Cellular and viral requirements for rapid endocytic entry of herpes simplex virus

Journal of Virology
Anthony V Nicola, Stephen E Straus

Abstract

It was recently demonstrated that herpes simplex virus (HSV) successfully infects Chinese hamster ovary (CHO) cells expressing glycoprotein D (gD) receptors and HeLa cells by an endocytic mechanism (A. V. Nicola, A. M. McEvoy, and S. E. Straus, J. Virol. 77:5324-5332, 2003). Here we define cellular and viral requirements of this pathway. Uptake of intact, enveloped HSV from the cell surface into endocytic vesicles was rapid (t(1/2) of 8 to 9 min) and independent of the known cell surface gD receptors. Following uptake from the surface, recovery of intracellular, infectious virions increased steadily up to 20 min postinfection (p.i.), which corresponds to accumulation of enveloped virus in intracellular compartments. There was a sharp decline in recovery by 30 min p.i., suggesting loss of the virus envelope as a result of capsid penetration from endocytic organelles into the cytosol. In the absence of gD receptors, endocytosed virions did not successfully penetrate into the cytosol but were instead transported to lysosomes for degradation. Inhibitors of phosphatidylinositol (PI) 3-kinase, such as wortmannin, blocked transport of incoming HSV to the nuclear periphery and virus-induced gene expression but had no effect on virus bi...Continue Reading

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Citations

Oct 15, 2009·Amino Acids·Manjula Kalia, Shahid Jameel
Oct 29, 2013·Journal of Medicinal Chemistry·Marco CantisaniStefania Galdiero
Feb 17, 2007·Nature Reviews. Microbiology·Boerries Brandenburg, Xiaowei Zhuang
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