Association of HTLV-III with Epstein-Barr Virus Infection and Abnormalities of T Lymphocytes in Homosexual Men

Abstract

Homosexual men were studied for associations among human T-lymphotropic virus type III (HTLV-III) infection, Epstein-Barr virus (EBV) infection, and T cell abnormalities. The presence of IgG antibody to EBV capsid antigen and antibody to EBV early antigen was significantly associated with augmented counts of suppressor T cells in healthy HTLV-III-seronegative men. HTLV-III-seropositive asymptomatic subjects had significantly enhanced titers of antibody to EBV and lower ratios of helper to suppressor T cells compared with HTLV-III-seronegative homosexual men. Of three men who seroconverted to HTLV-III, two had a greater than fourfold increase in titer of IgG antibody to EBV capsid antigen after seroconversion. These results suggest that the interaction of HTLV-III and EBV and their immunologic perturbations are significant in the natural history of this retrovirus infection in homosexual men.

Relationship between antibody production to Epstein-Barr virus (EBV) early antigens and various EBV-related diseases

“…An enhanced IgG response to EAs or VCAs has been found in homosexual men [71] and particularly in AIDS cases [70,77]. In patients developing OHL, elevated titers of VCA-specific IgG were observed, while anti-EA IgG and EBNA antibody levels resembled those of healthy non-homosexual individuals [30].…”

An Epstein-Barr virus immediate-early gene product trans-activates gene expression from the human immunodeficiency virus long terminal repeat.

“…EBV also induces fatal B-cell lymphomas in immunocompromised patients (13) and is associated with both Burkitt lymphoma and nasopharyngeal carcinoma (14,15). Homosexual men, one of the main groups at risk for HIV infection, have a 50% prevalence of active EBV infection (EBV early antigen, 21:40) even when seronegative for HIV, whereas in healthy heterosexuals the prevalence of active EBV infection is only 5% (16).…”

Immunocytochemical detection of herpes viruses in oral smears of HIV‐infected patients

“…The increased load of EBV found in the oral CS of our patients may have various consequences: since EBV itself is an effective unspecific immunostimulant it may trigger the progression of the disease by activation of CD4"^ epithelial cells and thereby coactivating latent HIV which leads to destruction of these cells (17,29), The decreasing number of CD4 eells rnay in turn favor further Bcells already latently infected by EBV to complete a full lytic cycle of viral replication without prior immunoelimination. Whether the increased finding of oral lymphomas in HIV-infected patients may be related to the inereased EBV expression (30), is yet unknown, but may well relate to similar mechanisms, CMV can be transmitted via saliva as well as through blood and sexual contact (16), After the initial replication in epithelial cells CMV takes up long-term residence in circulating leukocytes.…”

“…There is ample evidence of EBV infection in patients with AIDS (16, 17); titers of EBV-related antibodies as well as numbers of EBV-infected cells in the peripheral blood of HIV-infected patients are higher than those in HI V-seronegative healthy persons (17). While human B lymphocytes are the usual target, EBV can also infect and replicate in epithelial cells of oropharyngeal and genital sites (18)(19)(20)(21).…”