Six newborn rhesus macaques were experimentally infected with pathogen
ic Simian immunodeficiency virus of macaques (SIVmac251), and three ne
wborn macaques were infected with avirulent SIVmac1A11. The former dev
eloped rapidly fatal simian AIDS and died within 26 wk of age, whereas
the latter remained clinically normal. Infant monkeys that developed
rapidly progressive disease had rapid declines in CD4(+) cells and wer
e unable to mount IgG and IgA antibody responses to SIV or to an unrel
ated antigen, tetanus toxoid. IgM antibody responses were near normal
to both SIV-specific and nonspecific antigens. Cytotoxic T lymphocyte
(CTL) responses to SN envelope were observed in animals infected with
either virulent or avirulent SIV. These studies demonstrated that viru
lent SIVmac infection induced a rapid immunosuppression that was both
SIV-specific and nonspecific in nature. The observation that virulent
strains of SIV can rapidly induce a global immunosuppression provides
one explanation for the rapid disease course in some HIV-infected chil
dren and supports the strategy of early and vigorous antiviral drug th
erapy to alter the disease course even if this does not prevent infect
ion.