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
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.