The devastating effects of HIV infection worldwide are reason enough for AIDS researchers to grasp at thin rays of hope. But seldom has a single anecdotal case stimulated as much hope as the 1999 report of an acutely infected patient who appeared to control HIV replication after two short treatment interruptions . This report generated the hypothesis that early antiretroviral treatment (during or very soon after symptomatic seroconversion) allows the incompletely damaged immune system to recover and respond appropriately to virus antigens during treatment interruptions. This, in turn, according to the hypothesis, leads to control of viral replication by a healed and appropriately stimulated immune response to the patient's HIV infection.
Consistent with this hypothesis was the prior finding that early antiretroviral therapy led to induction of HIV-specific proliferative responses similar to those that had been observed in patients with long-term, non-progressing HIV . This led Rosenberg and colleagues to ask whether HIV-specific proliferative responses were a necessary and sufficient cause of long-term non-progression or just an immunologic consequence of controlled virus replication. Their report of virologic control in patients who interrupted therapy after early treatment raised hope that if HIV infection was treated early enough, the immune system could be repaired sufficiently to allow for long-term immunologic control of HIV replication . Unfortunately, that's where the good news ends.