CD4+ T cells and gamma interferon in the long-term control of persistent friend retrovirus infection

被引:47
作者
Iwashiro, M [1 ]
Peterson, K [1 ]
Messer, RJ [1 ]
Stromnes, IM [1 ]
Hasenkrug, KJ [1 ]
机构
[1] NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, NIH, Hamilton, MT 59840 USA
关键词
D O I
10.1128/JVI.75.1.52-60.2001
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
We have used the Friend virus model to determine the basic mechanisms by which the immune system can control persistent retroviral infections. Previously we showed that CD4(+) T cells play an essential role in keeping persistent retrovirus in check, The present in vitro experiments with a Friend virus-specific CD4(+) T-cell clone revealed that these cells produce gamma interferon (IPN-gamma), which acts with two distinct mechanisms of antiviral activity. First, IFN-gamma had a direct inhibitory effect on virus production. This inhibitory effect was noncytolytic and, interestingly, was not associated with decreased cell surface expression of viral antigens. The second mechanism of IFN-gamma -mediated antiviral activity was an enhancement of CD4(+) T-cell-mediated cytolytic activity. We also found an in vivo role for IFN-gamma in the control of persistent Friend virus infections, Neutralization of IFN-gamma in persistently infected mice resulted in significantly increased levels of virus in the spleen, and a significant percentage of IFN-gamma -deficient mice were unable to maintain long-term control over Friend virus infections.
引用
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页码:52 / 60
页数:9
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