Functional Genomic Analysis of Herpes Simplex Virus Type 1 Counteraction of the Host Innate Response

Pasieka, Tracy Jo; Baas, Tracey; Carter, Victoria S.; Proll, Sean; Katze, Michael G.; Leib, David A.

doi:10.1128/jvi.00333-06

Cited by 55 publications

(62 citation statements)

References 65 publications

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“…Therefore, at the early stages of HSV infection, it acts to inhibit or alleviate the induction of antiviral immunity. This idea is in line with the observation that a ␥ 1 34.5 null mutant induced differential gene expression as compared with wild type HSV-1 (27). These results lend support to the hypothesis that inhibition of the induction of antiviral immunity by the ␥ 1 34.5 protein contributes to the pathogenesis of HSV infection.…”

Section: Discussionsupporting

confidence: 79%

“…In this context, it is notable that an HSV mutant, lacking a leaky late gene ␥ 1 34.5, replicates efficiently in cells devoid of IFN-␣/␤ genes (26). Additionally, the ␥ 1 34.5 null mutant induces differential cytokine expression as compared with wild type virus (27). Thus, HSV modulation of cytokine expression is a complex process that involves multiple viral components.…”

mentioning

confidence: 99%

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Control of TANK-binding Kinase 1-mediated Signaling by the γ134.5 Protein of Herpes Simplex Virus 1

Verpooten

Hou

et al. 2009

Journal of Biological Chemistry

173

187

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Control of TANK-binding Kinase 1-mediated Signaling by the γ134.5 Protein of Herpes Simplex Virus 1

Verpooten

Hou

et al. 2009

Journal of Biological Chemistry

173

187

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“…Previously, it has been demonstrated that ISG56 mRNA expression was much stronger and longer than ISG54 in response to viruses such as influenza virus and herpes simplex virus type 1 (29,30). It has also been noted that ISG56 mRNA is the most abundant IFN-induced mRNAs in a gene array analysis (16).…”

Section: Discussionmentioning

confidence: 99%

ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response

Xue

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

182

154

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“…If C. trachomatis-infected murine cells are exposed to IFN-c early in the developmental cycle, inclusions remain small (Nelson et al, 2005). Recent studies indicate that Iigp1 is upregulated in HSV-1-infected murine cells at 3 h post-infection (Pasieka et al, 2006). Although a human Iigp1 homologue has not been identified, it is possible that HSV/host cell interaction activates human p47 GTPases that function similarly.…”

Section: Inclusions Within Co-infected Cells Continue To Enlarge and mentioning

confidence: 99%

Herpes simplex virus co-infection-induced Chlamydia trachomatis persistence is not mediated by any known persistence inducer or anti-chlamydial pathway

et al. 2008

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Several inducers of chlamydial persistence have been described, including interferon-c (IFN-c), IFN-a, IFN-b, and tumour necrosis factor-a (TNF-a) exposure, and iron, amino acid or glucose deprivation. A tissue-culture model of Chlamydia trachomatis/herpes simplex virus type-2 (HSV-2) co-infection indicates that viral co-infection stimulates the formation of persistent chlamydiae. This study was designed to ascertain whether co-infection-induced persistence is mediated by a previously characterized mechanism. Luminex assays indicate that IFN-c, IFN-a, and TNF-a are not released from co-infected cells. Semiquantitative RT-PCR studies demonstrate that IFN-b, IFN-c, indoleamine 2,3-dioxygenase, lymphotoxin-a and inducible nitric oxide synthase are not expressed during co-infection. These data indicate that viral-induced persistence is not stimulated by any persistence-associated cytokine. Supplementation of co-infected cells with excess amino acids, iron-saturated holotransferrin, glucose or a combination of amino acids and iron does not restore chlamydial infectivity, demonstrating that HSV-2-induced persistence is not mediated by depletion of these nutrients. Finally, inclusions within co-infected cells continue to enlarge and incorporate C 6 -NBD-ceramide, indicating that HSV-2 co-infection does not inhibit vesicular transport to the developing inclusion. Collectively these data demonstrate that co-infection-induced persistence is not mediated by any currently characterized persistence inducer or anti-chlamydial pathway. Previous studies indicate that HSV-2 attachment and/or entry into the host cell is sufficient for stimulating chlamydial persistence, suggesting that viral attachment and/or entry may trigger a novel host pathway which restricts chlamydial development.

show abstract

Functional Genomic Analysis of Herpes Simplex Virus Type 1 Counteraction of the Host Innate Response

Cited by 55 publications

References 65 publications

Control of TANK-binding Kinase 1-mediated Signaling by the γ134.5 Protein of Herpes Simplex Virus 1

Control of TANK-binding Kinase 1-mediated Signaling by the γ134.5 Protein of Herpes Simplex Virus 1

ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response

Herpes simplex virus co-infection-induced Chlamydia trachomatis persistence is not mediated by any known persistence inducer or anti-chlamydial pathway

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