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ARS Home » Pacific West Area » Pullman, Washington » Animal Disease Research » Research » Publications at this Location » Publication #288431
Title: Molecular requirement for sterols in herpes simplex virus entry and infectivity

Author
item WUDIRI, G.A. - Washington State University
item PRITCHARD, S.M. - Washington State University
item Li, Hong
item LIU, J - Rocky Mountain Laboratory
item AGUILAR, H.C. - Washington State University
item GILK, S.D. - Washington State University
item NICOLA, A.V. - Washington State University

Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/11/2014
Publication Date: 12/2/2014
Citation: Wudiri, G., Pritchard, S., Li, H., Liu, J., Aguilar, H., Gilk, S., Nicola, A. 2014. Molecular requirement for sterols in herpes simplex virus entry and infectivity. Journal of Virology. 88(23):13918-13922.

Interpretive Summary: Herpes simplex virus (HSV) has been proposed to enter human epithelial cells via endocytosis and neurons by direct penetration at the plasma membrane. However, the selection of entry route is complex and multifactorial. Cholesterol-altering agents inhibiting HSV entry have been observed, but the mechanistic role of host cholesterol in HSV entry remains unclear. This study is designed to determine the role of cell cholesterol in direct fusion of HSV with the cell surface and entry by virion endocytosis. The results showed that HSV successfully entered DHCR24-/-cells, which lack a desmosterol-to-cholesterol conversion enzyme, indicating entry can occur independently of cholesterol. Depletion of desmosterol from these cells resulted in diminished HSV-1 entry, suggesting a general sterol requirement for HSV-1 entry and that desmosterol can operate in virus entry. Cholesterol functioned more effectively than desmosterol, suggesting that the hydrocarbon tail of cholesterol influences viral entry.

Technical Abstract: Herpes simplex virus 1 (HSV-1) required cholesterol for virion-induced membrane fusion. HSV successfully entered DHCR24-/-cells, which lack a desmosterol-to-cholesterol conversion enzyme, indicating entry can occur independently of cholesterol. Depletion of desmosterol from these cells resulted in diminished HSV-1 entry, suggesting a general sterol requirement for HSV-1 entry and that desmosterol can operate in virus entry. Cholesterol functioned more effectively than desmosterol, suggesting that the hydrocarbon tail of cholesterol influences viral entry.