Early Events in Herpes Simplex Virus Lifecycle with Implications for an Infection of Lifetime



Sarah Salameh1, 3, Urmi Sheth1, 3, Deepak Shukla*, 1, 2
1 Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois at Chicago, 60612, USA
2 Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, 60612, USA
3 Illinois Mathematics and Science Academy, 1500 Sullivan Rd., Aurora, IL 60506-1000, USA


Article Metrics

CrossRef Citations:
0
Total Statistics:

Full-Text HTML Views: 513
Abstract HTML Views: 352
PDF Downloads: 121
Total Views/Downloads: 986
Unique Statistics:

Full-Text HTML Views: 322
Abstract HTML Views: 231
PDF Downloads: 100
Total Views/Downloads: 653



© Salameh et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Ophthalmology and Visual Sciences (M/C 648), University of Illinois at Chicago, 1855 W. Taylor Street, Chicago, IL 60612, USA; Tel: 312-355-0908; E-mail: dshukla@uic.edu


Abstract

Affecting a large percentage of human population herpes simplex virus (HSV) types -1 and -2 mainly cause oral, ocular, and genital diseases. Infection begins with viral entry into a host cell, which may be preceded by viral “surfing” along filopodia. Viral glycoproteins then bind to one or more of several cell surface receptors, such as herpesvirus entry mediator (HVEM), nectin-1, 3-O sulfated heparan sulfate (3-OS HS), paired immunoglobulin-like receptor α, and non-muscle myosin-IIA. At least five viral envelope glycoproteins participate in entry and these include gB, gC, gD and gH-gL. Post-entry, these glycoproteins may also facilitate cell-to-cell spread of the virus, which helps in the evasion of physical barriers as well as several components of the innate and adaptive immune responses. The spread may be facilitated by membrane fusion, movement across tight junctions, transfer across neuronal synapses, or the recruitment of actin-containing structures. This review summarizes some of the recent advances in our understanding of HSV entry and cell-to-cell spread.

Keywords: HSV, viral entry, glycoproteins, membrane fusion, viral surfing..