Preferential replication of FIV in activated CD4⁺CD25⁺T cells independent of cellular proliferation

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• 作者：Joshi ; Anjali ; Vahlenkamp ; Thomas W. ; Garg ; Himanshu ; Tompkins ; Wayne A.F. ; Tompkins ; Mary B.
• 关键词：FIV ; HIV ; AIDS ; Latency ; Stimulation ; Anergy ; Apoptosis ; Reservoir
• 刊名：Virology
• 出版年：2004
• 出版时间：April 10, 2004
• 年：2004
• 卷：321
• 期：2
• 页码：307-322
• 全文大小：724 K

文摘

Studies attempting to identify reservoirs of HIV-1 latency have documented that the virus persists as both a latent and productive infection in subsets of CD4⁺ cells. Reports regarding establishment of a stable HIV-1 infection in quiescent T cells in vitro, however, are controversial. In the present study, we investigated the susceptibility of naive and activated CD4⁺ cell subsets (distinguished by differential expression of CD25) to feline immunodeficiency virus (FIV) infection, their ability to replicate the virus, and potentially act as a reservoir for virus persistence in infected animals. While both CD4⁺CD25⁺ and CD4⁺CD25⁻ cells are susceptible to FIV infection in vitro and in vivo, only CD4⁺CD25⁺ cells produce infectious virions when cultured with interleukin-2 (IL-2). Latently infected CD4⁺CD25⁻ cells produce infectious virions following ConcanvalinA (ConA) stimulation, which correlates with upregulated surface expression of CD25. In contrast to CD4⁺CD25⁻ cells, CD4⁺CD25⁺ cells remain unresponsive to mitogen stimulation and are relatively resistant to apoptosis whether or not infected with FIV. The ability of CD4⁺CD25⁺ cells to replicate FIV efficiently in the presence of IL-2 but remain anergic and unresponsive to apoptotic signaling suggests that these cells may provide a reservoir of productive FIV infection. On the contrary, CD4⁺CD25⁻ cells seem to establish as latent viral reservoirs capable of being reactivated after stimulation.