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Thyroid hormone (T 3 ) has been suggested to play a role in herpes simplex virus 1 (HSV-1) replication. It was previously reported that HSV-1 replication was suppressed by T 3 in mouse neuroblastoma cells overexpressing thyroid hormone receptor β1 (TRβ1). Using a human neuro-endocrine cells LNCaP differentiated by androgen deprivation, HSV-1 replication was active but decreased by T 3 at very low moi, probably due to low copy of TRβ1. In this study, a recombinant HSV-1 was constructed expressing TRβ1 (HSV-1/TRβ1). Infection of Vero cells (very little TRβ1 expression) with HSV-1/TRβ1 exhibited increased replication in the presence of T 3 compared to the counterpart without TRβ1 overexpression. Interestingly, HSV-1/TRβ1 infection of differentiated LNCaP cells showed strong suppression of viral replication by T 3 and the removal of hormone did not fully reversed the suppression as was observed in parent virus. Quantitative analyses indicated that ICP0 expression was blocked using HSV-1/TRβ1 for infection during T 3 washout, suggesting that overexpression of TRβ1 is likely to delay its inhibitory effect on viral gene expression. Together these results emphasized the importance of TRβ1 in the regulation of HSV-1 replication in differentiated environment with neuronal phenotype.

journal of neurovirology

Overexpression of thyroid hormone receptor β1 altered thyroid hormone-mediated regulation of herpes simplex virus-1 replication in differentiated cells