E. Scala et al., C-C CHEMOKINES, IL-16, AND SOLUBLE ANTIVIRAL FACTOR ACTIVITY ARE INCREASED IN CLONED T-CELLS FROM SUBJECTS WITH LONG-TERM NONPROGRESSIVE HIV-INFECTION, The Journal of immunology, 158(9), 1997, pp. 4485-4492
A combination of three beta, or C-C, chemokines, as well as IL-16, hav
e been shown to inhibit HIV replication in vitro. Cellular antiviral f
actor is a more potent agent, and acts on all HIV strains. All are mai
nly, but not exclusively, produced by CD8(+) T cells, both in HIV+ and
healthy subjects. We studied the production of these HIV-suppressive
factors in patients with HIV infection at different stages of disease,
No difference in production by PBMC stimulated with PHA has been obse
rved in asymptomatic HIV+, long-term nonprogressors (LTnP), and AIDS p
atients. When T cell line supernatants from these three groups were st
udied, no significant difference was found for C-C chemokines or IL-16
production, and viral suppression. However, T cell clones from LTnP s
ecreted higher levels of all three chemokines, IL-16, and exerted a st
ronger inhibition on HIV replication. CD8(+) clones showed a higher pr
oduction than CD4(+) clones. These clones were able to produce all ant
iviral factors irrespective of the secretion of type 1 or type 2 cytok
ines, The antiviral activities were not correlated, implying that vira
l suppression did not depend solely on C-C chemokines or IL-16. We pos
tulate that all factors are needed to prevent HIV disease progression.