title: Lack of selective V beta deletion in CD4+ or CD8+ T lymphocytes and functional integrity of T-cell repertoire during acute HIV syndrome.
abstract: OBJECTIVE
  To study the V beta T-cell repertoire in peripheral blood lymphocytes (PBL) during acute HIV syndrome by using several anti-V beta monoclonal antibodies (MAb) and to analyse its functionality by stimulating PBL with superantigens (SAg) such as Staphylococcus aureus enterotoxins.
  
  
  METHODS
  Cytofluorimetric analysis of V beta T-cell-receptor expression was performed on PBL from eight patients with symptomatic, acute HIV-1 primary infection, showing a dramatic decrease of CD4+ PBL accompanied by a marked increase in activated/memory CD8+ T cells, and on 12 age- and sex-matched healthy controls. PBL were then isolated, stimulated with different SAg, anti-CD3 MAb or phytohaemagglutinin and cultured for 3 days. PBL capability to progress through cell cycle was studied by the classic cytofluorimetric method of bromodeoxyuridine incorporation and DNA staining with propidium iodide.
  
  
  RESULTS
  Despite the presence of a few expansions of some V beta families among CD8+ T lymphocytes, no gross alterations in T-cell repertoire were present in patients with acute HIV syndrome. Its functionality was maintained overall, as PBL responsiveness to SAg was well preserved. Interestingly, all CD8+ T cells, although bearing different V beta T-cell receptors, expressed marked signs of activation, i.e., CD45R0, CD38 and major histocompatibility complex class II molecules, and also high amounts of CD11a and CD18.
  
  
  CONCLUSIONS
  Our data suggest, at least in the early phases and in the acute form of the infection, that HIV is not likely to act as a SAg. However, further studies are needed to analyse other sites, such as lymph nodes, where HIV could exert other, significant effects, and to study the expression of other V beta families than those investigated here.
authors.affiliation: Department of Biomedical Sciences, University of Modena School of Medicine, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Cossarizza
authors.forename: C
authors.initials: C
authors.lastname: Ortolani
authors.forename: C
authors.initials: C
authors.lastname: Mussini
authors.forename: G
authors.initials: G
authors.lastname: Guaraldi
authors.forename: N
authors.initials: N
authors.lastname: Mongiardo
authors.forename: V
authors.initials: V
authors.lastname: Borghi
authors.forename: D
authors.initials: D
authors.lastname: Barbieri
authors.forename: E
authors.initials: E
authors.lastname: Bellesia
authors.forename: M G
authors.initials: MG
authors.lastname: Franceschini
authors.forename: B
authors.initials: B
authors.lastname: De Rienzo
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D000208:Acute Disease; D000328:Adult; D016516:CD4-CD8 Ratio; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D005260:Female; D015497:HIV-1 / Q000276:immunology*; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D007135:Immunoglobulin Variable Region / Q000276:immunology; D016130:Immunophenotyping; D008213:Lymphocyte Activation; D008297:Male; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D018089:Superantigens / Q000276:immunology
chemical_list: D006684:HLA-DR Antigens; D007135:Immunoglobulin Variable Region; D016693:Receptors, Antigen, T-Cell, alpha-beta; D018089:Superantigens