Inhibition of porcine reproductive and respiratory syndrome virus by interferon-gamma and recovery of virus replication with 2-aminopurine |
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Authors: | R R R Rowland B Robinson J Stefanick T S Kim L Guanghua S R Lawson D A Benfield |
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Institution: | (1) Department of Biology-Microbiology, South Dakota State University, Brookings, South Dakota, U.S.A., US;(2) Department of Veterinary Science, South Dakota State University, Brookings, South Dakota, U.S.A., US |
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Abstract: | Summary. Porcine reproductive and respiratory syndrome virus (PRRSV) belongs to a group of RNA viruses that establish persistent infections.
A proposed strategy for evading immunity during persistent PRRSV infection is by preventing the induction of IFN activity
in pigs and/or by blocking the activation of antiviral proteins in permissive cells. IFN-γ mRNA expression was observed in
the lymph nodes and lungs of pigs infected with wild-type PRRSV strain SDSU-23983. Pretreatment of MARC-145 cells with IFN-γ
inhibited wild-type (SDSU-23983 P6) and culture-adapted (SDSU-23983 P136) PRRS viruses in a dose-dependent manner and at relatively
low concentrations. The effect of IFN-γ on virus replication included reductions in the number of infected cells, virus yield,
and RNA content in single cells. Virus replication was partially restored by the addition of 2-aminopurine (2-AP), an inhibitor
of dsRNA inducible protein kinase (PKR). The addition of 2-AP also restored the viral RNA content per cell to near normal
levels, suggesting that inhibition of viral RNA synthesis was through PKR. The principal difference between P6 and P136 isolates
was the recovery of P136 replication with lower concentrations of 2-AP. Immunostaining with anti-PKR antibody showed a redistribution
of PKR from the cytoplasm into nucleoli of infected cells.
Received March 7, 2000 Accepted August 16, 2000 |
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