OBJECTIVES: To study herpes simplex virus (HSV) growth in human T lymphocytes (Jurkat cells) with and without phytohemagglutinin (PHA) activation and to investigate the possible mechanism of viral growth. METHODS: The levels of HSV-1 production and adsorption were determined by plaque titration assay. The number of HSV-1-infected cells was assayed using flow cytometry. The expression of herpesvirus entry mediator A (HveA) mRNA was detected by RT-PCR. RESULTS: HSV-1 production as well as the number of HSV-1-infected Jurkat cells were enhanced after the cells were activated by PHA. Moreover, the amount of viral entry was demonstrated to increase in PHA-activated cells. An increase in HveA mRNA was observed in PHA-activated Jurkat cells. CONCLUSIONS: We found that HSV-1 can replicate in human T lymphocytes, and the replication was increased following PHA activation. This finding may be due to an increase in viral entry via HveA receptor. Copyright 2004 S. Karger AG, Basel
OBJECTIVES: To study herpes simplex virus (HSV) growth in human T lymphocytes (Jurkat cells) with and without phytohemagglutinin (PHA) activation and to investigate the possible mechanism of viral growth. METHODS: The levels of HSV-1 production and adsorption were determined by plaque titration assay. The number of HSV-1-infected cells was assayed using flow cytometry. The expression of herpesvirus entry mediator A (HveA) mRNA was detected by RT-PCR. RESULTS:HSV-1 production as well as the number of HSV-1-infected Jurkat cells were enhanced after the cells were activated by PHA. Moreover, the amount of viral entry was demonstrated to increase in PHA-activated cells. An increase in HveA mRNA was observed in PHA-activated Jurkat cells. CONCLUSIONS: We found that HSV-1 can replicate in human T lymphocytes, and the replication was increased following PHA activation. This finding may be due to an increase in viral entry via HveA receptor. Copyright 2004 S. Karger AG, Basel