Antibody spectrum against the viral transactivator protein in patients with human immunodeficiency virus type 1 infection and Kaposi's sarcoma

We analyzed patterns of antibody response to recombinant transactivator pro tein (human Immunodeficiency virus type 1 [HIV-1] tat) in serum samples fro m HIV-1-negative subjects (n = 60), HIV-1-infected asymptomatic patients (n = 20), HTV-1-infected patients with Kaposi's sarcoma (n = 25), and patient s with Kaposi's sarcoma without HN-I infection. None of the: healthy subjec ts possessed antitat immunoglobulin G (IgG) in their serum. AU asymptomatic patients with HN-I infection were anti-tar IgG-positive. Epitope mapping r evealed that these sera had anti-rat IgG to all the functional domains of t ar protein. Histochemical studies on lymph nodes from five asymptomatic HIV -1-infected patients showed that, in all cases, rat-positive cells were pre sent within the germinal center at the stage of follicular fragmentation co ntaining immunoblasts and small lymphocytes. Of the 25 HIV-1-infected patie nts with Kaposi's sarcoma, 4 were anti-tar TgG-positive; however, the epito pe analysis revealed that IgG to functional domains of tar protein-in parti cular to transactivating response element (TAR)binding site-were absent. Al l patients with Kaposi's sarcoma without HIV-1 infection were anti-rat IgG- negative. Presence or absence of anti-rat IgG and a prevalence of different antibody profiles in different groups of patients indicated the pathophysi ologic role of rat protein. Thus, a passive immunization with anti-tar IgG could be a useful strategy to influence the pathophysiologic state of the d isease.