OBJECTIVES: To explore the host transcription factor E2F-1 and/or any mechanisms that may support viral entry and its effect on the HSV-1 production in anti-CD3-activated Jurkat cells. METHODS: The expressions of ICP4, HVEM and E2F-1 were studied using reverse transcription-PCR and Western blot. HSV-1 production was determined by plaque titration assay and HSV-1 DNA load was quantified by real-time PCR. The viral uptake was observed by electron microscopy. RESULTS: In anti-CD3-activated Jurkat cells, there was a significant increase in the HSV-1 production. The expression of ICP4 mRNA after HSV-1 infection occurred 2 h prior to the synthesis of the ICP4 protein, which was significantly higher in activated than nonactivated T cells. There were no significant differences in the expressions of E2F-1 mRNA. The HVEM expression was positively correlated with the HSV-1 DNA in the activated T cells. From the electron micrograph, the formations of filopodia were observed only in HSV-1-infected, activated cells. CONCLUSIONS: High expressions of viral receptor protein and filopodia formations are the key factors that enhance the HSV-1 entry into activated T lymphocytes, resulting in an increased production of the virus.
OBJECTIVES: To explore the host transcription factor E2F-1 and/or any mechanisms that may support viral entry and its effect on the HSV-1 production in anti-CD3-activated Jurkat cells. METHODS: The expressions of ICP4, HVEM and E2F-1 were studied using reverse transcription-PCR and Western blot. HSV-1 production was determined by plaque titration assay and HSV-1 DNA load was quantified by real-time PCR. The viral uptake was observed by electron microscopy. RESULTS: In anti-CD3-activated Jurkat cells, there was a significant increase in the HSV-1 production. The expression of ICP4 mRNA after HSV-1 infection occurred 2 h prior to the synthesis of the ICP4 protein, which was significantly higher in activated than nonactivated T cells. There were no significant differences in the expressions of E2F-1 mRNA. The HVEM expression was positively correlated with the HSV-1 DNA in the activated T cells. From the electron micrograph, the formations of filopodia were observed only in HSV-1-infected, activated cells. CONCLUSIONS: High expressions of viral receptor protein and filopodia formations are the key factors that enhance the HSV-1 entry into activated T lymphocytes, resulting in an increased production of the virus.