Characterization of the subcellular localization of herpes simplex virus type 1 proteins in living cells

Xing, Junji; Wang, Shuai; You, Li; Guo, Hongbo; Zhao, Lei; Pan, Weiwei; Lin, Fusen; Zhu, Hua; Wang, Lei; Li, Meili; Wang, Lin; Zheng, Chunfu

doi:10.1007/s00430-010-0175-9

Cited by 33 publications

(31 citation statements)

References 66 publications

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“…To construct US3-Flag, the US3 open reading frame (ORF) of HSV-1 F strain (GenBank accession no. GU734771.1) was amplified from plasmid US3-EYFP as previously described (58) and cloned into the BglII and EcoRI sites of the pCMV-Flag vector (Beyotime, Shanghai, China). Other plasmids were constructed similarly.…”

Section: Methodsmentioning

confidence: 99%

Herpes Simplex Virus 1 Protein Kinase US3 Hyperphosphorylates p65/RelA and Dampens NF-κB Activation

Wang

et al. 2014

J Virol

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Nuclear factor B (NF-B) plays important roles in innate immune responses by regulating the expression of a large number of target genes involved in the immune and inflammatory response, apoptosis, cell proliferation, differentiation, and survival. To survive in the host cells, viruses have evolved multiple strategies to evade and subvert the host immune response. Herpes simplex virus 1 (HSV-1) bears a large DNA genome, with the capacity to encode many different viral proteins to counteract the host immune responses. In the present study, we demonstrated that HSV-1 protein kinase US3 significantly inhibited NF-B activation and decreased the expression of inflammatory chemokine interleukin-8 (IL-8). US3 was also shown to hyperphosphorylate p65 at serine 75 and block its nuclear translocation. Two US3 mutants, K220M and D305A, still interacted with p65; however, they could not hyperphosphorylate p65, indicating that the kinase activity of US3 was indispensable for the function. The attenuation of NF-B activation by HSV-1 US3 protein kinase may represent a critical adaptation to enable virus persistence within the host. IMPORTANCEThis study demonstrated that HSV-1 protein kinase US3 significantly inhibited NF-B activation and decreased the expression of inflammatory chemokine interleukin-8 (IL-8). US3 hyperphosphorylated p65 at serine 75 to inhibit NF-B activation. The kinase activity of US3 was indispensable for its hyperphosphorylation of p65 and abrogation of the nuclear translocation of p65. The present study elaborated a novel mechanism of HSV-1 US3 to evade the host innate immunity.

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Section: Methodsmentioning

confidence: 99%

Herpes Simplex Virus 1 Protein Kinase US3 Hyperphosphorylates p65/RelA and Dampens NF-κB Activation

Wang

et al. 2014

J Virol

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“…All enzymes, except for the T4 DNA ligase (New England BioLabs, Massachusetts), used for cloning procedures were purchased from TaKaRa (Dalian, China). To construct ICP0-Flag and ICP0-Myc, the open reading frame (ORF) of ICP0 was amplified from plasmid ICP0-enhanced yellow fluorescent protein (EYFP) as previously described (44) and cloned into the BamHI and EcoRI sites of the pCMVFlag and pCMV-Myc vectors (Beyotime, Shanghai, China). To construct Flag-p65 RHD, the ORF of the p65 RHD was amplified from plasmid pFlag-p65 and cloned into the BamHI and EcoRI sites of the pCMVFlag.…”

Section: Methodsmentioning

confidence: 99%

Herpes Simplex Virus 1 E3 Ubiquitin Ligase ICP0 Protein Inhibits Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Interacting with p65/RelA and p50/NF-κB1

Zhang

Wang

et al. 2013

J Virol

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“…Indirect immunofluorescent assay was performed as previously described (Clase et al, 2003;Zhao et al, 2008;Shen et al, 2009;Kang and Banfield, 2010;Xing et al, 2011). DEF cells were seeded onto glass coverslips and grown to a confluence of 30-40% prior to mock infection or infection with DEV in 6-well plates.…”

Section: Indirect Immunofluorescence Assaymentioning

confidence: 99%

Identification and characterization of the duck enteritis virus (DEV) US2 gene

Gao¹,

Cheng²,

Wang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The US2 protein has been reported to contribute to duck enteritis virus (DEV) infection; however, its kinetics and localization during infection, and whether it is a component of virion, have not been previously reported. To elucidate the function of DEV US2, US2 was amplified by polymerase chain reaction (PCR) and inserted into pET-32a(+); this was expressed, the recombinant US2 protein was purified, and a polyclonal antibody generated. In addition, the kinetics and localization of the US2 gene and protein were determined by quantitative real-time fluorescent PCR, ganciclovir (GCV), and cycloheximide (CHX) treatment, westernblot, and indirect immunofluorescence assay. The packaging of US2 into DEV virions was revealed by a protease protection assay. US2 was found to be transcribed 24 h post-infection (pi) and peaked at 72 h pi; the US2 protein was detected 48 h pi, except in the presence of GCV or CHX. US2 was packed into virions and also localized to the plasma membrane and 13779-13790 (2015) cytoplasm in infected cells. The results showed that the DEV US2 is a late gene, and that its encoding protein could be a tegument component localized mainly in the cytoplasm. This study provides useful data for the further analysis of DEV US2, including an explanation for the genetic conservation among alphaherpesviruses.

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Characterization of the subcellular localization of herpes simplex virus type 1 proteins in living cells

Cited by 33 publications

References 66 publications

Herpes Simplex Virus 1 Protein Kinase US3 Hyperphosphorylates p65/RelA and Dampens NF-κB Activation

Herpes Simplex Virus 1 Protein Kinase US3 Hyperphosphorylates p65/RelA and Dampens NF-κB Activation

Herpes Simplex Virus 1 E3 Ubiquitin Ligase ICP0 Protein Inhibits Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Interacting with p65/RelA and p50/NF-κB1

Identification and characterization of the duck enteritis virus (DEV) US2 gene

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