Important note: Information in this article was accurate in February 1999. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, February 22, 1999
Daniel J. DeNoon, Senior Editor
The studies were presented in a session devoted to cell-mediated immunity at the 6th Conference on Retroviruses and Opportunistic Infections, held January 31-February 4, 1999, in Chicago, Illinois.
In two of the studies, researchers essentially drained off monkeys' CD8(+) T cells by giving them potent anti-CD8 monoclonal antibodies.
In animals chronically infected with simian immunodeficiency virus (SIV), the loss of T cells resulted in a rapid increase in viral load that declined only when CD8(+) cells began to reappear. In animals infected with SIV within six days of CD8(+) cell depletion, most failed to develop anti-HIV immune responses and had rapid disease progression.
"These results demonstrate conclusively that CD8 cells play a crucial role in suppressing SIV replication in vivo," said Xia Jin of the Aaron Diamond AIDS Research Center, New York. "CD8 cells have a major influence on viral setpoint."
Among the chronically infected animals studied by Jin et al., two of three animals with undetectable virus load had the huge increases in viral load seen in other animals. But one of these monkeys maintained an undetectable viral load even in the absence of CD8(+) cells. How the animal managed to do this is not yet understood.
Further evidence on the dynamics of CD8(+) lymphocyte control of HIV came from Harvard researcher J. Schmitz, who depleted monkeys of CD8(+) cells six days before or six days after pathogenic SIV infection.
Initially, the peak levels of viremia after infection did not differ from control animals. But the CD8 depleted animals had a much different disease course. Those who were slow to recover their CD8(+) T-cell responses had the shortest survival. Those with more rapid recovery of CD8(+) T-cell responses still had shorter survival times than control animals.
When Schmitz et al. repeated the experiment in monkeys with chronic SIV infection, they obtained results similar to those of the ADARC team with all animals exhibiting a 4 log[10] increase in viral load.
"These observations provide direct evidence for the role of CD8(+) lymphocytes in controlling AIDS virus replication in primary and chronic infection," Schmitz et al. concluded.
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