Document 0050
 DOCN  M9460050
 TI    [Mechanisms of lymphopenia in HIV infection]
 DT    9404
 AU    Roger PM; Pradier C; Dellamonica P; Service des Maladies infectieuses et
       tropicales, Hopital de; l'Archet, Nice.
 SO    Presse Med. 1994 Jan 22;23(2):89-94. Unique Identifier : AIDSLINE
       MED/94188330
 AB    Blood counts of CD4 cells remain the best prognostic factor in patients
       infected with human immunodeficiency virus (HIV). However, the small
       number of infected cells contrasts with the importance of lymphocyte
       depletion. Several mechanisms might explain this depletion including:
       antibody-dependent cytotoxicity. Twenty to 50% of the antibodies
       produced in vitro by B lymphocytes are directed against HIV antigens,
       especially the gp120 and gp41 viral envelope antigen. If this
       cytotoxicity effect occurs in vivo, it could reduce of lymphocytes
       carrying the viral genome and partially explain the major lymphopenia in
       HIV-infected patients. It is not yet known whether the long-term effect
       of these antibodies is immunoprotective or deleterious, but they may
       play a protective role at least in the initial stages of the disease.
       autoimmunity. Sequence homology between the HLA II molecules and the
       glycoproteins of the viral envelope has been clinically and biologically
       documented in many manifestations of HIV infection. It has been
       suggested that alloreactivity, similar to the graft-versus-host reaction
       could be involved. In addition, programmed cell-death of the CD4
       lymphocytes appears to be overactivated in HIV-positive subjects,
       possibly because the gp120 viral antigen perturbs the CD4-dependent
       signal for cell death. deleterious effects of cytokines. Tumour necrosis
       factor, for example, is known to play a role in the regulation of viral
       replication; it may favour the destruction of contaminated cells but
       also the initiation of provirus replication and integration into the
       cell genome. supra-antigens and/or infectious factors. Supra-antigenes,
       which can link with HLA molecules, are capable of oligoclonal activation
       without being processed in the cell presenting the antigen. This
       activation might affect cell death. Certain germ toxins could also play
       a role as cofactors. Cohort studies of asymptomatic HIV patients are
       needed to improve our understanding of these mechanisms. A therapeutic
       approach tailored to the stage reached by HIV-infected subjects will
       then be possible.
 DE    Acquired Immunodeficiency Syndrome/*IMMUNOLOGY  Antigens, CD4/IMMUNOLOGY
       Apoptosis/IMMUNOLOGY  Autoimmunity/IMMUNOLOGY  AIDS-Related
       Opportunistic Infections/IMMUNOLOGY  English Abstract  Human  HIV
       Infections/*COMPLICATIONS/IMMUNOLOGY  HIV-1/DRUG
       EFFECTS/IMMUNOLOGY/*PATHOGENICITY  Lymphopenia/*ETIOLOGY/IMMUNOLOGY
       T-Lymphocytes, Cytotoxic/IMMUNOLOGY  T4 Lymphocytes/IMMUNOLOGY  JOURNAL
       ARTICLE  REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).