Acute Human Immunodeficiency Virus Replication Causes a Rapid and Persistent Impairment of Vγ9Vδ2 T Cells in Chronically Infected Patients Undergoing Structured Treatment Interruption
Author(s) -
Federico Martini,
Fabrizio Poccia,
Delia Goletti,
Stefania Carrara,
Donatella Vincenti,
Gianpiero D’Offizi,
Chiara Agrati,
Giuseppe Ippolito,
Vittorio Colizzi,
Leopoldo Paolo Pucillo,
Carla Montesano
Publication year - 2002
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/342410
Subject(s) - viremia , viral replication , virology , lytic cycle , immunology , virus , biology , t cell , immunodeficiency , viral load , antigen , immune system
T cells expressing Vgamma9Vdelta2 display lytic and proliferative responses against human immunodeficiency virus (HIV)-infected cells and release antiviral soluble factors. Chronic HIV-positive patients have deep changes in the composition and function of the circulating gammadelta T cell pool that are restored by highly active antiretroviral therapy (HAART). gammadelta T cells were analyzed during the rapid plasma HIV RNA rebound in HIV-infected patients undergoing structured treatment interruption (STI). A loss in circulating Vgamma9Vdelta2 T cells was observed, indicating that acute HIV replication may influence Vgamma9Vdelta2 homeostasis. These cells were lost among CD45RA(-)CD27(-) Vgamma9Vdelta2 T cell effectors, and a significant unresponsiveness, measured as antigen-driven interferon-gamma production, was observed during STI. After HAART resumption and consequent inhibition of HIV replication, Vgamma9Vdelta2 T cell reactivity was restored both quantitatively and functionally. These observations indicate that Vgamma9Vdelta2 T cells are activated early after active HIV replication but are rapidly lost when viremia is not controlled.
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