Effect of herpes simplex virus on cultured Burkitt tumor cells and its failure to influence the Epstein-Barr virus carrier state.

Abstract

Summary Various lines of blastoid cells of Burkitt tumor or leukemic origins were exposed to herpes simplex virus (HSV) in an attempt to improve or activate replication of the Epstein-Barr virus (EBV) present in a small fraction of cells in some of the cultures and not, or no longer, detectable in the others. The effects of HSV on these cell lines ranged from rapid loss (in 3–6 days), to delayed destruction (in 2–7 weeks), to transitory infection and survival. The differential behavior of the cultures was apparently unrelated to ( a ) the extents of the indigenous EBV infection, ( b ) production of autogenous interferon or other antiviral factors, and ( c ) the degrees of adsorption of HSV. The initial resistance to HSV of some of the lines and its ultimate loss remain unexplained. It is reduced temporarily when cells are exposed to HSV in the presence of diethylaminoethyl dextran. As evident from EBV-specific immunofluorescence, the HSV infection neither increased the extent of the carrier state in EBV-positive cell lines, nor did it cause the appearance of EBV antigen-containing cells in EBV-negative lines. Passage of viral progeny from HSV-infected cultures with or without addition of anti-HSV serum to monolayer cultures of human or rabbit cells failed to induce EBV antigen synthesis in the exposed cell populations.