Document 0053 DOCN M9480053 TI Ability of HIV to promote a TH1 to TH0 shift and to replicate preferentially in TH2 and TH0 cells [see comments] DT 9410 AU Maggi E; Mazzetti M; Ravina A; Annunziato F; de Carli M; Piccinni MP; Manetti R; Carbonari M; Pesce AM; del Prete G; et al; Division of Clinical Immunology and Allergy, University of; Florence, Italy. SO Science. 1994 Jul 8;265(5169):244-8. Unique Identifier : AIDSLINE MED/94294788 CM Comment in: Science 1994 Jul 8;265(5169):193-4 AB Both interferon gamma (IFN-gamma) produced by T helper 1 (TH1) lymphocytes and interleukin-4 (IL-4) produced by TH2 lymphocytes were reduced in either bulk circulating mononuclear cells or mitogen-induced CD4+ T cell clones from the peripheral blood of individuals infected with human immunodeficiency virus (HIV). There was a preferential reduction in clones producing IL-4 and IL-5 in the advanced phases of infection. However, enhanced proportions of CD4+ T cell clones producing both TH1-type and TH2-type cytokines (TH0 clones) were generated from either skin-infiltrating T cells that had been activated in vivo or peripheral blood T cells stimulated by antigen in vitro when cells were isolated from HIV-infected individuals. All TH2 and most TH0 clones supported viral replication, although viral replication was not detected in any of the TH1 clones infected in vitro with HIV. These results suggest that HIV (i) does not induce a definite TH1 to TH2 switch, but can favor a shift to the TH0 phenotype in response to recall antigens, and (ii) preferentially replicates in CD4+ T cells producing TH2-type cytokines (TH2 and TH0). DE Acquired Immunodeficiency Syndrome/IMMUNOLOGY Cell Line Cells, Cultured Human HIV/*PHYSIOLOGY HIV Infections/*IMMUNOLOGY/MICROBIOLOGY HIV Seropositivity/IMMUNOLOGY Immunologic Memory Interferon Type II/*BIOSYNTHESIS Interleukin-4/BIOSYNTHESIS Interleukin-5/BIOSYNTHESIS Interleukins/*BIOSYNTHESIS Lymphocyte Transformation Phenotype Support, Non-U.S. Gov't T-Lymphocytes, Helper-Inducer/*IMMUNOLOGY/MICROBIOLOGY Virus Replication JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).