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319 Detection of Mucosal Antibodies in HIV-Infected Individuals
P. Wright*, P. Kozlowski, E. Sannella, G. Rybczyk, P. Goepfert, H. Staats , T. VanCott , D. Trabattoni, and J. Mestecky
NIAID HIV Vaccine Trials Network
Background: There is data indicating that HIV-specific mucosal IgA antibodies may be impaired in HIV-infected people and important, though contradictory, evidence that IgA antibodies correlate with protection in highly exposed individuals. To determine the best approach for detection of IgA antibodies in mucosal samples a panel of rectal washes from infected and uninfected individuals was distributed to 6 investigators with experience in detection of mucosal IgA.
Methods: Rectal washes were collected from 16 HIV-infected and 14 uninfected volunteers following instillation of 100 ml of saline into the rectal vault. The infected volunteers were in good clinical and virologic control; 6 had CD4 counts below 300. Total, HIV-specific and influenzavirus-specific IgA and IgG were performed in a blinded fashion according to established protocols in each laboratory.
Results: All samples had detectable total IgA (median 68 mug/ml). Values did not vary between infected and uninfected. IgA was always dominant with concentrations >10 times IgG. Total IgA values were comparable to rectal collections using wicks. HIV-specific IgA antibodies were difficult only to detect. One laboratory identified sig. number (8/13) samples from infected subjects, i.e., with HIV-specific IgA values 2 SD above mean uninfecteds. In spite of lower total IgG, all but 1 laboratory identified the infected subjects on the basis of HIV-specific IgG. Comparable levels of influenza-specific IgA antibodies were identified in nasal secretions and in rectal secretions in both infected and uninfected volunteers.
Conclusions: There is a defect in production of HIV-specific IgA antibodies in HIV-infected individuals. Obviously many variables enter into collection and detection of mucosal antibodies, however, the observations that HIV-specific IgG antibodies and influenza IgA antibodies were seen in the rectal wash samples implies that the defect is real. This observation does not directly address whether vaccination or exposure without infection may stimulate HIV-specific IgA mucosal antibodies nor does it provide a mechanism for this defect. It does provide a strong incentive to better understand the role of mucosal immunity in HIV acquisition and the clinical course of disease.
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