Open AccessCD8+ cells from asymptomatic human immunodeficiency virus-infected individuals suppress superinfection of their peripheral blood mononuclear cells
Author(s) -
Edward Barker,
Katharine N. Bossart,
Christopher P. Locher,
Bruce K. Patterson,
Jay A. Levy
Publication year - 1996
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/0022-1317-77-12-2953
Subject(s) - superinfection , biology , peripheral blood mononuclear cell , virology , asymptomatic , human immunodeficiency virus (hiv) , virus , cd8 , immunology , peripheral blood , immune system , medicine , in vitro , pathology , genetics
Most human immunodeficiency virus (HIV)-infected individuals show evidence of infection by only one strain of the virus despite possible frequent contact with multiple strains. The reason(s) for the emergence of a dominant strain of virus in HIV-infected people and the mechanism(s) which prevent other strains from establishing an infection is not known. In the present study, we demonstrate that peripheral blood mononuclear cells (PBMC) of asymptomatic HIV-infected individuals can resist productive infection by HIV-1 and HIV-2 strains. Although the PBMC of these individuals are resistant to superinfection, their CD4+ cells are susceptible to infection. Moreover, two weeks after infection of their PBMC in culture, the superinfecting virus can be recovered from isolated CD4+ cells. When CD8+ cells from asymptomatic individuals are added to the superinfected CD4+ cells, replication of the exogenously introduced virus is inhibited. In contrast, PBMC from individuals who have progressed to disease (Progressors) do not resist superinfection and their CD8+ cells do not showthe antiviral activity which controls productive HIV infection. These findings suggest that CD8+ cells suppressing HIV replication in infected individuals may be critical in preventing the establishment of infection by other strains of HIV by blocking virus replication.