       Document 0127
 DOCN  M9650127
 TI    Relation between changes in cellular load, evolution of viral phenotype,
       and the clonal composition of virus populations in the course of human
       immunodeficiency virus type 1 infection.
 DT    9605
 AU    Koot M; van 't Wout AB; Kootstra NA; de Goede RE; Tersmette M;
       Schuitemaker H; Department of Clinical Viro-Immunology, Netherlands Red
       Cross; Blood Transfusion Service, University of Amsterdam, Netherlands.
 SO    J Infect Dis. 1996 Feb;173(2):349-54. Unique Identifier : AIDSLINE
       MED/96162092
 AB    The relationship between the evolution of human immunodeficiency virus
       type 1 (HIV-1) biologic phenotype, changes in the proportion of infected
       peripheral blood mononuclear cells, and the relative contribution of
       non-syncytium-inducing (NSI) and syncytium-inducing (SI) HIV-1 variants
       to virus load was studied during the course of HIV-1 infection. In 65
       HIV-1-infected subjects, the proportion of infected CD4 T cells was
       higher in persons who carried SI variants. Longitudinal studies revealed
       that the emergence of SI HIV-1 variants can occur at relatively low
       numbers of HIV-1-infected cells. Emergence of SI variants frequently
       coincided with an increase of virus load due to an expansion of both NSI
       and SI variants, although the contribution of SI viruses to the total
       virus population significantly increased with time after SI phenotype
       conversion. These data indicate that NSI to SI phenotype conversion,
       rather than resulting from high virus load, is part of the sequence of
       events that leads to increased virus load and CD4 cell depletion.
 DE    Cross-Sectional Studies  CD4 Lymphocyte Count  CD4-Positive
       T-Lymphocytes/*VIROLOGY  Giant Cells/VIROLOGY  Human  HIV
       Infections/IMMUNOLOGY/*VIROLOGY  HIV-1/*CLASSIFICATION/ISOLATION & PURIF
       Longitudinal Studies  Phenotype  Support, Non-U.S. Gov't  JOURNAL
       ARTICLE

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

