Role of CD4+CD25+ and CD4+CD25- T Cells in Feline Immunodeficiency Virus Infection.

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Title: Role of CD4+CD25+ and CD4+CD25- T Cells in Feline Immunodeficiency Virus Infection.
Author: Joshi, Anjali
Advisors: Dr. Wayne Tompkins, Committee Chair
Abstract: Treatment of HIV infected individuals with HAART reduces the levels of plasma viral loads to below the limit of detection by standard clinical assays. HAART however, does not result in virus eradication as a small but detectable virus reservoir persists in all individuals receiving therapy. 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+ T cells. However, reports regarding establishment of a stable HIV-1 infection in quiescent T cells in vitro remain controversial. In the present study, we investigated the susceptibility of naive (CD4+CD25-) and activated (CD4+CD25+) feline T cells to 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 in the absence of a strong mitogenic stimulus like ConA. In contrast to CD4+CD25- cells, CD4+CD25+ cells display the key characteristics of Treg cells in that they remain unresponsive to mitogenic stimulation, and are relatively resistant to apoptosis. Mechanisms regulating infection of these cells revealed that CD4+CD25- cells are less susceptible to FIV infection, both at the level at viral entry and cellular transcriptional activity. 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. CD4+CD25- cells, on the contrary, seem to establish as latent viral reservoirs capable of being reactivated after stimulation.
Date: 2005-01-30
Degree: PhD
Discipline: Immunology

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