Termination of Transcription of LAT Increases the Amounts of ICP0 mRNA but Does Not Alter the Course of HSV-1 Infection in Latently Infected Murine Ganglia  

作　　者：Haifang Jiang Jiaming Wu Xianjie Liu Ruitao Lu Manling Zhou Meiling Chen Yonghong Liu Grace Guoying Zhou Wenmin Fu 

机构地区：[1]School of Basic Medical Sciences,Guangzhou Medical University,Guangzhou 511436,China [2]Shenzhen International Institute for Biomedical Research,Shenzhen 518116,China

出　　处：《Virologica Sinica》2021年第2期264-272,共9页中国病毒学（英文版）

基　　金：supported by grants from Shenzhen Overseas High-Caliber Peacock Foundation KQTD2015071414385495;Shenzhen Science and Innovation Commission Project Grants JCYJ20180306173333907 to Shenzhen International Institute for Biomedical Research。

摘　　要：On entering sensory ganglia,herpes simplex viruses 1(HSV-1)establishes a latent infection with the synthesis of a latency associated transcript(LAT)or initiates productive infection with expression of a set of immediate early viral proteins.The precise mechanisms how expression of a genes is suppressed during the latency are unknown.One mechanism that has been proposed is illustrated in the case of ICP0,a key immediate early viral regulatory protein.Specifically,the 2 kb LAT intron is complementary to the 30 terminal portion of ICP0 m RNA.To test the hypothesis that accumulation of LAT negatively affects the accumulation of ICP0 m RNA,we inserted a DNA fragment encoding two poly(A)sequences into LAT to early terminate LAT transcript without interrupting the complementary sequence of ICP0 transcript(named as SR1603).Comparisons of the parent(SR1601)and mutant(SR1603)HSV-1 viruses showed the following:Neurons harboring latent SR1603 virus accumulated equivalent amounts of viral DNA but higher amounts of ICP0 m RNA and lower amounts of LAT,when compared to neurons harboring the SR1601 virus.One notable difference between the two viruses is that viral RNA accumulation in explanted ganglia harboring SR1603 virus initiated significantly sooner than that in neurons harboring SR1601 virus,suggesting that ICP0 may act as an activator of viral gene expression in permissive cells.Collectively,these data suggest that increased ICP0 m RNA by suppressed LAT did not affect the establishment of latency in latently infected murine ganglia.

关 键 词：Herpes simplex viruses 1(HSV-1) Latency associated transcript(LAT) ICP0 LATENCY 

分 类 号：R373.11[医药卫生—病原生物学]