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Porcine circovirus 2

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Postweaning multisystemic wasting syndrome

3. Introduction

Porcine Circovirus (PCV) is a single stranded DNA virus (class II), that is non-enveloped with an un-segmented circular genome. The viral capsid is icosahedral and approximately 17 nm in diameter. PCV is a member of the virus family Circoviridae. PCV are the smallest viruses replicating autonomously in eukaryotic cells. They replicate in the nucleus of infected cells, utilising the host polymerase for genome amplification. There are 2 strains: Type 1 PCV and Type 2 PCV. It is still unclear whether type 2 PCV (first isolated in 1997) actually causes PMWS, as infection with the virus alone causes no clinical signs, it appears to work synergistically with parvovirus, perhaps with parvovirus activating a latent form of circovirus or weakening the immune system enough for PCV to take hold. PCV1 and PCV2 show a high degree of sequence identity and a similar genomic organisation; nevertheless, the basis of the distinct pathogenicity has not yet been unravelled (Wiki: Porcine circovirus).

4. Microbial Pathogenesis

PCV2 binds to heparin sulfate and chondroitin sulfate, which are glycosaminoglycans (GAGs), as a 1st step of attachment. However, as PCV2 is found in cells that lack GAGs, it is thought that another coreceptor is also used for viral entry. The hallmark lesion of PCV2 infection is lymphoid depletion with histiocytic replacement. In affected lymph organs, dendritic cells, and macrophages that replace the lymphocytes contain large amounts of PCV2 virus. There is no viral degradation in these cells, and because dendritic cells are highly mobile, it is thought that dendritic mobility may be a method of viral dissemination in tissues. It is still unknown how PCV2 causes a reduction in lymphocytes. Hypotheses include induced apoptosis, decreased lymphocyte production in the bone marrow, or reduced lymphocyte proliferation in secondary lymphoid tissue (Gillespie et al., 2009).

5. Host Protective Immunity

Because most breeding age sows are seropositive for PCV2, most piglets are born with maternal antibodies against PCV2. In weaned piglets, the mean half life of antibodies is 19 days. Antibody levels will wane at 4–6 weeks in pigs with initially low levels of antibody, at 6–10 weeks with moderate antibody levels, and by 8.5–13.5 weeks in pigs with high antibody levels. Piglets do not typically demonstrate clinical signs of disease before 4 weeks of age, suggesting that maternally derived antibodies are protective. Experimental studies found that maternal antibody protection is dependent on the level of maternal antibodies present. High levels of maternal antibodies are more protective than low levels, but do not completely prevent infection, whereas low levels of antibodies did not provide any protection against infection (Gillespie et al., 2009).

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