Presentation by Tina Dillas ('18) delivered at the Rhodes College Undergraduate Research and Creative Activity Symposium (URCAS).Herpes simplex virus 1 (HSV-1) is a neuroinvasive human pathogen that evades host immune
responses and results in life-long infection. Primary infections generally occur around the mouth
and lips from viral transmission though oral secretions. Following infection, HSV-1 spreads to
the host nervous system and establishes latency. The virus’s ability to reactivate infection
depends on the site of infection, virus strain, and host immunity. HSV-1 infection normally
causes mild symptoms; however, in rare cases the virus enters the central nervous system and, if
untreated, can lead to fatal encephalitis. The purpose of this study was to explore genetic
variation in HSV-1 and consider how frequently differences that may contribute to central
nervous system virulence occur in circulating viral strains.Twenty-two HSV strains were
obtained from collaborators at the Centers for Disease Control and Prevention. These strains
vary in their neurovirulence as determined previously in mouse studies. Here, we assessed
variation in the DNA sequences of two viral genes designated UL39 and UL53 (encoding
ribonucleotide reductase and glycoprotein K, respectively) due to their involvement in HSV-1
neurovirulence. Sequences of these genes from the twenty-two viral strains were compared to
identify variations that correlate with high or low neurovirulence
