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Macaque resists SIV challenge by blocking viral replication postentry.(Brief Article)

Vaccine Weekly

| August 07, 2002 | COPYRIGHT 2002 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2002 AUG 7 - (NewsRx.com & NewsRx.net) -- by Maria G. Essig, MS, ELS, senior medical writer - A rhesus macaque resisted two intravaginal and one intrarectal challenge with SIV, yet failed to seroconvert, a result attributed to cellular inhibition by CD4+ T cells.

"Elucidation of the host factors which influence susceptibility to human immunodeficiency virus or simian immunodeficiency virus (SIV) infection and disease progression has important theoretical and practical implications," commented B. Peng and colleagues at the National Cancer Institute.

The investigators challenged a macaque (identified as 359) being used as a vaccine control animal with two successive intravaginal deliveries of the highly pathogenic SIV[subscript]mac251, but no seroconversion occurred. A third challenge with SIV[subscript]mac32H done intrarectally also failed to provoke an SIV infection.

Peng and collaborators able to detect viral RNA (10[superscript]6 copies/mL) in the plasma only at 2 weeks after the challenge, could isolate virus and detect proviral DNA only 8 weeks postchallenge. The macaque cleared SIV naturally and continued to be seronegative.

When blood and lymph node cells collected from the macaque 49 weeks after the intrarectal challenge were given to another, naive animal, the naive macaque did not develop SIV infection (Rhesus macaque resistance to mucosal simian immunodeficiency virus infection is associated with a postentry block in viral replication. Journal of Virology, 2002;76(12):6016-6026).

In vivo and in vitro investigations indicated that "the resistance of macaque 359 to SIV infection was not due to a high level of CD8+ suppressor activity but to an inherent resistance of its CD4+ T cells," said Peng et al. No ...

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