CONSERVED T-CELL RECEPTOR REPERTOIRE IN SIMIAN IMMUNODEFICIENCY VIRUS-INFECTED RHESUS-MONKEYS

Citation
Zw. Chen et al., CONSERVED T-CELL RECEPTOR REPERTOIRE IN SIMIAN IMMUNODEFICIENCY VIRUS-INFECTED RHESUS-MONKEYS, The Journal of immunology, 151(4), 1993, pp. 2177-2187
Citations number
37
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
151
Issue
4
Year of publication
1993
Pages
2177 - 2187
Database
ISI
SICI code
0022-1767(1993)151:4<2177:CTRRIS>2.0.ZU;2-C
Abstract
Studies to assess the possibility that the HIV may encode a superantig en that plays a role in the depletion of functional CD4+ lymphocytes i n the infected individual have yielded discrepant results. The problem in performing conclusive examinations of this issue may be attributed , at least in part, to the difficulty of prospectively studying indivi duals from before their infection until the time of profound CD4+ lymp hocyte loss. To determine whether the AIDS virus deletes particular su bpopulations of Vbeta-expressing lymphocytes, we have employed an anim al model of AIDS, the simian immunodeficiency virus (SIV)-infected mac aque monkey. Rhesus monkeys were experimentally infected with SIV(mac) and studied prospectively. A PCR-based quantitative method for assess ing TCR repertoire was employed to analyze the expression of 24 Vbeta and 30 Valpha gene families in the monkeys. Although circulating PBL w ere increased in number by 3 wk after SIV(mac) infection, the expanded lymphocyte populations exhibited no significant perturbation in their TCR Vbeta repertoires. PBL obtained from monkeys before and 0.5 to 3 years after infection displayed no significant change in Vbeta and Val pha gene family expression. Finally, no deletion of Vbeta-expressing c ell subpopulations could be demonstrated in purified CD4+ lymphocytes from infected monkeys. This was true even for monkeys whose blood cont ained less than 200 CD4+ lymphocytes/mul. These results indicate that the TCR repertoire is conserved in SIV(mac)-infected rhesus monkeys an d suggests that mechanisms other than superantigen-induced deletion mu st be responsible for CD4+ lymphocyte loss in these animals.