Important note: Information in this article was accurate in March 1999. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, March 1, 1999
Daniel J. DeNoon, Senior Editor
AIDS surveillance by the U.S. Centers for Disease Control and Prevention (CDC) has turned up several people who test negative on most FDA-licensed HIV screening assays and on the usually-definitive Western blot assay.
It had been feared that these rare individuals were infected with a mutant virus that was extremely adept at hiding from the immune system - and from HIV tests. But extensive studies by CDC researcher D.L. Ellenberger and colleagues suggest that this is not the case.
"These data suggest that the lack of a detectable antibody response may be a result of immune dysfunction rather than viral factors," they suggested.
Ellenberger reported the findings in a poster presentation to the 6th Conference on Retroviruses and Opportunistic Infections, held January 31-February 4, 1999, in Chicago, Illinois.
AIDS case surveillance identified several HIV infected persistently seronegative (HIPS) patients. Infections could be confirmed in all of these cases by PCR or other diagnostic methods.
Ellenberger et al. studied six of these persistently seronegative individuals. Interestingly, four of the six had measurable serum antibodies to one or more common pathogens.
But in vitro stimulation of two patients' peripheral blood mononuclear cells (PBMC) could not elicit HIV specific antibody production, although potent T-dependent and direct B-cell mitogens were used. These tests readily elicited HIV specific antibody from the PBMC of a person who remained asymptomatic despite longstanding HIV infection (a long-term nonprogressor). Similarly, in vitro stimulation of PBMC with the cytokines IL-4 and IL-12 failed to elicit anti-HIV antibodies despite eliciting marked T-cell proliferation.
Analysis of viral isolates from all six patients showed they were infected with clade B isolates. Analysis of sequences from structural and regulatory genes showed no specific mutations. Thus Ellenberger et al. concluded that even though most of the HIPS patients made antibody to another antigen, they shared an immune incompetence responsible for failure to produce anti-HIV antibody.
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