Once an individual is infected with herpes simplex virus (HSV), the virus establishes a latent infection in sensory neurons. Periodically, various stimuli may induce lytic reactivation resulting in mild recurrent lesions to more severe disease. The factors which determine the establishment of latency and reactivation are poorly understood. However, considering the requirements for the viral IE gene products in productive infection, it is likely that the regulation of this latency-reactivation cycle is dependent upon the components which regulate the expression of the IE genes. The critical component of this regulatory process is HCF-1. Analyses of this protein in a mouse model have shown that the protein is specifically sequestered in the cytoplasm of sensory neurons and rapidly transported to the nucleus in response to reativation stimuli. ? ? Recent work has resulted in the establishment of a primary sensory neuronal cell culture which allowed for the specific localization of HCF-1 in the cytoplasm. Additional studies have determined that the nuclear transport of HCF-1 in latently infected neurons correlates with viral reactivation.
| Whitlow, Zackary; Kristie, Thomas M (2009) Recruitment of the transcriptional coactivator HCF-1 to viral immediate-early promoters during initiation of reactivation from latency of herpes simplex virus type 1. J Virol 83:9591-5 |
| Nogueira, Mauricio L; Wang, Victoria E H; Tantin, Dean et al. (2004) Herpes simplex virus infections are arrested in Oct-1-deficient cells. Proc Natl Acad Sci U S A 101:1473-8 |
| Vogel, J L; Kristie, T M (2000) The novel coactivator C1 (HCF) coordinates multiprotein enhancer formation and mediates transcription activation by GABP. EMBO J 19:683-90 |
| Kristie, T M; Vogel, J L; Sears, A E (1999) Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency. Proc Natl Acad Sci U S A 96:1229-33 |
