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ARS Home » Pacific West Area » Pullman, Washington » Animal Disease Research » Research » Publications at this Location » Publication #297940
Title: Contributions of herpes simplex virus type 1 envelope proteins to entry by endocytosis

Author
item TRI KOMALA, SARI - Washington State University
item PRITCHARD, SUZANNE - Washington State University
item CUNHA, CRISTINA - Washington State University
item WUDIRI, GEORGE - Washington State University
item AGUILAR, HECTOR - Washington State University
item Taus, Naomi
item NICOLA, ANTHONY - Washington State University

Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/10/2013
Publication Date: 12/18/2013
Citation: Tri Komala, S., Pritchard, S.M., Cunha, C.W., Wudiri, G.A., Aguilar, H.C., Taus, N.S., Nicola, A.V. 2013. Contributions of herpes simplex virus type 1 envelope proteins to entry by endocytosis. Journal of Virology. 87(24):13922-13926.

Interpretive Summary: Herpes simplex virus (HSV) entry into cells is a complex process and relies on multiple proteins located on the surface of the virus particle. There are four viral proteins known to be required for entry by the pathway referred to as direct penetration. However, additional specific proteins needed for an alternative pathway known as endocytic entry are unknown. This study used HSVs missing one of seven different viral proteins to determine whether any of them had a role in endocytic entry. All of the viruses entered cells, thus the same four viral proteins needed for direct penetration may also be sufficient for endocytic entry, which is different from the way other herpesviruses use multiple entry pathways.

Technical Abstract: Herpes simplex virus (HSV) proteins specifically required for endocytic entry but not direct penetration have not been identified. HSVs deleted of gE, gG, gI, gJ, gM, UL45, or Us9 entered cells via either pH-dependent or pH-independent endocytosis and were inactivated by mildly acidic pH. Thus, the required HSV glycoproteins, gB, gD, and gH-gL, may be sufficient for entry regardless of entry route taken. This may be distinct from entry mechanisms employed by other human herpesviruses.