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Herpes Simplex Virus 1 Counteracts Viperin via Its Virion Host Shutoff Protein UL41

Guanghui Shen  Kezhen Wang  Shuai Wang  Mingsheng Cai  Mei-li Li  Chunfu Zheng  
【摘要】:Herpes simplex virus 1(HSV-1)is a member of the Alphaerpesviridae subfamily of herpseviruses with a large dsDNA genome encoding over 80 viral proteins.During infection,HSV-1 initiates a lytic cycle in the mucosal tissues where viral replication,transcription,assembly and egress follows.Then the latent infection established in sensory ganglia where reactivation may happen of which HSV-1 will interact with host cells.The first line of innate immune system defense against the invading pathogens is the interferon(IFN)response,which triggers the expression of a wide array of interferon-stimulating genes(ISGs).Viperin is a highly conserved,361-aminoacid protein.It is first identified as an IFN-γ-inducible protein,which is directly induced by HCMV(human cytomegalovirus)and its constitutive expression is low.Viperin(also known as cig5 or RASD2)can also be categorized as an ISG which limits the replication of many DNA and RNA viruses.However,whether viperin plays a role during herpes simplex virus type 1(HSV-1)infection is unknown.In our study,ectopic expression of UL41 significantly inhibited viperin-Luciferase expression,but other HSV-1 proteinsdid not.Meanwhile,HEK293T cells were cotransfected with viperin-Flag and UL41-His or ICPO-Flag plasmids.As expected,ectopic expression of UL41-His,but not ICPO-Flag,significantly reduced the expression of viperin-Flag in a dose dependent manner It was shown for the first time that WT HSV-1 infection couldn't induce viperin production and ectopicly expressed viperin inhibited the replication of UL41-null HSV-1,but not WT viruses through luciferase reporter assay,Western blot and titer.The molecular mechanism underneath is that WT HSV-1 counteracts viperin by degrading its mRNA via UL41protein with RT-PCR.

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