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Herpes simplex virus type 1 can either suppress or enhance human immunodeficiency virus type 1 replication in CD4‐positive T lymphocytes
Author(s) -
Calistri Arianna,
Parolin Cristina,
Palù Giorgio
Publication year - 2003
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10350
Subject(s) - virology , herpes simplex virus , superinfection , biology , coinfection , virus , transactivation , hsl and hsv , viral replication , multiplicity of infection , immunology , gene , gene expression , biochemistry
Abstract It was proposed recently that CEM CD4‐positive T cells infected chronically by herpes simplex virus type 1 (HSV‐1) and human immunodeficiency virus type 1 (HIV‐1) (CEM HSV/HIV ) may be used as a model for studying HIV/HSV interactions. To ascertain whether HSV‐HIV coinfection of T lymphocytes has a role in promoting progression of lentiviral infection, T cells infected chronically by either HSV‐1 (CEM HSV ) or HIV‐1 (CEM HIV ) were challenged with a superinfecting dose of HIV‐1 or HSV‐1. The results show a positive influence on HIV growth when CEM HIV cells were superinfected with HSV‐1 to an extent that was dependent on the multiplicity of superinfection used. In contrast, HIV superinfection of CEM HSV cells resulted in a delay of HIV‐1 production and in a lack of HSV‐mediated LTR transactivation. These effects were due to cell growth inhibition and apoptosis, resulting from persistent HSV‐1 infection. Treatment of CEM HSV with acyclovir inhibited completely the HSV‐1 cytopathic effects and allowed efficient HIV‐1 replication. These data may be relevant in clarifying the role of HIV/HSV interaction in the pathogenesis of AIDS. J. Med. Virol. 70:163–170, 2003. © 2003 Wiley‐Liss, Inc.