ABSTRACT
Both arms of the immune system, humoral and cell-mediated, are invoked in response to infection by HIV. The humoral response, involving both immunoglobulin M (IgM) and IgG, is detectable within weeks of acute infection and IgG antibodies generally persist throughout the individual’s life. High levels of HIV-specific IgA can be found in the gut secretions and breast milk. Antibodies are directed against the structural, regulatory and enzymatic elements of the virus. Some of the envelope-reactive antibodies have neutralizing activity; that is, they can block viral infection. The part played by neutralizing antibodies in the pathogenesis of HIV infection has been a matter of controversy in the past, largely as a result of variation of assay systems from one laboratory to another. Greater standardization of laboratory tests in recent years has produced a clearer picture of the true role of the antibody in HIV infection. However, there are still pitfalls. Neutralization assays against laboratory-adapted strains of the virus give different results for the same tests performed against autologous virus isolated from the patient or ‘near patient’ isolates from other individuals. Vaccineinduced antibodies usually only neutralize the virus strain which was used for vaccination, and are not cross-neutralizing with other isolates. It is unlikely that antibodies have any role in protection from cell-cell transmission of HIV (via the fusion of infected and uninfected cells), which may be the main way in which HIV is spread once infection is established in vivo. However, antibodies in secretions may prevent the initial infection. The stimulation of secretory antibodies by local vaccination is of great interest. The communication of Blymphocytes between all sites of mucosa-associated lymphoid tissue (MALT) means that vaccination at one site leads to a generalized response [1].
