HERPES-SIMPLEX VIRUS TYPE-1 AND PSEUDORABIES VIRUS BIND TO A COMMON SATURABLE RECEPTOR ON VERO CELLS THAT IS NOT HEPARAN-SULFATE

Authors
Citation
Wc. Lee et Ao. Fuller, HERPES-SIMPLEX VIRUS TYPE-1 AND PSEUDORABIES VIRUS BIND TO A COMMON SATURABLE RECEPTOR ON VERO CELLS THAT IS NOT HEPARAN-SULFATE, Journal of virology, 67(9), 1993, pp. 5088-5097
Citations number
54
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Virology
Journal title
ISSN journal
0022-538X
Volume
67
Issue
9
Year of publication
1993
Pages
5088 - 5097
Database
ISI
SICI code
0022-538X(1993)67:9<5088:HVTAPV>2.0.ZU;2-M
Abstract
Herpes simplex virus type 1 (HSV-1) and pseudorabies virus (PRV) infec t different natural hosts but are very similar in structure, replicati ve cycle, and entry into cultured cells. We determined whether HSV-1 a nd PRV use the same cellular components during entry into Vero cells, which are highly susceptible to each virus but are not from native hos ts for either. UV-inactivated virions of either HSV-1 or PRV could sat urate cell surfaces to block infection of challenge HSV-1 or PRV. In t he presence of saturating levels for infection of either virus, radiol abeled virus bound well and in a heparin-sensitive manner. This result shows that heparan sulfate proteoglycans on Vero cells are not the li miting cellular component. To identify the virus component required fo r blocking, we used an HSV-1 null mutant virus lacking gB, gD, or gH a s blocking virus. Virions lacking gB were able to block infection of c hallenge virus to the same level as did virus containing gB. In contra st, virions lacking gD lost all and most of the ability to block infec tion of HSV-1 and PRV, respectively. HSV-1 lacking gH and PRV lacking gp50 also were less competent in blocking infection of challenge virus . We conclude that HSV-1 and PRV bind to a common receptor for infecti on of Vero cells. Although both viruses bind a heparin-like cell compo nent on many cells, including Vero cells, they also attach to a differ ent and limited cell surface component that is bound at least by HSV-1 gD and possibly gH and to some degree by PRV gp50 but not gB. These r esults clearly demonstrate binding of both HSV-1 and PRV to a common c ell receptor that is not heparan sulfate and demonstrate that several types of attachment occur for both viruses during infectious entry.