       Document 0386
 DOCN  M9610386
 TI    Oligoclonal CD8 lymphocytes from persons with asymptomatic human
       immunodeficiency virus (HIV) type 1 infection inhibit HIV-1 replication.
 DT    9601
 AU    Toso JF; Chen CH; Mohr JR; Piglia L; Oei C; Ferrari G; Greenberg ML;
       Weinhold KJ; Department of Pathology, Duke Center for AIDS Research,
       Duke; University Medical Center, Durham, North Carolina 27710-2996,;
       USA.
 SO    J Infect Dis. 1995 Oct;172(4):964-73. Unique Identifier : AIDSLINE
       MED/96029362
 AB    CD8 lymphocytes from asymptomatic human immunodeficiency virus (HIV)
       type 1-infected patients can suppress virus production from infected CD4
       cells. Suppressive activity is separate and distinct from cytotoxic T
       lymphocyte (CTL) reactivities and is likely mediated by a soluble
       factor(s). The majority of HIV-1 suppression studies have been done in
       the context of bulk CD8 cell cultures. In this study, viral suppression
       was characterized by clonal populations of CD8 cells derived from
       HIV-1-infected patients. Most of the suppressive clones were devoid of
       detectable CTL reactivity against env-, gag-, pol-, and nef-expressing
       targets. Among the suppressive clones derived from an individual
       patient, a marked heterogeneity was evident with respect to phenotypic
       markers, cytokine production, and T cell receptor V beta expression.
       These results suggest that noncytolytic virus suppression is oligoclonal
       in nature. Clones provide tools for future studies aimed at
       understanding the mechanism of suppression and identifying the
       suppressive factor.
 DE    Clone Cells  Cytokines/BIOSYNTHESIS  CD8-Positive
       T-Lymphocytes/CYTOLOGY/*IMMUNOLOGY  Human  HIV Infections/*IMMUNOLOGY
       HIV-1/DRUG EFFECTS/*GROWTH & DEVELOPMENT  Phenotype  RNA-Directed DNA
       Polymerase/ANALYSIS  Support, U.S. Gov't, P.H.S.  Suppressor Factors,
       Immunologic/*PHARMACOLOGY  T-Lymphocytes, Cytotoxic/IMMUNOLOGY  JOURNAL
       ARTICLE

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

