Sequence variability in UL39 and UL53 genes of Herpes simplex virus 1 may contribute to neurovirulence

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

Assessment of the activity of secondary caries lesions with short-wavelength infrared, thermal, and optical coherence tomographic imaging.

Significance: Leakage in the interfaces between restorative materials and tooth structure allows for fluid and bacterial acid infiltration, causing restoration failure due to secondary caries. Dentists spend more time replacing composite restorations than placing new ones. Previous in vitro and in vivo studies on enamel and root surfaces using shortwave-infrared (SWIR) and thermal imaging during dehydration with forced air have been promising for assessing lesion activity. Aim: We hypothesized that SWIR reflectance and thermal imaging methods can be used to monitor the activity of secondary caries lesions around composite restorations. The objective of this study was to employ these methods to measure the rate of fluid loss from lesions during dehydration with forced air to assess lesion activity. Approach: Sixty-three extracted human teeth with total of 109 suspected secondary lesions were examined using SWIR and thermal imaging during dehydration. The thickness of the highly mineralized transparent surface layer (TSL) at lesion interfaces indicative of lesion activity was measured by optical coherence tomography (OCT). Micro-computed tomography (MicroCT) was used to further confirm lesion severity and structure. OCT and MicroCT measurements of lesion structure, depth, and severity were correlated with fluid loss rates measured with SWIR reflectance and thermal imaging. Results: TSL thickness measured with OCT correlated with both SWIR reflectance and thermal measurements of rates of fluid loss ( p<0.05 ). Increasing TSL thickness led to decreased permeability of lesions, potentially indicating full lesion arrest at TSL≥70  μm . SWIR performed better than thermal imaging for secondary lesion activity assessment, although both methods performed best on smooth surface lesions. Conclusions: Nondestructive SWIR reflectance and OCT imaging methods are promising for clinically monitoring the activity of secondary caries lesions