AIDSWEEKLY Plus, 3 June 1996
Daniel J. DeNoon, Senior Editor

A new finding overturns a long-held belief about the natural history of HIV infection.

Soon after a person is first infected with HIV there is a short burst of high-titer viremia. This viremia quickly subsides.

Common wisdom has held that a neutralizing antibody response is what controls the virus. According to this scenario, the subsequent escape of the virus from immune surveillance is due to mutations that permit it to avoid neutralization.

But now a French research team studying 12 patients with primary HIV infection reports that neutralizing antibodies are in no way associated with this early decline in HIV viremia.

University of Bordeaux researchers Isabelle Pellegrin and colleagues reported their findings in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology ("Kinetics of Appearance of Neutralizing Antibodies in 12 Patients with Primary or Recent HIV-1 Infection and Relationship with Plasma and Cellular Viral Loads," JAIDS, 1996;11(5):438-447).

"There is apparently no relationship between the emergence of neutralizing activity and the decrease of plasma viral load," Pellegrin et al. reported. "The clearance of the initial plasma viral load is not associated with the emergence of neutralizing antibodies and, therefore, may not be mediated by them."

The researchers suggested that non-neutralizing antibodies recognizing the HIV envelope could form immune complexes with viral particles. If such immunoglobulins fix complement, the immune complexes would bind to complement-receptor molecules in lymphoid tissues where they would be trapped.

"To analyze the immune response during primary HIV infection and to specify the antiviral effects of the host immunity, further studies on the role of CTL [cytotoxic lymphocytes] in these patients are required," they concluded. "The results may have important consequences not only for a better understanding of the pathogenesis of HIV-1 infection but also for the development of preventive or therapeutic strategies against the virus."

This work was supported by ANRS (grant 94017), DRED, and private donations.

The corresponding author for this study is Herve J.A. Fleury, Laboratoire de Virologie, Universite de Bordeaux II, 146 rue Leo Saignat, 33076 Bordeaux Cedex, France.

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