Role of Us3 gene of herpes simplex virus type 1 for resistance to interferon.

Piroozmand, Ahmad; Koyama, A. Hajime; Shimada, Yoshiko; Fujita, Mikako; Arakawa, Tsutomu; Adachi, Akio

doi:10.3892/ijmm.14.4.641

Cited by 20 publications

(16 citation statements)

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“…Several lines of evidence indicate that Us3 participates in a variety of processes, such as promoting viral egress (36,37), enhancing viral protein synthesis (38), preventing apoptosis (39 -41), regulating the epigenetic modification of chromosomes (42,43), and suppressing innate immunity (9,44). In this study, we showed that Us3 negatively regulated TCR-mediated signaling, resulting in diminished calcium mobilization and IL-2 secretion.…”

Section: Discussionmentioning

confidence: 60%

The Us3 Protein of Herpes Simplex Virus 1 Inhibits T Cell Signaling by Confining Linker for Activation of T Cells (LAT) Activation via TRAF6 Protein

Yang

Wang

et al. 2015

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 60%

The Us3 Protein of Herpes Simplex Virus 1 Inhibits T Cell Signaling by Confining Linker for Activation of T Cells (LAT) Activation via TRAF6 Protein

Yang

Wang

et al. 2015

Journal of Biological Chemistry

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“…US3-deficient HSV-1 was more sensitive to alpha IFN (IFN-␣) and induced stronger activation of IFN regulatory factor 3 (IRF3) (26,27). Our recent work also demonstrated that US3 hyperphosphorylated IRF3 and inhibited IFN-␤ production (28).…”

mentioning

confidence: 84%

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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“…For VZV-and PRV-infected cells, the lack of US3 reduced the capacity of the virus to interfere with induction of the IFN signaling pathway following exposure to IFN (175,195). Recently, Peri et al reported that US3-null HSV-1 induces a strong activation of IRF-3 and type I IFN mRNA expression and that HSV-1 US3 downregulates the intracellular expression of TLR3 and the type I interferon-inducible protein MxA, which is known to posses antiviral activity (171).…”

Section: Herpesvirusesmentioning

confidence: 99%

Viral Serine/Threonine Protein Kinases

Jacob

Broeke

Favoreel

2011

J Virol

108

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Phosphorylation represents one the most abundant and important posttranslational modifications of proteins, including viral proteins. Virus-encoded serine/threonine protein kinases appear to be a feature that is unique to large DNA viruses. Although the importance of these kinases for virus replication in cell culture is variable, they invariably play important roles in virus virulence. The current review provides an overview of the different viral serine/threonine protein kinases of several large DNA viruses and discusses their function, importance, and potential as antiviral drug targets.

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Role of Us3 gene of herpes simplex virus type 1 for resistance to interferon.

Cited by 20 publications

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The Us3 Protein of Herpes Simplex Virus 1 Inhibits T Cell Signaling by Confining Linker for Activation of T Cells (LAT) Activation via TRAF6 Protein

The Us3 Protein of Herpes Simplex Virus 1 Inhibits T Cell Signaling by Confining Linker for Activation of T Cells (LAT) Activation via TRAF6 Protein

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

Viral Serine/Threonine Protein Kinases

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