A Herpes Simplex Virus 1 Recombinant Lacking the Glycoprotein G Coding Sequences Is Defective in Entry through Apical Surfaces of Polarized Epithelial Cells in Culture and in vivo

A Herpes Simplex Virus 1 Recombinant Lacking the Glycoprotein G Coding Sequences Is Defective in Entry through Apical Surfaces of Polarized Epithelial Cells in Culture and in vivo

During infection of a new host, the first surfaces encountered by herpes simplex viruses are the apical membranes of epithelial cells of mucosal surfaces. These cells are highly polarized, and the protein composition of their apical and basolateral membranes are very different, so that different vir...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS Vol. 97; no. 4; pp. 1818 - 1822
Main Authors: Tran, Lorren C., Kissner, Jennifer M., Westerman, Larry E., Sears, Amy E.
Format: Journal Article
Language:English
Published: United States National Academy of Sciences of the United States of America 15-02-2000
National Acad Sciences
National Academy of Sciences
The National Academy of Sciences
Subjects:
Animals
Biological Sciences
Cell culture techniques
Cell Division
Cell Line
Cell lines
Cells
Cultured cells
Dogs
Epithelial cells
Eye - virology
Female
glycoprotein G
Glycoproteins
Glycoproteins - genetics
Herpes simplex virus 1
Herpes viruses
Herpesvirus 1, Human - genetics
Human herpesvirus 1
Infections
Membrane proteins
Mice
Mice, Inbred Strains
Microbiology
Mutation
Proteins
Vero cells
Viral Envelope Proteins - genetics
Virus Replication
Viruses
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Summary:During infection of a new host, the first surfaces encountered by herpes simplex viruses are the apical membranes of epithelial cells of mucosal surfaces. These cells are highly polarized, and the protein composition of their apical and basolateral membranes are very different, so that different viral entry pathways have evolved for each surface. To determine whether the viral glycoprotein G (gG) is specifically required for efficient infection of a particular surface of polarized cells, apical and basal surfaces were infected with wild-type virus or a gG deletion mutant. After infection of polarized cells in culture, the gG-virus was deficient in infection of apical surfaces but was able to infect cells through basal membranes, replicate, and spread into surrounding cells. The gG-dependent step in apical infection was a stage beyond attachment. After in vivo infection of apical surfaces of epithelial cells of nonscarified mouse corneas, infection by glycoprotein C-or gG-virus was considerably reduced as compared with that observed after infection with wild-type virus. In contrast, when corneas were scarified, allowing virus access to other cell surfaces, the gG and glycoprotein C deletion mutants infected eyes as efficiently as wild-type viruses. A secondary mutation allowing infection of apical surfaces by gG-virus arose readily during passage of the virus in nonpolarized cells, indicating that either the gG-dependent step of apical infection can be bypassed or that another viral protein can acquire the same function.
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To whom reprint requests should be addressed at: 1510 Clifton Road, Atlanta, GA 30322. E-mail: sears@microbio.emory.edu.
Communicated by Bernard Roizman, The University of Chicago, Chicago, IL
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.020510297