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
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.
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* 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: email@example.com