Imagine that HIV was a “normal” virus. An infection begins and the body responds, without getting trapped in a cycle where CD4+ T cells are consumed and the immune system is crippled.
SIV can infect sooty mangabeys but it doesn't cripple their immune systems.
The attractiveness of this idea explains some of why scientists are interested in sooty mangabeys and other non-human primates. HIV’s relative SIV can infect them, but they usually don’t develop immunodeficiency.
At last week’s AIDS Vaccine 2010 conference, Cynthia Derdeyn reported her laboratory’s recent results investigating sooty mangabeys, which don’t develop high levels of neutralizing antibodies against SIV when infected. Derdeyn’s group at Emory Vaccine Center and Yerkes National Primate Research Center studies how HIV and SIV evade the immune system.
The implications of Derdeyn’s observations are sobering. Much of the AIDS vaccine research field is interested in figuring out how to goad the human immune system into producing neutralizing antibodies against HIV, with the idea that having those antibodies present pre-exposure would allow the body to keep the virus from establishing itself. However, achieving that goal has been elusive.
How sooty mangabeys are able to manage SIV infection without catastrophe is still an active area of research. In a review published in Nature Medicine, Guido Silvestri (a champion of this area of research who returned to Yerkes this year as a Georgia Research Alliance Eminent Scholar) and colleagues propose that the difference comes from an absence of CCR5, a molecule that needs to be on certain immune cells for HIV/SIV to infect them:
“It is conceivable that, in natural SIV hosts, a restriction of CCR5 expression to more activated effector and/or CD4+ T cells may confine SIV replication to a subset of more ‘expendable’ cells, thus better preserving the homeostasis of central memory CD4+ T cells despite similarly high levels of viremia.”
Scientists have found parallels in the body’s responses to other viruses. A recent Op Ed piece in the New York Times explains the idea that when the body is fighting a cold, the immune system, rather than the cold virus itself, produces most of the achy, sneezy symptoms we associate with a cold, and some people never experience those symptoms even while successfully fighting off the cold virus.
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