Viral Pathogenesis

To initiate a productive infection, a virus generally must attach to a specific receptor molecule on the host cell, cross the host cell membrane, and undergo a disassembly event, thereby exposing its genome to the host cell machinery. A better understanding of these events in the viral replication cycle will augment researchers' ability to develop agents that can prevent viral infections and, at a more basic level, will further the understanding of protein:protein interactions. To address these issues, undergraduate research assistants and I are characterizing a series of reovirus mutants that exhibit increased resistance to ethanol. Previous genetic studies have demonstrated that the increased ethanol resistance results from a single point mutation. Presumably, this mutation increases the stability of the viral outer capsid. Our preliminary results indicate that these mutants exhibit increased resistance to a series of harsh chemical and physical agents. Currently, undergraduate researchers are in the process of confirming these findings. We also are interested in determining whether these mutant viruses exhibit altered disassembly properties in vitro and in vivo. Perhaps, the mutations conferring increased resistance to ethanol also impede the normal disassembly pathway. Finally, we hope to investigate the replication kinetics of these viruses. If the observed mutations alter the stability of the outer capsid, then the ability of these viruses to replicate may be impeded. Through these studies, we hope to gain a better understanding of the assembly and disassembly of non-enveloped viruses. Such an increase in our knowledge of these events will further our understanding of viral pathogenesis and potentially aid in the development of anti-viral agents.

You can find out more about Dr. Wessner's research interests by visiting his homepage or contacting him by email.