Towson University

Faculty Member, Biological Sciences

Associate Professor

Fisher College of Science and Mathematics

About

The Towson University Herpes Virus Laboratory studies multiple aspects of human and animal herpesvirus research.  Current projects involve developing better long-term therapies to treat human and veterinary alphaherpesvirus infection; basic cellular, molecular, and biochemical characterization of envelope glycoproteins of human cytomegalovirus; and characterizing oligodendrocyte infection by human herpesvirus 6.

All herpesviruses establish a latent infection that is capable of being reactivated after the host is first infected by the agent.  In the cases of the alphaherpesvirus group, these latent infections reside in ganglia, from which newly replicating virus can then cause cutaneous lesions on the locally enervated epithelia.  For herpes simplex virus-1 (HSV-1), these signs appear as recurrent cold sores and fever blisters; HSV-2 causes genital lesions; varicella zoster virus (VZV) is the etiologic agent for chicken pox and shingles; feline herpesvirus-1 (FHV) causes debilitating conjunctivitis in domestic and wild cats.  Acyclovir and valacyclovir (for HSV and VZV) or penciclovir (for FHV), dosed daily, can be used clinically to actively suppress recurrent infections.  However, these drugs have short in vivo half lives and require high patient compliance to keep suppressive levels of the drugs present at all times.  We have developed silicone-acyclovir subcutaneous implants that deliver enough daily drug consistently over the course of 3-5 years to keep recurrent outbreaks in check in vitro and in animal models.  Our studies continue, though, to examine more fully the kinetics of drug release, better assays for low-level detection of these drugs, and improvements in the engineering of the implants to extend their utility.

Human cytomegalovirus (CMV) expresses four envelope glycoproteins akin to cellular chemokine receptors, G protein-coupled receptors utilized for immune system signaling and chemoattraction.  Previous studies showed basic biology of these receptors, including presumed subcellular localization and extent of glycosylation.  Current research is geared towards a better understanding of the cell biology of these receptors, especially with regard to expression kinetics within the herpesvirus system (i.e., immediate-early, early, late), subcellular localization during all stages of viral infection (from binding of the virus to a target cell through egress of mature virions), molecular expression characteristics of specialized mRNA splicing and translation at internal start sites, and the biochemistry of post-translational modifications of these glycoproteins.

It has been hypothesized that infection with human herpesvirus-6A (and most likely not –6B; HHV-6A and HHV-6B) is linked to the clinical symptoms of multiple sclerosis (MS).  This chronic demyelinating disease is characterized by the degeneration of oligodendrocytes, glial cells that are responsible for creating and maintaining the myelin sheath around neurons.  We are studying HHV-6 infection of these cells in culture to determine their relative susceptibility to infection with either HHV-6A or –6B, and how that may relate to MS.  To determine relative infectivity and to monitor the course of infection, we are using immunofluorescence to monitor the appearance and relative levels of viral antigens expressed during immediate early, early, and late stages of infection.  We expect that quantifying the levels of these various viral proteins will help us determine whether HHV-6 may be more credibly linked to MS, and whether that link involves infection of oligodendrocytes.

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