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.
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