Porcine Circovirus 2 Prevalence and Host-cell Interaction.

摘要

Porcine Circovirus type 2 (PCV2) is a small, non-enveloped virus with a single-stranded DNA genome. It causes a variety of disease syndromes collectively referred as Porcine Circovirus Associated Disease (PCVAD) and has been identified in most swine producing countries worldwide. The mechanism of pathogenesis is unclear, though it is believed that high viral loads contribute to histological lesions. The prevalence of PCV1 and PCV2 infection and exposure in the U.S. finishing swine herd was studied. The results revealed that over 82% of sera from 185 farms were positive for PCV2 by PCR, whereas only 2.4% were positive for PCV1. More than 80% of PCV2 DNA-positive swine were also positive for anti-PCV2 antibodies. PCV1 was only rarely present. Since PCV2 is widespread in in swine population, an in vitro cell culture system was developed to study PCV2-host cell interaction. R1BL cells were highly permissive and more effective for PCV2 growth than commonly used PK-15 cells. Genome-wide transcriptional profiling of R1BL cells in the presence and absence of PCV2 infection was performed to gain molecular insights into the PCV2-host cell interaction. R1BL cells were characterized as endothelial cells based on the expression of endothelial specific genes. A total of 214 genes were differentially expressed in all three infected libraries. A strong host response was observed with the induction of multiple genes involved in interferon beta (IFN beta)-induced innate antiviral, pro-inflammatory and adaptive immune responses. These genes include IFN , ZDBP, DDX60, Mx2, OAS1, Mx1, OAS2, IFI27, IFI44, IRF1, IRF7, IRF9, IFIT1, IFIT2, IFIT3, CCL10, and CCL5. Other differentiallay expressed genes were involved in various biological and molecular functions such as transcription, cell signaling and apoptosis. Taken together, the results suggest that the strong innate immune response itself may contribute to the pathogenesis of PCV2, but surprisingly does not stimulate an effective adaptive immune response.