17-beta estradiol promotion of herpes simplex virus type 1 reactivation is estrogen receptor dependent.
Vicetti Miguel RD1, Sheridan BS, Harvey SA, Schreiner RS, Hendricks RL, Cherpes TL.
1Graduate Program in Immunology, Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA. [corrected].
Abstract
Correlations
between estrogen and herpes simplex virus (HSV) reactivation from
latency have been suggested by numerous clinical reports, but causal
associations are not well delineated. In a murine HSV-1 corneal
infection model, we establish 17-beta estradiol (17-betaE) treatment of
latently infected ovariectomized mice induces viral reactivation, as
demonstrated by increased viral load and increased immediate-early viral
gene expression in the latently infected trigeminal ganglia (TG).
Interestingly, the increased HSV reactivation occurred in the absence of
inhibition of viral specific CD8(+) T-cell effector function. 17-betaE
administration increased HSV reactivation in CD45(+) cell-depleted TG
explant cultures, providing further support that leukocyte-independent
effects on latently infected neurons were responsible for the increased
reactivation. The drug-induced increases in HSV copy number were not
recapitulated upon in vivo treatment of latently infected estrogen
receptor alpha-deficient mice, evidence that HSV reactivation promoted
by 17-betaE was estrogen receptor dependent. These findings provide
additional framework for the emerging conceptualization of HSV latency
as a dynamic process maintained by complex interactions among multiple
cooperative and competing host, viral, and environmental forces.
Additional research is needed to confirm whether pregnancy or hormonal
contraceptives containing 17-betaE also promote HSV reactivation from
latency in an estrogen receptor-dependent manner.
J Virol. 2010 Jan;84(1):565-72. doi: 10.1128/JVI.01374-09.
http://jvi.asm.org/content/84/1/565.long
Md. Rodolfo Vicetti. Ex-miembro del GII.
