A number of physiological factors have been suggested to participate in the Herpes Simplex Virus Type-1 (HSV-1) reactivation. Of particular interest is the effect of hormonal aberration on gene expression and activati...A number of physiological factors have been suggested to participate in the Herpes Simplex Virus Type-1 (HSV-1) reactivation. Of particular interest is the effect of hormonal aberration on gene expression and activation. Thyroid hormone (TH) was shown to play a role in HSV-1 gene expression and replication in cell culture and animal models. We hypothesize that TH participates in the control of HSV latency and reactivation in humans by regulating viral gene expression and replication. Prior to implementing a full-scale population-based inquiry into this hypothesis, a pilot study using a pharmacy claims data base and a case-controlled, retrospective cohort preliminary investigation was conducted to develop further the hypothetical link between TH and HSV-1 reactivation. Using prescriptions for treating thyroid disorders and HSV-1 infections as proxies for biologic functions, we queried a prescription data base to construct two patient cohorts: Cohort 1 was comprised of patients receiving prescription drugs for thyroid disorders over a three-month period, and Cohort 2 was composed of patients not receiving thyroid medications during this period. HSV-1 medications were recorded for each cohort and the difference in the frequency of HSV-1 prescription drug utilization was examined for statistical significance. Using a 2 × 2 contingency table, a chi-square of 10.12 was calculated that was significant at p = 0.0015, confirming that a significant difference was found in HSV-1 utilization between these two cohorts, suggesting that patients who receive thyroid drugs have a greater chance of receiving antiviral drugs for HSV-1 infection/reactivation. Since this pilot study has inherent limitations in the data set, this finding is descriptive, not explanatory, and further research involving more detailed patient records in a larger patient population will be implemented to explore the relationship more robustly.展开更多
文摘A number of physiological factors have been suggested to participate in the Herpes Simplex Virus Type-1 (HSV-1) reactivation. Of particular interest is the effect of hormonal aberration on gene expression and activation. Thyroid hormone (TH) was shown to play a role in HSV-1 gene expression and replication in cell culture and animal models. We hypothesize that TH participates in the control of HSV latency and reactivation in humans by regulating viral gene expression and replication. Prior to implementing a full-scale population-based inquiry into this hypothesis, a pilot study using a pharmacy claims data base and a case-controlled, retrospective cohort preliminary investigation was conducted to develop further the hypothetical link between TH and HSV-1 reactivation. Using prescriptions for treating thyroid disorders and HSV-1 infections as proxies for biologic functions, we queried a prescription data base to construct two patient cohorts: Cohort 1 was comprised of patients receiving prescription drugs for thyroid disorders over a three-month period, and Cohort 2 was composed of patients not receiving thyroid medications during this period. HSV-1 medications were recorded for each cohort and the difference in the frequency of HSV-1 prescription drug utilization was examined for statistical significance. Using a 2 × 2 contingency table, a chi-square of 10.12 was calculated that was significant at p = 0.0015, confirming that a significant difference was found in HSV-1 utilization between these two cohorts, suggesting that patients who receive thyroid drugs have a greater chance of receiving antiviral drugs for HSV-1 infection/reactivation. Since this pilot study has inherent limitations in the data set, this finding is descriptive, not explanatory, and further research involving more detailed patient records in a larger patient population will be implemented to explore the relationship more robustly.
