Hoshino, Y., Pesnicak, L., Straus, S.E. and Cohen, J.I. (2009) Impairment in Reactivation of a Latency Associated Transcript (LAT)-Deficient HSV-2 Is Not Solely Dependent on the Latent Viral Load or the Number of CD8+ T Cells Infiltrating the Ganglia. Virology, 387, 193-199.
https://doi.org/10.1016/j.virol.2009.02.004

has been cited by the following article:

• TITLE: The Role, Mechanism and Transcriptional Regulation of LAT in Herpes Simplex Virus Latency and Reactivation

  AUTHORS: Ying Zhang, Yingying Wang, Junting Cheng, Wenqi Cai, Ziwen Han, Yang Zhou, Qi Huang, Moyu Wang, Xiaochun Peng, Xianwang Wang, Zhaowu Ma, Ying Xiang, Hongwu Xin

  KEYWORDS: Herpes Simplex Virus (HSV), Oncolytic Herpes Simplex Virus (oHSV), Latency-Associated Transcript (LAT), Reactivation, Immediate-Early Gene (IE Gene)

  JOURNAL NAME: Yangtze Medicine, Vol.4 No.1, March 10, 2020

  ABSTRACT: Herpes simplex virus (HSV) infection in the human body can be latent in neurons for long time and be reactivated leading to recurrence at high rate. Currently there is no effective clinical strategy for the prevention and treatment of the disease relapse. HSV LAT gene is expressed in large quantities and lytic genes are turned off leading to HSV latency. Disruption of the gene expression is thought to cause HSV reactivation and disease relapse. To reveal the essence of HSV latency and reactivation, we summarized and innovatively classified the role, mechanism and transcriptional regulation of LAT in HSV latency and reactivation. This review may have important implications for future studies on HSV latency and reactivation, HSV disease prevention and treatment, and safer and more effective oncolytic HSVs (oHSVs).