruses and parvoviruses are small viruses having one capsid protein (Cp) and short genomic ssDNA. Vaccines against both viruses have been developed. However, a new vaccine should be designed, as a response to new genetically different genotypes having been identified which either have demonstrably different or yet unknown pathogenicity. In contrast, the African swine fever virus and pseudorabies virus are large viruses composed of a trilayer envelope and long linear genomic dsDNA. In the case of the African swine fever virus, there are many approaches to vaccine development. However, the effectiveness of every preparation was not sufficient for commercial purposes. In other words, there is no commercial vaccine for combating the viral infection and its disease. Further research is needed in this area to rectify this deficit. In the case of the pseudorabies virus, the majority of developed vaccines are live attenuated vaccines, due to their efficiency.
Abrams C.C., Goatley L., Fishbourne E., Chapman D., Cooke L., Oura C.A., Netherton C.L., Takamatsu H.-H., Dixon L.K.: Deletion of virulence associated genes from attenuated African swine fever virus isolate OUR T88/3 decreases its ability to protect against challenge with virulent virus. Virology 2013, 443, 99–105, doi: 10.1016/j.virol.2013.04.028.AbramsC.C.GoatleyL.FishbourneE.ChapmanD.CookeL.OuraC.A.NethertonC.L.TakamatsuH.-H.DixonL.K.Deletion of virulence associated genes from attenuated African swine fever virus isolate OUR T88/3 decreases its ability to protect against challenge with virulent virusVirology20134439910510.1016/j.virol.2013.04.028370909023725691Open DOISearch in Google Scholar
Achenbach J.E., Gallardo C., Nieto-Pelegrín E., Rivera-Arroyo B., Degefa-Negi T., Arias M., Jenberie S., Mulisa D.D., Gizaw D., Gelaye E., Chibssa T.R., Belaye A., Loitsch A., Forsa M., Yami M., Diallo A., Soler A., Lamien C.E., Sánchez-Vizcaíno J.M.: Identification of a new genotype of African swine fever virus in domestic pigs from Ethiopia. Transbound Emerg Dis 2017, 64, 1393–1404, doi: 10.1111/tbed.12511.AchenbachJ.E.GallardoC.Nieto-PelegrínE.Rivera-ArroyoB.Degefa-NegiT.AriasM.JenberieS.MulisaD.D.GizawD.GelayeE.ChibssaT.R.BelayeA.LoitschA.ForsaM.YamiM.DialloA.SolerA.LamienC.E.Sánchez-VizcaínoJ.M.Identification of a new genotype of African swine fever virus in domestic pigs from EthiopiaTransbound Emerg Dis2017641393140410.1111/tbed.1251127211823Open DOISearch in Google Scholar
Alcamí A., Angulo A., López-Otín C., Muñoz M., Freije J.M.P., Carrascosa A.L., Viñuela E.: Amino-acid-sequence and structural-properties of protein p12, an African swine fever virus attachment protein. J Virol 1992, 66, 3860–3868, doi: 10.1128/JVI.66.6.3860-3868.1992.AlcamíA.AnguloA.López-OtínC.MuñozM.FreijeJ.M.P.CarrascosaA.L.ViñuelaE.Amino-acid-sequence and structural-properties of protein p12, an African swine fever virus attachment proteinJ Virol1992663860386810.1128/JVI.66.6.3860-3868.19922411711583732Open DOISearch in Google Scholar
Allan G.M., Ellis J.A.: Porcine circoviruses: a review. J Vet Diagn Invest 2000, 12, 3–14, doi: 10.1177/104063870001200102.AllanG.M.EllisJ.A.Porcine circoviruses: a reviewJ Vet Diagn Invest20001231410.1177/10406387000120010210690769Open DOISearch in Google Scholar
Alonso C., Miskin J., Hernáez B., Fernandez-Zapatero P., Soto L., Cantó C., Rodríguez-Crespo I., Dixon L., Escribano J.M.: African swine fever virus protein p54 interacts with the microtubular motor complex through direct binding to light-chain dynein. J Virol 2001, 75, 9819–9827, doi: 10.1128/JVI.75.20.9819-9827.2001.AlonsoC.MiskinJ.HernáezB.Fernandez-ZapateroP.SotoL.CantóC.Rodríguez-CrespoI.DixonL.EscribanoJ.M.African swine fever virus protein p54 interacts with the microtubular motor complex through direct binding to light-chain dyneinJ Virol2001759819982710.1128/JVI.75.20.9819-9827.200111455411559815Open DOISearch in Google Scholar
Andrés G.: African swine fever virus gets undressed: new insights on the entry pathway. J Virol 2017, 91, e01906-16, doi: 10.1128/JVI.01906-16.AndrésG.African swine fever virus gets undressed: new insights on the entry pathwayJ Virol201791e019061610.1128/JVI.01906-16528689127974557Open DOISearch in Google Scholar
Andrés G., García-Escudero R., Viñuela E., Salas M.L., Rodríguez J.M.: African swine fever virus structural protein pE120R is essential for virus transport from assembly sites to plasma membrane but not for infectivity. J Virol 2001, 75, 6758–6768, doi: 10.1128/JVI.75.15.6758-6768.2001.AndrésG.García-EscuderoR.ViñuelaE.SalasM.L.RodríguezJ.M.African swine fever virus structural protein pE120R is essential for virus transport from assembly sites to plasma membrane but not for infectivityJ Virol2001756758676810.1128/JVI.75.15.6758-6768.200111440211435554Open DOISearch in Google Scholar
Argilaguet J.M., Pérez-Martín E., Gallardo C., Salguero F.J., Borrego B., Lacasta A., Accensi F., Díaz I., Nofrarías M., Pujols J., Blanco E., Pérez-Filgueira M., Escribano J.M., Rodríguez F.: Enhancing DNA immunization by targeting ASFV antigens to SLA-II bearing cells. Vaccine 2011, 29, 5379–5385, doi: 10.1016/j.vaccine.2011.05.084.ArgilaguetJ.M.Pérez-MartínE.GallardoC.SalgueroF.J.BorregoB.LacastaA.AccensiF.DíazI.NofraríasM.PujolsJ.BlancoE.Pérez-FilgueiraM.EscribanoJ.M.RodríguezF.Enhancing DNA immunization by targeting ASFV antigens to SLA-II bearing cellsVaccine2011295379538510.1016/j.vaccine.2011.05.08421679736Open DOISearch in Google Scholar
Arias M., de la Torre A., Dixon L., Gallardo C., Jori F., Laddomada A., Martins C., Parkhouse R.M., Revilla Y., Rodriguez F., Sanchez-Vizcaino J.M.: Approaches and perspectives for development of African swine fever virus vaccines. Vaccines 2017, 5, 35, doi: 10.3390/vaccines5040035.AriasM.de laTorre A.DixonL.GallardoC.JoriF.LaddomadaA.MartinsC.ParkhouseR.M.RevillaY.RodriguezF.Sanchez-VizcainoJ.M.Approaches and perspectives for development of African swine fever virus vaccinesVaccines201753510.3390/vaccines5040035574860228991171Open DOISearch in Google Scholar
Banjara S., Caria S., Dixon L.K., Hinds M.G., Kvansakul M.: Structural insight into African swine fever virus A179L-mediated inhibition of apoptosis. J Virol 2017, 91, e02228-16, doi: 10.1128/JVI.02228-16.BanjaraS.CariaS.DixonL.K.HindsM.G.KvansakulM.Structural insight into African swine fever virus A179L-mediated inhibition of apoptosisJ Virol201791e022281610.1128/JVI.02228-16533181528053104Open DOISearch in Google Scholar
Bellini S., Rutili D., Guberti V.: Preventive measures aimed at minimizing the risk of African swine fever virus spread in pig farming systems. Acta Vet Scand 2016, 58, 82, doi: 10.1186/ s13028-016-0264-x.BelliniS.RutiliD.GubertiV.Preventive measures aimed at minimizing the risk of African swine fever virus spread in pig farming systemsActa Vet Scand2016588210.1186/s13028-016-0264-xOpen DOISearch in Google Scholar
Blome S., Gabriel C., Beer M.: Modern adjuvants do not enhance the efficacy of an inactivated African swine fever virus vaccine preparation. Vaccine 2014, 32, 3879–3882, doi: 10.1016/ j.vaccine.2014.05.051.BlomeS.GabrielC.BeerM.Modern adjuvants do not enhance the efficacy of an inactivated African swine fever virus vaccine preparationVaccine2014323879388210.1016/j.vaccine.2014.05.051Open DOISearch in Google Scholar
Borca M.V., Carrillo C., Zsak L., Laegreid W.W., Kutish G.F., Neilan J.G., Burrage T.G., Rock D.L.: Deletion of a CD2-like gene, 8-DR, from African swine fever virus affects viral infection in domestic swine. J Virol 1998, 72, 2881–2889, doi: 10.1128/JVI.72.4.2881-2889.1998.BorcaM.V.CarrilloC.ZsakL.LaegreidW.W.KutishG.F.NeilanJ.G.BurrageT.G.RockD.L.Deletion of a CD2-like gene, 8-DR, from African swine fever virus affects viral infection in domestic swineJ Virol1998722881288910.1128/JVI.72.4.2881-2889.1998Open DOISearch in Google Scholar
Boshoff C.I., Bastos A.D.S., Gerber L.J., Vosloo W.: Genetic characterization of African swine fever viruses from outbreaks in southern Africa (1973–1999). Vet Microbiol 2007, 121, 45–55, doi: 10.1016/j.vetmic.2006.11.007.BoshoffC.I.BastosA.D.S.GerberL.J.VoslooW.Genetic characterization of African swine fever viruses from outbreaks in southern Africa (1973–1999)Vet Microbiol2007121455510.1016/j.vetmic.2006.11.007Open DOISearch in Google Scholar
Brookes S.M., Sun H., Dixon L.K., Parkhouse R.M.E.: Characterization of African swine fever virion proteins j5R and j13L: immuno-localization in virus particles and assembly sites. J Gen Virol 1998, 79, 1179–1188, doi: 10.1099/0022-131779-5-1179.BrookesS.M.SunH.DixonL.K.ParkhouseR.M.E.Characterization of African swine fever virion proteins j5R and j13L: immuno-localization in virus particles and assembly sitesJ Gen Virol1998791179118810.1099/0022-131779-5-1179Open DOISearch in Google Scholar
Burmakina G., Malogolovkin A., Tulman E.R., Zsak L., Delhon G., Diel D.G., Shobogorov N.M., Morgunov Y.P., Morgunov S.Y., Kutish G.F., Kolbasov D., Rock D.L.: African swine fever virus serotype-specific proteins are significant protective antigens for African swine fever. J Gen Virol 2016, 97, 1670–1675, doi: 10.1099/jgv.0.000490.BurmakinaG.MalogolovkinA.TulmanE.R.ZsakL.DelhonG.DielD.G.ShobogorovN.M.MorgunovY.P.MorgunovS.Y.KutishG.F.KolbasovD.RockD.L.African swine fever virus serotype-specific proteins are significant protective antigens for African swine feverJ Gen Virol2016971670167510.1099/jgv.0.000490Open DOISearch in Google Scholar
Camacho A., Viñuela E.: Protein P22 of African swine fever virus – an early structural protein that is incorporated into the membrane of infected cells. Virology 1991, 181, 251–257, doi: 10.1016/ 0042-6822(91)90490-3.CamachoA.ViñuelaE.Protein P22 of African swine fever virus – an early structural protein that is incorporated into the membrane of infected cellsVirology199118125125710.1016/0042-6822(91)90490-3Open DOISearch in Google Scholar
Cao W., Cao H., Yi X., Zhuang Y.: Development of a simple and high‑yielding fed‑batch process for the production of porcine circovirus type 2 virus‑like particle subunit vaccine. AMB Express 2019, 9, 164, doi: 10.1186/s13568-019-0880-8.CaoW.CaoH.YiX.ZhuangY.Development of a simple and high‑yielding fed‑batch process for the production of porcine circovirus type 2 virus‑like particle subunit vaccineAMB Express2019916410.1186/s13568-019-0880-8678905831605297Open DOISearch in Google Scholar
Chae C.: Porcine respiratory disease complex: Interaction of vaccination and porcine circovirus type 2, porcine reproductive and respiratory syndrome virus, and Mycoplasma hyopneumoniae Vet J 2016, 212, 1–6, doi: 10.1016/j.tvjl.2015.10.030.ChaeC.Porcine respiratory disease complex: Interaction of vaccination and porcine circovirus type 2, porcine reproductive and respiratory syndrome virus, and Mycoplasma hyopneumoniaeVet J20162121610.1016/j.tvjl.2015.10.03027256017Open DOISearch in Google Scholar
Chapman D.A.G., Tcherepanov V., Upton C., Dixon L.K.: Comparison of the genome sequences of nonpathogenic and pathogenic African swine fever virus isolates. J Gen Virol 2008, 89, 397–408, doi: 10.1099/vir.0.83343-0.ChapmanD.A.G.TcherepanovV.UptonC.DixonL.K.Comparison of the genome sequences of nonpathogenic and pathogenic African swine fever virus isolatesJ Gen Virol20088939740810.1099/vir.0.83343-018198370Open DOISearch in Google Scholar
Chen G.H., Mai K.J., Zhou L., Wu R.T., Tang X.Y., Wu J.L., He L.L., Lan T., Xie Q.M., Sun Y., Ma J.Y.: Detection and genome sequencing of porcine circovirus 3 in neonatal pigs with congenital tremors in South China. Transbound Emerg Dis 2017, 64, 1650–1654, doi: 10.1111/tbed.12702.ChenG.H.MaiK.J.ZhouL.WuR.T.TangX.Y.WuJ.L.HeL.L.LanT.XieQ.M.SunY.MaJ.Y.Detection and genome sequencing of porcine circovirus 3 in neonatal pigs with congenital tremors in South ChinaTransbound Emerg Dis2017641650165410.1111/tbed.12702Open DOISearch in Google Scholar
Chen Y., Xu Q., Chen H., Luo X., Wu Q., Tan C., Pan Q., Chen J.L.: Evolution and genetic diversity of porcine circovirus 3 in China. Viruses 2019, 11, 786, doi: 10.3390/v11090786.ChenY.XuQ.ChenH.LuoX.WuQ.TanC.PanQ.ChenJ.L.Evolution and genetic diversity of porcine circovirus 3 in ChinaViruses20191178610.3390/v11090786Open DOISearch in Google Scholar
Cheung A. K., Wu G., Wang D., Bayles D.O., Lager K.M., Vincent A.L.: Identification and molecular cloning of a novel porcine parvovirus. Arch Virol 2010, 155, 801–806, doi: 10.1007/s00705-010-0646-8.CheungA. K.WuG.WangD.BaylesD.O.LagerK.M.VincentA.L.Identification and molecular cloning of a novel porcine parvovirusArch Virol201015580180610.1007/s00705-010-0646-8Open DOISearch in Google Scholar
Cobbold C., Wileman T.: The major structural protein of African swine fever virus, p73, is packaged into large structures, indicative of viral capsid or matrix precursors, on the endoplasmic reticulum. J Virol 1998, 72, 5215–5223, doi: 10.1128/JVI.72.6.5215-5223.1998.CobboldC.WilemanT.The major structural protein of African swine fever virus, p73, is packaged into large structures, indicative of viral capsid or matrix precursors, on the endoplasmic reticulumJ Virol1998725215522310.1128/JVI.72.6.5215-5223.1998Open DOISearch in Google Scholar
Crandell R.A.: Pseudorabies (Aujeszky’s disease). Vet Clin North Am Large Anim Pract 1982, 4, 321–331, doi: 10.1016/s0196-9846(17)30108-8.CrandellR.A.Pseudorabies (Aujeszky’s disease)Vet Clin North Am Large Anim Pract1982432133110.1016/s0196-9846(17)30108-8Open DOISearch in Google Scholar
Cuesta-Geijo M.A., Chiappi M., Galindo I., Barrado-Gil L., Muñoz-Moreno R., Carrascosa J.L., Alonso C.: Cholesterol flux is required for endosomal progression of African swine fever virions during the initial establishment of infection. J Virol 2016, 90, 1534–1543, doi: 10.1128/JVI.02694-15.Cuesta-GeijoM.A.ChiappiM.GalindoI.Barrado-GilL.Muñoz-MorenoR.CarrascosaJ.L.AlonsoC.Cholesterol flux is required for endosomal progression of African swine fever virions during the initial establishment of infectionJ Virol2016901534154310.1128/JVI.02694-15471963026608317Open DOISearch in Google Scholar
Cui J., Biernacka K., Fan J., Gerber P.F., Stadejek T., Opriessnig T.: Circulation of porcine parvovirus types 1 through 6 in serum samples obtained from six commercial Polish pig farms. Transbound Emerg Dis 2017, 64, 1945–1952, doi: 10.1111/tbed.12593.CuiJ.BiernackaK.FanJ.GerberP.F.StadejekT.OpriessnigT.Circulation of porcine parvovirus types 1 through 6 in serum samples obtained from six commercial Polish pig farmsTransbound Emerg Dis2017641945195210.1111/tbed.1259327882679Open DOISearch in Google Scholar
Cui J., Fan J., Gerber P.F., Biernacka K., Stadejek T., Xiao C.-T., Opriessnig T.: First identification of porcine parvovirus 6 in Poland. Virus Genes 2017, 53, 100–104, doi: 10.1007/s11262-016-1386-y.CuiJ.FanJ.GerberP.F.BiernackaK.StadejekT.XiaoC.-T.OpriessnigT.First identification of porcine parvovirus 6 in PolandVirus Genes20175310010410.1007/s11262-016-1386-y530618127590228Open DOISearch in Google Scholar
Dixon L.K., Chapman D.A.G., Netherton C.L., Upton C.: African swine fever virus replication and genomics. Virus Res 2013, 173, 3–14, doi: 10.1016/j.virusres.2012.10.020.DixonL.K.ChapmanD.A.G.NethertonC.L.UptonC.African swine fever virus replication and genomicsVirus Res201317331410.1016/j.virusres.2012.10.02023142553Open DOISearch in Google Scholar
Dixon L.K., Islam M., Nash R., Reis A.L.: African swine fever virus evasion of host defences. Virus Res 2019, 266, 25–33, doi: 10.1016/j.virusres.2019.04.002.DixonL.K.IslamM.NashR.ReisA.L.African swine fever virus evasion of host defencesVirus Res2019266253310.1016/j.virusres.2019.04.002650568630959069Open DOISearch in Google Scholar
Faccini S., Barbieri I., Gilioli A., Sala G., Gibelli L.R., Moreno A., Sacchi C., Rosignoli C., Franzini G., Nigrelli A.: Detection and genetic characterization of porcine circovirus type 3 in Italy. Transbound Emerg Dis 2017, 64, 1661–1664, doi: 10.1111/tbed.12714.FacciniS.BarbieriI.GilioliA.SalaG.GibelliL.R.MorenoA.SacchiC.RosignoliC.FranziniG.NigrelliA.Detection and genetic characterization of porcine circovirus type 3 in ItalyTransbound Emerg Dis2017641661166410.1111/tbed.1271428921870Open DOISearch in Google Scholar
Fenaux M., Halbur P.G., Haqshenas G., Royer R., Thomas P., Nawagitgul P., Gill M., Toth T.E., Meng X.J.: Cloned genomic DNA of type 2 Porcine circovirus is infectious when injected directly into the liver and lymph nodes of pigs: characterization of clinical disease, virus distribution, and pathologic lesions. J Virol 2002, 76, 541–551, doi: 10.1128/jvi.76.2.541-551.2002.FenauxM.HalburP.G.HaqshenasG.RoyerR.ThomasP.NawagitgulP.GillM.TothT.E.MengX.J.Cloned genomic DNA of type 2 Porcine circovirus is infectious when injected directly into the liver and lymph nodes of pigs: characterization of clinical disease, virus distribution, and pathologic lesionsJ Virol20027654155110.1128/jvi.76.2.541-551.200213683111752145Open DOISearch in Google Scholar
Fenaux M., Opriessnig T., Halbur P.G., Elvinger F., Meng X.J.: A chimeric porcine circovirus (PCV) with the immunogenic capsid gene of the pathogenic PCV type 2 (PCV2) cloned into the genomic backbone of the non-pathogenic PCV1 induces protective immunity against PCV2 infection in pigs. J Virol 2004, 78, 6297–6303, doi: 10.1128/JVI.78.12.6297-6303.2004.FenauxM.OpriessnigT.HalburP.G.ElvingerF.MengX.J.A chimeric porcine circovirus (PCV) with the immunogenic capsid gene of the pathogenic PCV type 2 (PCV2) cloned into the genomic backbone of the non-pathogenic PCV1 induces protective immunity against PCV2 infection in pigsJ Virol2004786297630310.1128/JVI.78.12.6297-6303.200441654715163723Open DOISearch in Google Scholar
Fenaux M., Opriessnig T., Halbur P.G., Meng X.J.: Immunogenicity and pathogenicity of chimeric infectious DNA clones of pathogenic porcine circovirus type 2 (PCV2) and nonpathogenic PCV1 in weanling pigs. J Virol 2003, 77, 11232–11243, doi: 10.1128/JVI.77.20.11232-11243.2003.FenauxM.OpriessnigT.HalburP.G.MengX.J.Immunogenicity and pathogenicity of chimeric infectious DNA clones of pathogenic porcine circovirus type 2 (PCV2) and nonpathogenic PCV1 in weanling pigsJ Virol200377112321124310.1128/JVI.77.20.11232-11243.2003Open DOISearch in Google Scholar
Foerster T., Streck A.F., Speck S., Selbitz H.-J., Lindner T., Truyen U.: An inactivated whole-virus porcine parvovirus vaccine protects pigs against disease but does not prevent virus shedding even after homologous virus challenge. J Gen Virol 2016, 97, 1408–1413, doi: 10.1099/jgv.0.000446.FoersterT.StreckA.F.SpeckS.SelbitzH.-J.LindnerT.TruyenU.An inactivated whole-virus porcine parvovirus vaccine protects pigs against disease but does not prevent virus shedding even after homologous virus challengeJ Gen Virol2016971408141310.1099/jgv.0.00044626939976Open DOISearch in Google Scholar
Fonseca Jr.A.A., Camargos M.F., Sales M.L., Heinemann M.B., Leite R.C., Reis J.K.P.: Pseudorabies virus can be classified into five genotypes using partial sequences of UL44. Braz J Microbiol 2012, 43, 1632–1640, doi: 10.1590/S1517-838220120004000048.FonsecaJr.A.A.CamargosM.F.SalesM.L.HeinemannM.B.LeiteR.C.ReisJ.K.P.Pseudorabies virus can be classified into five genotypes using partial sequences of UL44Braz J Microbiol2012431632164010.1590/S1517-838220120004000048376903824031995Open DOISearch in Google Scholar
Frant M., Woźniakowski G., Pejsak Z.: African swine fever (ASF) and ticks. No risk of tick-mediated ASF spread in Poland and Baltic states. J Vet Res 2017, 61, 375–380, doi: 10.1515/jvetres-2017-0055.FrantM.WoźniakowskiG.PejsakZ.African swine fever (ASF) and ticksNo risk of tick-mediated ASF spread in Poland and Baltic states. J Vet Res20176137538010.1515/jvetres-2017-0055593733329978098Open DOISearch in Google Scholar
Freuling C.M., Müller T.F., Mettenleiter T.C.: Vaccines against pseudorabies virus (PrV). Vet Microbiol 2017, 206, 3–9, doi: 10.1016/j.vetmic.2016.11.019.FreulingC.M.MüllerT.F.MettenleiterT.C.Vaccines against pseudorabies virus (PrV)Vet Microbiol20172063910.1016/j.vetmic.2016.11.01927890448Open DOISearch in Google Scholar
Fux R., Söckler C., Link E.K., Renken C., Krejci R., Sutter G., Ritzmann M., Eddicks M.: Full genome characterization of porcine circovirus type 3 isolates reveals the existence of two distinct groups of virus strains. Virol J 2018, 15, 25, doi: 10.1186/s12985-018-0929-3.FuxR.SöcklerC.LinkE.K.RenkenC.KrejciR.SutterG.RitzmannM.EddicksM.Full genome characterization of porcine circovirus type 3 isolates reveals the existence of two distinct groups of virus strainsVirol J2018152510.1186/s12985-018-0929-3578963429378597Open DOISearch in Google Scholar
Gagnon C., Tremblay D., Tijssen P.: PCV2 strain variation: What does it mean? Proc Am Assoc Swine Practitioners 2007, 38, 535–540.GagnonC.TremblayD.TijssenP.PCV2 strain variation: What does it mean?Proc Am Assoc Swine Practitioners200738535540Search in Google Scholar
Galindo I., Alonso C.: African swine fever virus: a review. Viruses 2017, 9, 103, doi: 10.3390/v9050103.GalindoI.AlonsoC.African swine fever virus: a reviewViruses2017910310.3390/v9050103545441628489063Open DOISearch in Google Scholar
Golding J.P., Goatley L., Goodbourn S., Dixon L.K., Taylor G., Netherton C.L.: Sensitivity of African swine fever virus to type I interferon is linked to genes within multigene families 360 and 505. Virology 2016, 493, 154–161, doi: 10.1016/j.virol.2016.03.019.GoldingJ.P.GoatleyL.GoodbournS.DixonL.K.TaylorG.NethertonC.L.Sensitivity of African swine fever virus to type I interferon is linked to genes within multigene families 360 and 505Virology201649315416110.1016/j.virol.2016.03.019486367827043071Open DOISearch in Google Scholar
Gómez-Puertas P., Rodríguez F., Oviedo J.M., Brun A., Alonso C., Escribano J.M.: The African swine fever virus proteins p54 and p30 are involved in two distinct steps of virus attachment and both contribute to the antibody-mediated protective immune response. Virology 1998, 243, 461–471, doi: 10.1006/viro.1998.9068.Gómez-PuertasP.RodríguezF.OviedoJ.M.BrunA.AlonsoC.EscribanoJ.M.The African swine fever virus proteins p54 and p30 are involved in two distinct steps of virus attachment and both contribute to the antibody-mediated protective immune responseVirology199824346147110.1006/viro.1998.90689568043Open DOISearch in Google Scholar
Gómez-Puertas P., Rodríguez F., Oviedo J.M., Ramiro-Ibáñez F., Ruiz-Gonzalvo F., Alonso C., Escribano J.M.: Neutralizing antibodies to different proteins of African swine fever virus inhibit both virus attachment and internalization. J Virol 1996, 70, 5689–5694, doi: 10.1128/JVI.70.8.5689-5694.1996.Gómez-PuertasP.RodríguezF.OviedoJ.M.Ramiro-IbáñezF.Ruiz-GonzalvoF.AlonsoC.EscribanoJ.M.Neutralizing antibodies to different proteins of African swine fever virus inhibit both virus attachment and internalizationJ Virol1996705689569410.1128/JVI.70.8.5689-5694.19961905368764090Open DOISearch in Google Scholar
Gómez-Villamandos J.C., Bautista M.J., Sánchez-Cordón P.J., Carrasco L.: Pathology of African swine fever: the role of monocyte-macrophage. Virus Res 2013, 173, 140–149, doi: 10.1016/j.virusres.2013.01.017.Gómez-VillamandosJ.C.BautistaM.J.Sánchez-CordónP.J.CarrascoL.Pathology of African swine fever: the role of monocyte-macrophageVirus Res201317314014910.1016/j.virusres.2013.01.01723376310Open DOISearch in Google Scholar
Harding J.C., Clark E.G., Strokappe J.H., Willson P.I., Ellis J.A.: Postweaning multisystemic wasting syndrome: Epidemiology and clinical presentation. Swine Health Prod 1998, 6, 249–254, https://www.aasv.org/jshap/issues/v6n6/v6n6p249.pdfHardingJ.C.ClarkE.G.StrokappeJ.H.WillsonP.I.EllisJ.A.Postweaning multisystemic wasting syndrome: Epidemiology and clinical presentationSwine Health Prod19986249254https://www.aasv.org/jshap/issues/v6n6/v6n6p249.pdfSearch in Google Scholar
Hernáez B., Guerra M., Salas M.L., Andrés G.: African swine fever virus undergoes outer envelope disruption, capsid disassembly and inner envelope fusion before core release from multivesicular endosomes. PLoS Pathog 2016, 12, e1005595, doi: 10.1371/journal.ppat.1005595.HernáezB.GuerraM.SalasM.L.AndrésG.African swine fever virus undergoes outer envelope disruption, capsid disassembly and inner envelope fusion before core release from multivesicular endosomesPLoS Pathog201612e100559510.1371/journal.ppat.1005595484416627110717Open DOISearch in Google Scholar
Hijikata M., Abe K., Win K.M., Shimizu Y.K., Keicho N., Yoshikura H.: Identification of new parvovirus DNA sequence in swine sera from Myanmar. Jpn J Infect Dis 2001, 54, 244–245.HijikataM.AbeK.WinK.M.ShimizuY.K.KeichoN.YoshikuraH.Identification of new parvovirus DNA sequence in swine sera from MyanmarJpn J Infect Dis200154244245Search in Google Scholar
Huang L., Sun Z., Xia D., Wei Y., Sun E., Liu C., Zhu H., Bian H., Wu H., Feng L., Wang J., Liu C.: Neutralization mechanism of a monoclonal antibody targeting a porcine circovirus type 2 cap protein conformational epitope. J Virol 2020, 94, e01836-19, doi: 10.1128/JVI.01836-19.HuangL.SunZ.XiaD.WeiY.SunE.LiuC.ZhuH.BianH.WuH.FengL.WangJ.LiuC.Neutralization mechanism of a monoclonal antibody targeting a porcine circovirus type 2 cap protein conformational epitopeJ Virol202094e018361910.1128/JVI.01836-19716315032075932Open DOISearch in Google Scholar
Joo H.S., Donaldson-Wood C.R., Johnson R.H.: Observations on the pathogenesis of porcine parvovirus infection. Arch Vir 1976, 51, 123–129, doi: /10.1007/BF01317841.JooH.S.Donaldson-WoodC.R.JohnsonR.H.Observations on the pathogenesis of porcine parvovirus infectionArch Vir197651123129doi: /10.1007/BF0131784110.1007/BF01317841986801Search in Google Scholar
Jóźwik A., Manteufel J., Selbitz H.-J., Truyen U.: Vaccination against porcine parvovirus protects against disease, but does not prevent infection and virus shedding after challenge infection with a heterologous virus strain. J Gen Virol 2009, 90, 2437–2441, doi: 10.1099/vir.0.012054-0.JóźwikA.ManteufelJ.SelbitzH.-J.TruyenU.Vaccination against porcine parvovirus protects against disease, but does not prevent infection and virus shedding after challenge infection with a heterologous virus strainJ Gen Virol2009902437244110.1099/vir.0.012054-019535504Open DOISearch in Google Scholar
Kedkovid R., Woonwong Y., Arunorat J., Sirisereewan C., Sangpratum N., Lumyai M., Kesdangsakonwut S., Teankum K., Jittimanee S., Thanawongnuwech R.: Porcine circovirus type 3 (PCV3) infection in grower pigs from a Thai farm suffering from porcine respiratory disease complex (PRDC). Vet Microbiol 2018, 215, 71–76, doi: 10.1016/j.vetmic.2018.01.004.KedkovidR.WoonwongY.ArunoratJ.SirisereewanC.SangpratumN.LumyaiM.KesdangsakonwutS.TeankumK.JittimaneeS.ThanawongnuwechR.Porcine circovirus type 3 (PCV3) infection in grower pigs from a Thai farm suffering from porcine respiratory disease complex (PRDC)Vet Microbiol2018215717610.1016/j.vetmic.2018.01.00429426409Open DOISearch in Google Scholar
King K., Chapman D., Argilaguet J.M., Fishbourne E., Hutet E., Cariolet R., Hutchings G., Oura C.A., Netherton C.L., Moffat K., Taylor G., Le Potier M.F., Dixon L.K., Takamatsu H.H.: Protection of European domestic pigs from virulent African isolates of African swine fever virus by experimental immunisation. Vaccine 2011, 29, 4593–4600, doi: 10.1016/ j.vaccine.2011.04.052.KingK.ChapmanD.ArgilaguetJ.M.FishbourneE.HutetE.CarioletR.HutchingsG.OuraC.A.NethertonC.L.MoffatK.TaylorG.Le PotierM.F.DixonL.K.TakamatsuH.H.Protection of European domestic pigs from virulent African isolates of African swine fever virus by experimental immunisationVaccine2011294593460010.1016/j.vaccine.2011.04.052312096421549789Open DOISearch in Google Scholar
Kresse J.I., Taylor W.D., Stewart W.W., Eernisse K.A.: Parvovirus infection in pigs with necrotic and vesicle-like lesions. Vet Microbiol 1985, 10, 525–531, doi: 10.1016/03781135(85)90061-6.KresseJ.I.TaylorW.D.StewartW.W.EernisseK.A.Parvovirus infection in pigs with necrotic and vesicle-like lesionsVet Microbiol19851052553110.1016/03781135(85)90061-6Open DOISearch in Google Scholar
Ku X., Chen F., Li P., Wang Y., Yu X., Fan S., Qian P., Wu M., He Q.: Identification and genetic characterization of porcine circovirus type 3 in China. Transbound Emerg Dis 2017, 64, 703–708, doi: 10.1111/tbed.12638.KuX.ChenF.LiP.WangY.YuX.FanS.QianP.WuM.HeQ.Identification and genetic characterization of porcine circovirus type 3 in ChinaTransbound Emerg Dis20176470370810.1111/tbed.12638716976828317326Open DOISearch in Google Scholar
Kvansakul M., Caria S., Hinds M.G.: The Bcl-2 family in host-virus interactions. Viruses 2017, 9, 290, doi: 10.3390/v9100290.KvansakulM.CariaS.HindsM.G.The Bcl-2 family in host-virus interactionsViruses2017929010.3390/v9100290569164128984827Open DOISearch in Google Scholar
Lacasta A., Ballester M., Monteagudo P.L., Rodríguez J.M., Salas M.L., Accensi F., Pina-Pedrero S., Bensaid A., Argilaguet J., López-Soria S., Hutet E., Le Potier M.F., Rodríguez F.: Expression library immunization can confer protection against lethal challenge with African swine fever virus. J Virol 2014, 88, 13322–13332, doi: 10.1128/JVI.01893-14.LacastaA.BallesterM.MonteagudoP.L.RodríguezJ.M.SalasM.L.AccensiF.Pina-PedreroS.BensaidA.ArgilaguetJ.López-SoriaS.HutetE.Le PotierM.F.RodríguezF.Expression library immunization can confer protection against lethal challenge with African swine fever virusJ Virol201488133221333210.1128/JVI.01893-14424911225210179Open DOISearch in Google Scholar
Ladekjær-Mikkelsen A.S., Nielsen J.: A longitudinal study of cell-mediated immunity in pigs infected with porcine parvovirus. Vir Immunol 2002, 15, 373–384, doi: 10.1089/08828240260066297.Ladekjær-MikkelsenA.S.NielsenJ.A longitudinal study of cell-mediated immunity in pigs infected with porcine parvovirusVir Immunol20021537338410.1089/0882824026006629712081019Open DOISearch in Google Scholar
Lau S.K., Woo P.C., Tse H., Fu C.T., Au W.K., Chen X.C., Tsoi H.W., Tsang T.H., Chan J.S., Tsang D.N., Li K.S., Tse C.W., Ng T.K., Tsang O.T., Zheng B.J., Tam S., Chan K.H., Zhou B., Yuen K.Y.: Identification of novel porcine and bovine parvoviruses closely related to human parvovirus 4. J Gen Virol 2008, 89, 1840–1848, doi: 10.1099/vir.0.2008/000380-0.LauS.K.WooP.C.TseH.FuC.T.AuW.K.ChenX.C.TsoiH.W.TsangT.H.ChanJ.S.TsangD.N.LiK.S.TseC.W.NgT.K.TsangO.T.ZhengB.J.TamS.ChanK.H.ZhouB.YuenK.Y.Identification of novel porcine and bovine parvoviruses closely related to human parvovirus 4J Gen Virol2008891840184810.1099/vir.0.2008/000380-018632954Open DOISearch in Google Scholar
LeCann P., Albina E., Madec F., Cariolet R., Jestin A.: Piglet wasting disease. Vet Rec 1997, 141, 660.LeCannP.AlbinaE.MadecF.CarioletR.JestinA.Piglet wasting diseaseVet Rec1997141660Search in Google Scholar
Leitão A., Cartaxeiro C., Coelho R., Cruz B., Parkhouse R.M.E., Portugal F.C., Vigário J.D., Martins C.L.V.: The non-haemadsorbing African swine fever virus isolate ASFV/NH/P68 provides a model for defining the protective anti-virus immune response. J Gen Virol 2001, 82, 513–523, doi: 10.1099/00221317-82-3-513.LeitãoA.CartaxeiroC.CoelhoR.CruzB.ParkhouseR.M.E.PortugalF.C.VigárioJ.D.MartinsC.L.V.The non-haemadsorbing African swine fever virus isolate ASFV/NH/P68 provides a model for defining the protective anti-virus immune responseJ Gen Virol20018251352310.1099/00221317-82-3-513Open DOISearch in Google Scholar
Nawagitgul P., Morozov I., Bolin S.R., Harms P.A., Sorden S.D., Paul P.S.: Open reading frame 2 of porcine circovirus type 2 encodes a major capsid protein. J Gen Virol 2000, 81, 2281–2287, doi: 10.1099/0022-1317-81-9-2281.NawagitgulP.MorozovI.BolinS.R.HarmsP.A.SordenS.D.PaulP.S.Open reading frame 2 of porcine circovirus type 2 encodes a major capsid proteinJ Gen Virol2000812281228710.1099/0022-1317-81-9-228110950986Open DOISearch in Google Scholar
Li J., Song D., Wang S., Dai Y., Zhou J., Gu J.: Antiviral effect of epigallocatechin gallate via impairing porcine circovirus type 2 attachment to host cell receptor. Viruses 2020, 12, 176, doi: 10.3390/v12020176.LiJ.SongD.WangS.DaiY.ZhouJ.GuJ.Antiviral effect of epigallocatechin gallate via impairing porcine circovirus type 2 attachment to host cell receptorViruses20201217610.3390/v12020176707727632033244Open DOISearch in Google Scholar
MacLachlan N.J., Dubovi E.J.: Chapter 8: Asfarviridae and Iridoviridae In: Fenner’s Veterinary Virology 5th ed., edited by N.J. MacLachlan, E.J. Dubovi, Academic Press, Cambridge, MA, 2011, pp. 167–177.MacLachlanN.J.DuboviE.J.Chapter 8: Asfarviridae and IridoviridaeInFenner’s Veterinary Virology5th ed., edited byMacLachlanN.J.DuboviE.J.Academic PressCambridge, MA2011pp16717710.1016/B978-0-12-375158-4.00008-0Search in Google Scholar
MacLachlan N.J., Dubovi E.J.: Chapter 12: Parvoviridae In: Fenner’s Veterinary Virology 5th ed., edited by N.J. MacLachlan, E.J. Dubovi, Academic Press, Cambridge, MA, 2011, pp. 225–237.MacLachlanN.J.DuboviE.J.Chapter 12: ParvoviridaeInFenner’s Veterinary Virology5th ed., edited byMacLachlanN.J.DuboviE.J.Academic PressCambridge, MA2011pp22523710.1016/B978-0-12-375158-4.00012-2Search in Google Scholar
Madson D.M., Opriessnig T.: Effect of porcine circovirus type 2 (PCV2) infection on reproduction: disease, vertical transmission, diagnostics and vaccination. Anim Health Res Rev 2011, 12, 47–65, doi: 10.1017/S1466252311000053.MadsonD.M.OpriessnigT.Effect of porcine circovirus type 2 (PCV2) infection on reproduction: disease, vertical transmission, diagnostics and vaccinationAnim Health Res Rev201112476510.1017/S1466252311000053Open DOISearch in Google Scholar
Madson D.M., Patterson A.R., Ramamoorthy S., Pal N., Meng X.J., Opriessnig T.: Effect of porcine circovirus type 2 (PCV2) vaccination of the dam on PCV2 replication in utero. Clin Vac Immunol 2009, 16, 830–834, doi: 10.1128/CVI.00455-08.MadsonD.M.PattersonA.R.RamamoorthyS.PalN.MengX.J.OpriessnigT.Effect of porcine circovirus type 2 (PCV2) vaccination of the dam on PCV2 replication in uteroClin Vac Immunol20091683083410.1128/CVI.00455-08Open DOISearch in Google Scholar
Madson D.M., Patterson A.R., Ramamoorthy S., Pal N., Meng X.J., Opriessnig T.: Reproductive failure experimentally induced in sows via artificial insemination with semen spiked with porcine circovirus type 2 (PCV2). Vet Pathol 2009, 46, 707–716, doi: 10.1354/vp.08-VP-0234-O-FL.MadsonD.M.PattersonA.R.RamamoorthyS.PalN.MengX.J.OpriessnigT.Reproductive failure experimentally induced in sows via artificial insemination with semen spiked with porcine circovirus type 2 (PCV2)Vet Pathol20094670771610.1354/vp.08-VP-0234-O-FLOpen DOISearch in Google Scholar
Mandrioli L., Sarli G., Panarese S., Baldoni S., Marcato P.S.: Apoptosis and proliferative activity in lymph node reaction in postweaning multisystemic wasting syndrome (PMWS). Vet Immunol Immunopathol 2004, 97, 25–37, doi: 10.1016/j.vetimm.2003.08.017.MandrioliL.SarliG.PanareseS.BaldoniS.MarcatoP.S.Apoptosis and proliferative activity in lymph node reaction in postweaning multisystemic wasting syndrome (PMWS)Vet Immunol Immunopathol200497253710.1016/j.vetimm.2003.08.017Open DOISearch in Google Scholar
Masuda A., Lee J.M., Miyata T., Sato T., Hayashi S., Hino M., Morokuma D., Karasaki N., Mon H., Kusakabe T.: Purification and characterization of immunogenic recombinant virus-like particles of porcine circovirus type 2 expressed in silkworm pupae. J Gen Virol 2018, 99, 917–926, doi: 10.1099/jgv.0.001087.MasudaA.LeeJ.M.MiyataT.SatoT.HayashiS.HinoM.MorokumaD.KarasakiN.MonH.KusakabeT.Purification and characterization of immunogenic recombinant virus-like particles of porcine circovirus type 2 expressed in silkworm pupaeJ Gen Virol20189991792610.1099/jgv.0.001087Open DOISearch in Google Scholar
Mayr A., Bachmann P.A., Siegl G., Mahnel H., Sheffy B.E.: Characterization of a small porcine DNA virus. Arch Gesamte Virusforsch 1968, 25, 38–51, doi: 10.1007/BF01243088.MayrA.BachmannP.A.SieglG.MahnelH.SheffyB.E.Characterization of a small porcine DNA virusArch Gesamte Virusforsch196825385110.1007/BF01243088Open DOISearch in Google Scholar
McNeilly F., Allan G.M., Foster J.C., Adair B.M., McNulty M.S.: Effect of porcine circovirus infection on porcine alveolar macrophage function. Vet Immunol Immunopathol 1996, 49, 295–306, doi: 10.1016/0165-2427(95)05476-6.McNeillyF.AllanG.M.FosterJ.C.AdairB.M.McNultyM.S.Effect of porcine circovirus infection on porcine alveolar macrophage functionVet Immunol Immunopathol19964929530610.1016/0165-2427(95)05476-6Open DOISearch in Google Scholar
McNeilly F., McNair I., Mackie D.P., Meehan B.M., Kennedy S., Moffett D., Ellis J., Krakowka S., Allan G.M.: Production, characterisation and applications of monoclonal antibodies to porcine circovirus 2. Arch Virol 2001, 146, 909–922, doi: 10.1007/s007050170124.McNeillyF.McNairI.MackieD.P.MeehanB.M.KennedyS.MoffettD.EllisJ.KrakowkaS.AllanG.M.Production, characterisation and applications of monoclonal antibodies to porcine circovirus 2Arch Virol200114690992210.1007/s00705017012411448029Open DOISearch in Google Scholar
Meehan B.M., McNeilly F., Todd D., Kennedy S., Jewhurst V.A., Ellis J.A., Hassard L.E., Clark E.G., Haines D.M., Allan G.M.: Characterization of novel circovirus DNAs associated with wasting syndromes in pigs. J Gen Virol 1998, 79, 2171–2179, doi: 10.1099/0022-1317-79-9-2171.MeehanB.M.McNeillyF.ToddD.KennedyS.JewhurstV.A.EllisJ.A.HassardL.E.ClarkE.G.HainesD.M.AllanG.M.Characterization of novel circovirus DNAs associated with wasting syndromes in pigsJ Gen Virol1998792171217910.1099/0022-1317-79-9-21719747726Open DOISearch in Google Scholar
Meehan B.M., Todd D., Creelan J.L., Earle J.A P., Hoey E.M., McNulty M.S.: Characterization of viral DNAs from cells infected with chicken anaemia agent: sequence analysis of the cloned replicative form and transfection capabilities of cloned genome fragments. Arch Virol 1992, 124, 301–319, doi: 10.1007/BF01309811.MeehanB.M.ToddD.CreelanJ.L.EarleJ.A P.HoeyE.M.McNultyM.S.Characterization of viral DNAs from cells infected with chicken anaemia agent: sequence analysis of the cloned replicative form and transfection capabilities of cloned genome fragmentsArch Virol199212430131910.1007/BF01309811Open DOISearch in Google Scholar
Mima K.A., Burmakina G.S., Titov I.A., Malogolovkin A.S.: African swine fever virus glycoproteins p54 and CD2v in the context of immune response modulation: bioinformatic analysis of genetic variability and heterogeneity. Agrobiol 2015, 50, 785–793, doi: 10.15389/agrobiology.2015.6.785eng.MimaK.A.BurmakinaG.S.TitovI.A.MalogolovkinA.S.African swine fever virus glycoproteins p54 and CD2v in the context of immune response modulation: bioinformatic analysis of genetic variability and heterogeneityAgrobiol20155078579310.15389/agrobiology.2015.6.785engOpen DOISearch in Google Scholar
Monteagudo P.L., Lacasta A., López E., Bosch L., Collado J., Pina-Pedrero S., Correa-Fiz F., Accensi F., Navas M.J., Vidal E., Bustos M.J., Rodríguez J.M., Gallei A., Nikolin V., Salas M.L., Rodríguez, F.: BA71ΔCD2: A new recombinant live attenuated African swine fever virus with cross-protective capabilities. J Virol 2017, 91, e01058-17, doi: 10.1128/JVI.01058-17.MonteagudoP.L.LacastaA.LópezE.BoschL.ColladoJ.Pina-PedreroS.Correa-FizF.AccensiF.NavasM.J.VidalE.BustosM.J.RodríguezJ.M.GalleiA.NikolinV.SalasM.L.RodríguezF.BA71ΔCD2: A new recombinant live attenuated African swine fever virus with cross-protective capabilitiesJ Virol201791e010581710.1128/JVI.01058-17Open DOISearch in Google Scholar
Montgomery R.E.: On a form of swine fever occurring in British East Africa (Kenya colony). J Comp Pathol Therap 1921, 34, 159–191, doi: 10.1016/S0368-1742(21)80031-4.MontgomeryR.E.On a form of swine fever occurring in British East Africa (Kenya colony)J Comp Pathol Therap19213415919110.1016/S0368-1742(21)80031-4Open DOISearch in Google Scholar
Mulumba-Mfumu L.K., Goatley L.C., Saegerman C., Takamatsu H.H., Dixon L.K.: Immunization of African indigenous pigs with attenuated genotype I African swine fever virus OURT88/3 induces protection against challenge with virulent strains of genotype I. Transbound Emerg Dis 2015, 63, e323–7, doi: 10.1111/tbed.12303.Mulumba-MfumuL.K.GoatleyL.C.SaegermanC.TakamatsuH.H.DixonL.K.Immunization of African indigenous pigs with attenuated genotype I African swine fever virus OURT88/3 induces protection against challenge with virulent strains of genotype ITransbound Emerg Dis201563e323710.1111/tbed.1230325691347Open DOISearch in Google Scholar
Nakatsu F., Ohno H.: Adaptor protein complexes as the key regulators of protein sorting in the post-Golgi network. Cell Struct Funct 2003, 25, 419–429, doi: 10.1247/csf.28.419.NakatsuF.OhnoH.Adaptor protein complexes as the key regulators of protein sorting in the post-Golgi networkCell Struct Funct20032541942910.1247/csf.28.41914745134Open DOISearch in Google Scholar
Neilan J.G., Lu Z., Kutish G.F., Zsak L., Burrage T.G., Borca M.V., Carrillo C., Rock D.L.: A BIR motif containing gene of African swine fever virus, 4CL, is nonessential for growth in vitro and viral virulence. Virology 1997, 230, 252–264, doi: 10.1006/viro.1997.8481.NeilanJ.G.LuZ.KutishG.F.ZsakL.BurrageT.G.BorcaM.V.CarrilloC.RockD.L.A BIR motif containing gene of African swine fever virus, 4CL, is nonessential for growth in vitro and viral virulenceVirology199723025226410.1006/viro.1997.84819143281Open DOISearch in Google Scholar
Neilan J.G., Zsak L., Lu Z., Burrage T.G., Kutish G.F., Rock D.L.: Neutralizing antibodies to African swine fever virus proteins p30, p54, and p72 are not sufficient for antibody-mediated protection. Virology 2004, 319, 337–342, doi: 10.1016/j.virol.2003.11.011.NeilanJ.G.ZsakL.LuZ.BurrageT.G.KutishG.F.RockD.L.Neutralizing antibodies to African swine fever virus proteins p30, p54, and p72 are not sufficient for antibody-mediated protectionVirology200431933734210.1016/j.virol.2003.11.01114980493Open DOISearch in Google Scholar
Ni J., Qiao C., Han X., Han T., Kang W., Zi Z., Cao Z., Zhai X., Cai X.: Identification and genomic characterization of a novel porcine parvovirus (PPV6) in China. Virol J 2014, 11, 203, doi: 10.1186/s12985-014-0203-2.NiJ.QiaoC.HanX.HanT.KangW.ZiZ.CaoZ.ZhaiX.CaiX.Identification and genomic characterization of a novel porcine parvovirus (PPV6) in ChinaVirol J20141120310.1186/s12985-014-0203-2426536125442288Open DOISearch in Google Scholar
O’Donnell V., Holinka L.G., Sanford B., Krug P.W., Carlson J., Pacheco J.M., Reese B., Risatti G.R., Gladue D.P., Borca M.V.: African swine fever virus Georgia isolate harboring deletions of 9GL and MGF360/505 genes is highly attenuated in swine but does not confer protection against parental virus challenge. Virus Res 2016, 221, 8–14, doi: 10.1016/j.virusres.2016.05.014.O’DonnellV.HolinkaL.G.SanfordB.KrugP.W.CarlsonJ.PachecoJ.M.ReeseB.RisattiG.R.GladueD.P.BorcaM.V.African swine fever virus Georgia isolate harboring deletions of 9GL and MGF360/505 genes is highly attenuated in swine but does not confer protection against parental virus challengeVirus Res201622181410.1016/j.virusres.2016.05.01427182007Open DOISearch in Google Scholar
Olvera A., Cortey M., Segalés J.: Molecular evolution of porcine circovirus type 2 genomes: phylogeny and clonality. Virology 2007, 357, 175–185, doi: 10.1016/j.virol.2006.07.047.OlveraA.CorteyM.SegalésJ.Molecular evolution of porcine circovirus type 2 genomes: phylogeny and clonalityVirology200735717518510.1016/j.virol.2006.07.04716963096Open DOISearch in Google Scholar
Opriessnig T., Meng X.J., Halbur P.G.: Porcine circovirus type 2– associated disease: Update on current terminology, clinical manifestations, pathogenesis, diagnosis, and intervention strategies. J Vet Diagn Invest 2007, 19, 591–615, doi: 10.1177/ 104063870701900601.OpriessnigT.MengX.J.HalburP.G.Porcine circovirus type 2– associated disease: Update on current terminology, clinical manifestations, pathogenesis, diagnosis, and intervention strategiesJ Vet Diagn Invest20071959161510.1177/10406387070190060117998548Open DOISearch in Google Scholar
Opriessnig T., Patterson A.R., Madson D.M., Pal N., Ramamoorthy S., Meng X.J., Halbur P.G.: Comparison of the effectiveness of passive (dam) versus active (piglet) immunization against porcine circovirus type 2 (PCV2) and impact of passively derived PCV2 vaccine-induced immunity on vaccination. Vet Microbiol 2010, 142, 177–183, doi: 10.1016/j.vetmic.2009.09.056.OpriessnigT.PattersonA.R.MadsonD.M.PalN.RamamoorthyS.MengX.J.HalburP.G.Comparison of the effectiveness of passive (dam) versus active (piglet) immunization against porcine circovirus type 2 (PCV2) and impact of passively derived PCV2 vaccine-induced immunity on vaccinationVet Microbiol201014217718310.1016/j.vetmic.2009.09.05619913369Open DOISearch in Google Scholar
Ouh I.-O., Park S., Lee J.-Y., Song J.-Y.: Cho I.-S., Kim H.-R., Park C.-K.: First detection and genetic characterization of porcine parvovirus 7 from Korean domestic pig farms. J Vet Sci 2018, 19, 855–857, doi: 10.4142/jvs.2018.19.6.855.OuhI.-O.ParkS.LeeJ.-Y.SongJ.-Y.ChoI.-S.KimH.-R.ParkC.-K.First detection and genetic characterization of porcine parvovirus 7 from Korean domestic pig farmsJ Vet Sci20181985585710.4142/jvs.2018.19.6.855626557430304892Open DOISearch in Google Scholar
Oura C.A.L., Denyer M.S., Takamatsu H., Parkhouse R.M.E.: In vivo depletion of CD8+ T lymphocytes abrogates protective immunity to African swine fever virus. J Gen Virol 2005, 86, 2445–2450, doi: 10.1099/vir.0.81038-0.OuraC.A.L.DenyerM.S.TakamatsuH.ParkhouseR.M.E.In vivo depletion of CD8+ T lymphocytes abrogates protective immunity to African swine fever virusJ Gen Virol2005862445245010.1099/vir.0.81038-016099902Open DOISearch in Google Scholar
Palinski R., Piñeyro P., Shang P., Yuan F., Guo R., Fang Y., Byers E., Hause B.M.: A novel porcine circovirus distantly related to known circoviruses is associated with porcine dermatitis and nephropathy syndrome and reproductive failure. J Virol 2017, 91, e01879-16, doi: 10.1128/JVI.01879-16.PalinskiR.PiñeyroP.ShangP.YuanF.GuoR.FangY.ByersE.HauseB.M.A novel porcine circovirus distantly related to known circoviruses is associated with porcine dermatitis and nephropathy syndrome and reproductive failureJ Virol201791e018791610.1128/JVI.01879-16516520527795441Open DOISearch in Google Scholar
Pérez-Núñez D., García-Urdiales E., Martínez-Bonet M., María L., Nogal M.L., Barroso S., Revilla Y., Madrid R.: CD2v interacts with adaptor protein AP-1 during African swine fever infection. PLoS One 2015, 10, e0123714, doi: 10.1371/journal.pone.0123714.Pérez-NúñezD.García-UrdialesE.Martínez-BonetM.MaríaL.NogalM.L.BarrosoS.RevillaY.MadridR.CD2v interacts with adaptor protein AP-1 during African swine fever infectionPLoS One201510e012371410.1371/journal.pone.0123714441108625915900Open DOISearch in Google Scholar
Petrovan V., Yuan F., Li Y., Shang P., Murgia M.V., Misra S., Rowland R.R.R., Fang Y.: Development and characterization of monoclonal antibodies against p30 protein of African swine fever virus. Virus Res 2019, 269, 197632, doi: 10.1016/j.virusres.2019.05.010.PetrovanV.YuanF.LiY.ShangP.MurgiaM.V.MisraS.RowlandR.R.R.FangY.Development and characterization of monoclonal antibodies against p30 protein of African swine fever virusVirus Res201926919763210.1016/j.virusres.2019.05.01031129172Open DOISearch in Google Scholar
Pomeranz L.E., Reynolds A.E., Hengartner C.J.: Molecular biology of pseudorabies virus: impact on neurovirology and veterinary medicine. Microbiol Mol Biol Rev 2005, 69, 462–500, doi: 10.1128/MMBR.69.3.462–500.2005.PomeranzL.E.ReynoldsA.E.HengartnerC.J.Molecular biology of pseudorabies virus: impact on neurovirology and veterinary medicineMicrobiol Mol Biol Rev20056946250010.1128/MMBR.69.3.462–500.2005Open DOISearch in Google Scholar
Quembo C.J., Jori F., Vosloo W., Heath L.: Genetic characterization of African swine fever virus isolates from soft ticks at the wildlife/domestic interface in Mozambique and identification of a novel genotype. Transbound Emerg Dis 2018, 65, 420–431, doi: 10.1111/tbed.12700.QuemboC.J.JoriF.VoslooW.HeathL.Genetic characterization of African swine fever virus isolates from soft ticks at the wildlife/domestic interface in Mozambique and identification of a novel genotypeTransbound Emerg Dis20186542043110.1111/tbed.12700587339528921895Open DOISearch in Google Scholar
Reis A.L., Abrams C.C., Goatley L.C., Netherton C., Chapman D.G., Sanchez-Cordon P., Dixon L.K.: Deletion of African swine fever virus interferon inhibitors from the genome of a virulent isolate reduces virulence in domestic pigs and induces a protective response. Vaccine 2016, 34, 4698–4705, doi: 10.1016/j.vaccine.2016.08.011.ReisA.L.AbramsC.C.GoatleyL.C.NethertonC.ChapmanD.G.Sanchez-CordonP.DixonL.K.Deletion of African swine fever virus interferon inhibitors from the genome of a virulent isolate reduces virulence in domestic pigs and induces a protective responseVaccine2016344698470510.1016/j.vaccine.2016.08.011501289127521231Open DOISearch in Google Scholar
Rodriguez F., Alcaraz C., Eiras A., Yáñez R.J., Rodriguez J.M., Alonso C., Rodriguez J.F., Escribano J.M.: Characterization and molecular-basis of heterogeneity of the African swine fever virus envelope protein P54. J Virol 1994, 68, 7244–7252, doi: 10.1128/JVI.68.11.7244-7252.1994.RodriguezF.AlcarazC.EirasA.YáñezR.J.RodriguezJ.M.AlonsoC.RodriguezJ.F.EscribanoJ.M.Characterization and molecular-basis of heterogeneity of the African swine fever virus envelope protein P54J Virol1994687244725210.1128/JVI.68.11.7244-7252.19942371647933107Open DOISearch in Google Scholar
Rodríguez I., Nogal M.L., Redrejo-Rodríguez M., Bustos M.J., Salas M.L.: The African swine fever virus virion membrane protein pE248R is required for virus infectivity and an early postentry event. J Virol 2009, 83, 12290–12300, doi: 10.1128/JVI.01333-09.RodríguezI.NogalM.L.Redrejo-RodríguezM.BustosM.J.SalasM.L.The African swine fever virus virion membrane protein pE248R is required for virus infectivity and an early postentry eventJ Virol200983122901230010.1128/JVI.01333-09278671919793823Open DOISearch in Google Scholar
Rodríguez J.M., García-Escudero R., Salas M.L., Andrés G.: African swine fever virus structural protein p54 is essential for the recruitment of envelope precursors to assembly sites. J Virol 2004, 78, 4299–4313, doi: 10.1128/jvi.78.8.4299-4313.2004.RodríguezJ.M.García-EscuderoR.SalasM.L.AndrésG.African swine fever virus structural protein p54 is essential for the recruitment of envelope precursors to assembly sitesJ Virol2004784299431310.1128/jvi.78.8.4299-4313.200437426615047843Open DOISearch in Google Scholar
Rodríguez J.M., Yáñez R.J., Almazán F., Viñuela E., Rodriguez J.F.: African swine fever virus encodes a CD2 homolog responsible for the adhesion of erythrocytes to infected cells. J Virol 1993, 67, 5312–5320, doi: 10.1128/jvi.67.9.5312-5320.1993.RodríguezJ.M.YáñezR.J.AlmazánF.ViñuelaE.RodriguezJ.F.African swine fever virus encodes a CD2 homolog responsible for the adhesion of erythrocytes to infected cellsJ Virol1993675312532010.1128/jvi.67.9.5312-5320.19932379308102411Open DOISearch in Google Scholar
Rosell C., Segalés J., Ramos-Vara J.A., Folch J.M., Rodríguez-Arrioja G.M., Duran C.O., Balasch M., Plana-Durán J., Domingo M.: Identification of porcine circovirus in tissues of pigs with porcine dermatitis and nephropathy syndrome. Vet Rec 2000, 146, 40–43, doi: 10.1136/vr.146.2.40.RosellC.SegalésJ.Ramos-VaraJ.A.FolchJ.M.Rodríguez-ArriojaG.M.DuranC.O.BalaschM.Plana-DuránJ.DomingoM.Identification of porcine circovirus in tissues of pigs with porcine dermatitis and nephropathy syndromeVet Rec2000146404310.1136/vr.146.2.4010678809Open DOISearch in Google Scholar
Ruiz-Gonzalvo F., Rodríguez F., Escribano J.M.: Functional and immunological properties of the baculovirus-expressed hemagglutinin of African swine fever virus. Virology 1996, 218, 285–289, doi: 10.1006/viro.1996.0193.Ruiz-GonzalvoF.RodríguezF.EscribanoJ.M.Functional and immunological properties of the baculovirus-expressed hemagglutinin of African swine fever virusVirology199621828528910.1006/viro.1996.01938615037Open DOISearch in Google Scholar
Sánchez E.G., Pérez-Núñez D., Revilla Y.: Development of vaccines against African swine fever virus. Virus Res 2019, 265, 150–155, doi: 10.1016/j.virusres.2019.03.022.SánchezE.G.Pérez-NúñezD.RevillaY.Development of vaccines against African swine fever virusVirus Res201926515015510.1016/j.virusres.2019.03.02230922809Open DOISearch in Google Scholar
Sánchez-Cordón P.J., Chapman D., Jabbar T., Reis A.L., Goatley L., Netherton C.L., Taylor G., Montoya M., Dixon L.: Different routes and doses influence protection in pigs immunised with the naturally attenuated African swine fever virus isolate OURT88/3. Antiviral Res 2017, 138, 1–8, doi: 10.1016/j.antiviral.2016.11.021.Sánchez-CordónP.J.ChapmanD.JabbarT.ReisA.L.GoatleyL.NethertonC.L.TaylorG.MontoyaM.DixonL.Different routes and doses influence protection in pigs immunised with the naturally attenuated African swine fever virus isolate OURT88/3Antiviral Res20171381810.1016/j.antiviral.2016.11.021524508627908827Open DOISearch in Google Scholar
Sanford B., Holinka L.G., O’Donnell V., Krug P.W., Carlson J., Alfano M., Carrillo C., Wu P., Lowe A., Risatti G.R., Gladue D.P., Borca M.V.: Deletion of the thymidine kinase gene induces complete attenuation of the Georgia isolate of African swine fever virus. Virus Res 2016, 213, 165–171, doi: 10.1016/j.virusres.2015.12.002.SanfordB.HolinkaL.G.O’DonnellV.KrugP.W.CarlsonJ.AlfanoM.CarrilloC.WuP.LoweA.RisattiG.R.GladueD.P.BorcaM.V.Deletion of the thymidine kinase gene induces complete attenuation of the Georgia isolate of African swine fever virusVirus Res201621316517110.1016/j.virusres.2015.12.00226656424Open DOISearch in Google Scholar
Schirtzinger E.E., Suddith A.W., Hause B.M., Hesse R.A.: First identification of porcine parvovirus 6 in North America by viral metagenomic sequencing of serum from pigs infected with porcine reproductive and respiratory syndrome virus. Virol J 2015, 12, 170, doi: 10.1186/s12985-015-0401-6.SchirtzingerE.E.SuddithA.W.HauseB.M.HesseR.A.First identification of porcine parvovirus 6 in North America by viral metagenomic sequencing of serum from pigs infected with porcine reproductive and respiratory syndrome virusVirol J20151217010.1186/s12985-015-0401-6460908926475593Open DOISearch in Google Scholar
Shibahara T., Sato K., Ishikawa Y., Kadota K.: Porcine circovirus induces B lymphocyte depletion in pigs with wasting disease syndrome. J Vet Med Sci 2000, 62, 1125–1131, doi: 10.1292/jvms.62.1125.ShibaharaT.SatoK.IshikawaY.KadotaK.Porcine circovirus induces B lymphocyte depletion in pigs with wasting disease syndromeJ Vet Med Sci2000621125113110.1292/jvms.62.112511129853Open DOISearch in Google Scholar
Simón-Mateo C., Andrés G., Almazán F., Viñuela E.: Proteolytic processing in African swine fever virus: evidence for a new structural polyprotein, pp62. J Virol 1997, 71, 5799–5804, doi: 10.1128/JVI.71.8.5799-5804.1997.Simón-MateoC.AndrésG.AlmazánF.ViñuelaE.Proteolytic processing in African swine fever virus: evidence for a new structural polyprotein, pp62J Virol1997715799580410.1128/JVI.71.8.5799-5804.19971918349223468Open DOISearch in Google Scholar
Simón-Mateo C., Andrés G., Viñuela E.: Polyprotein processing in African swine fever virus: a novel strategy of gene expression for a DNA virus. EMBO J 1993, 12, 2977–2987, doi: 10.1002/j.1460-2075.1993.tb05960.x.Simón-MateoC.AndrésG.ViñuelaE.Polyprotein processing in African swine fever virus: a novel strategy of gene expression for a DNA virusEMBO J1993122977298710.1002/j.1460-2075.1993.tb05960.x4135538335009Open DOISearch in Google Scholar
Sorden S.D.: Update on porcine circovirus and postweaning multisystemic wasting syndrome (PMWS). Swine Health Prod 2000, 8, 133–136.SordenS.D.Update on porcine circovirus and postweaning multisystemic wasting syndrome (PMWS)Swine Health Prod20008133136Search in Google Scholar
Streck, A.F., Canal C.W., Truyen U.: Molecular epidemiology and evolution of porcine parvoviruses. Infect Genet Evol 2015, 36, 300–306, doi: 10.1016/j.meegid.2015.10.007.StreckA.F.CanalC.W.TruyenU.Molecular epidemiology and evolution of porcine parvovirusesInfect Genet Evol20153630030610.1016/j.meegid.2015.10.00726453771Open DOISearch in Google Scholar
Suárez C., Gutiérrez-Berzal J., Andrés G., Salas M.L., Rodríguez J.M.: African swine fever virus protein p17 is essential for the progression of viral membrane precursors toward icosahedral intermediates. J Virol 2010, 84, 7484–7499, doi: 10.1128/JVI.00600-10.SuárezC.Gutiérrez-BerzalJ.AndrésG.SalasM.L.RodríguezJ.M.African swine fever virus protein p17 is essential for the progression of viral membrane precursors toward icosahedral intermediatesJ Virol2010847484749910.1128/JVI.00600-10289761020504920Open DOISearch in Google Scholar
Sun H.C., Jenson J., Dixon L.K., Parkhouse R.M.E.: Characterization of the African swine fever virion protein j18L. J Gen Virol 1996, 77, 941–946, doi: 10.1099/0022-1317-77-5-941.SunH.C.JensonJ.DixonL.K.ParkhouseR.M.E.Characterization of the African swine fever virion protein j18LJ Gen Virol19967794194610.1099/0022-1317-77-5-9418609490Open DOISearch in Google Scholar
Tischer I., Rasch R., Tochtermann G.: Characterization of papovavirus- and picornavirus-like particles in permanent pig kidney cell lines. Zentralbl Bakteriol Orig A 1974, 226, 153–167.TischerI.RaschR.TochtermannG.Characterization of papovavirus- and picornavirus-like particles in permanent pig kidney cell linesZentralbl Bakteriol Orig A1974226153167Search in Google Scholar
Tischer I., Gelderblom H., Vettermann W., Koch M.A.: A very small porcine virus with circular single-stranded DNA. Nature 1982, 295, 64–66, doi: 10.1038/295064a0.TischerI.GelderblomH.VettermannW.KochM.A.A very small porcine virus with circular single-stranded DNANature1982295646610.1038/295064a07057875Open DOISearch in Google Scholar
Tochetto C., Lima D.A., Varela A.P.M., Loiko M.R., Paim W.P., Scheffer C.M., Herpich J.I., Cerva C., Schmitd C., Cibulski S.P., Santos A.C., Mayer F.Q., Roehe P.M.: Full-genome sequence of porcine circovirus type 3 recovered from serum of sows with stillbirths in Brazil. Transbound Emerg Dis 2018, 65, 5–9, doi: 10.1111/tbed.12735.TochettoC.LimaD.A.VarelaA.P.M.LoikoM.R.PaimW.P.SchefferC.M.HerpichJ.I.CervaC.SchmitdC.CibulskiS.P.SantosA.C.MayerF.Q.RoeheP.M.Full-genome sequence of porcine circovirus type 3 recovered from serum of sows with stillbirths in BrazilTransbound Emerg Dis2018655910.1111/tbed.1273529027372Open DOISearch in Google Scholar
Wang L., Zhao D., Sun B., Yu M., Wang Y., Ru Y., Jiang Y., Qiao X., Cui W., Zhou H., Li Y., Xu Y., Tang L.: Oral vaccination with the porcine circovirus type 2 (PCV-2) capsid protein expressed by Lactococcus lactis induces a specific immune response against PCV-2 in mice. J Appl Microbiol 2019, 128, 74–87, doi: 10.1111/jam.14473.WangL.ZhaoD.SunB.YuM.WangY.RuY.JiangY.QiaoX.CuiW.ZhouH.LiY.XuY.TangL.Oral vaccination with the porcine circovirus type 2 (PCV-2) capsid protein expressed by Lactococcus lactis induces a specific immune response against PCV-2 in miceJ Appl Microbiol2019128748710.1111/jam.1447331574195Open DOISearch in Google Scholar
Woźniakowski G., Frączyk M., Niemczuk K., Pejsak Z.: Selected aspects related to epidemiology, pathogenesis, immunity, and control of African swine fever. J Vet Res 2016, 60, 119–125, doi: 10.1515/jvetres-2016-0017.WoźniakowskiG.FrączykM.NiemczukK.PejsakZ.Selected aspects related to epidemiology, pathogenesis, immunity, and control of African swine feverJ Vet Res20166011912510.1515/jvetres-2016-0017Open DOISearch in Google Scholar
Xiao C.T., Giménez-Lirola L.G., Jiang Y.H., Halbur P.G., Opriessnig T.: Characterization of a novel porcine parvovirus tentatively designated PPV5. PLoS One 2013, 8, e65312, doi: 10.1371/journal.pone.0065312.XiaoC.T.Giménez-LirolaL.G.JiangY.H.HalburP.G.OpriessnigT.Characterization of a novel porcine parvovirus tentatively designated PPV5PLoS One20138e6531210.1371/journal.pone.0065312367641823762339Open DOISearch in Google Scholar
Xing X., Zhou H., Tong L., Chen Y., Sun Y., Wang H., Zhang G.: First identification of porcine parvovirus 7 in China. Arch Virol 2018, 163, 209–213, doi: 10.1007/s00705-017-3585-9.XingX.ZhouH.TongL.ChenY.SunY.WangH.ZhangG.First identification of porcine parvovirus 7 in ChinaArch Virol201816320921310.1007/s00705-017-3585-929022179Open DOISearch in Google Scholar
Yáñez R.J., Rodríguez J.M., Nogal M.L., Yuste L., Enríquez C., Rodriguez J.F., Viñuela E.: Analysis of the complete nucleotide-sequence of African swine fever virus. Virology 1995, 208, 249–278, doi: 10.1006/viro.1995.1149.YáñezR.J.RodríguezJ.M.NogalM.L.YusteL.EnríquezC.RodriguezJ.F.ViñuelaE.Analysis of the complete nucleotide-sequence of African swine fever virusVirology199520824927810.1006/viro.1995.114911831707Open DOISearch in Google Scholar
Ye X., Berg M., Fossum C., Wallgren P., Blomström A.L.: Detection and genetic characterisation of porcine circovirus 3 from pigs in Sweden. Virus Genes 2018, 54, 466–469, doi: 10.1007/s11262-018-1553-4.YeX.BergM.FossumC.WallgrenP.BlomströmA.L.Detection and genetic characterisation of porcine circovirus 3 from pigs in SwedenVirus Genes20185446646910.1007/s11262-018-1553-4595186829564688Open DOISearch in Google Scholar
Youle R.J., Strasser A.: The BCL-2 protein family: opposing activities that mediate cell death. Nat Rev Mol Cell Biol 2008, 9, 47–59, doi: 10.1038/nrm2308.YouleR.J.StrasserA.The BCL-2 protein family: opposing activities that mediate cell deathNat Rev Mol Cell Biol20089475910.1038/nrm230818097445Open DOISearch in Google Scholar
Zeeuw E.J.L., Leinecker N., Herwig V., Selbitz H.J., Truyen U.: Study of the virulence and cross-neutralization capability of recent porcine parvovirus field isolates and vaccine viruses in experimentally infected pregnant gilts. J Gen Virol 2007, 88, 420–427, doi: 10.1099/vir.0.82302-0.ZeeuwE.J.L.LeineckerN.HerwigV.SelbitzH.J.TruyenU.Study of the virulence and cross-neutralization capability of recent porcine parvovirus field isolates and vaccine viruses in experimentally infected pregnant giltsJ Gen Virol20078842042710.1099/vir.0.82302-017251558Open DOISearch in Google Scholar
Zhang H.H., Hu W.Q., Li J.Y., Liu T.N., Opriessnig T., Zhou J.Y., Xiao C.T.: Novel circovirus species identified in farmed pigs designated as Porcine circovirus 4, Hunan province, China. Transbound Emerg Dis 2020, 67, 1057–1061, doi: 10.1111/tbed.13446.ZhangH.H.HuW.Q.LiJ.Y.LiuT.N.OpriessnigT.ZhouJ.Y.XiaoC.T.Novel circovirus species identified in farmed pigs designated as Porcine circovirus 4, Hunan province, ChinaTransbound Emerg Dis2020671057106110.1111/tbed.1344631823481Open DOISearch in Google Scholar
Zhang J., Fan J., Li Y., Liang S., Huo S., Wang X., Zuo Y., Cui D., Li W., Zhong Z., Zhong F.: Porcine parvovirus infection causes pig placenta tissue damage involving nonstructural protein 1 (NS1)-induced intrinsic ROS/mitochondria-mediated apoptosis. Viruses 2019, 11, 389, doi: 10.3390/v11040389.ZhangJ.FanJ.LiY.LiangS.HuoS.WangX.ZuoY.CuiD.LiW.ZhongZ.ZhongF.Porcine parvovirus infection causes pig placenta tissue damage involving nonstructural protein 1 (NS1)-induced intrinsic ROS/mitochondria-mediated apoptosisViruses20191138910.3390/v11040389652072631027293Open DOISearch in Google Scholar
Zhang X., Shu X., Bai H., Li W., Li X., Wu C., Gao Y., Wang Y., Yang K., Song C.: Effect of porcine circovirus type 2 on the severity of lung and brain damage in piglets infected with porcine pseudorabies virus. Vet Microbiol 2019, 237, 108394, doi: 10.1016/j.vetmic.2019.108394.ZhangX.ShuX.BaiH.LiW.LiX.WuC.GaoY.WangY.YangK.SongC.Effect of porcine circovirus type 2 on the severity of lung and brain damage in piglets infected with porcine pseudorabies virusVet Microbiol201923710839410.1016/j.vetmic.2019.10839431585642Open DOISearch in Google Scholar
Zhang Z., Luo Y., Zhang Y., Guo K.: Enhanced protective immune response to PCV2 adenovirus vaccine by fusion expression of Cap protein with InvC in pigs. J Vet Sci 2019, 20, e35, doi: 10.4142/jvs.2019.20.e35.ZhangZ.LuoY.ZhangY.GuoK.Enhanced protective immune response to PCV2 adenovirus vaccine by fusion expression of Cap protein with InvC in pigsJ Vet Sci201920e3510.4142/jvs.2019.20.e35666920931364320Open DOISearch in Google Scholar
Zhao X., Xiang H., Bai X., Fei N., Huang Y., Song X., Zhang H., Zhang L., Tong D.: Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation. Vir J 2016, 13, 26, doi: 10.1186/s12985-016-0480-z.ZhaoX.XiangH.BaiX.FeiN.HuangY.SongX.ZhangH.ZhangL.TongD.Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulationVir J2016132610.1186/s12985-016-0480-z475502326880103Open DOISearch in Google Scholar
