A 14,700 MW protein from the E3 region of adenovirus inhibits cytolysis by tumor necrosis factor

Gooding, Linda R.; Elmore, Lynne W.; Tollefson, Ann E.; Brady, Helen; Wold, William S.M.

doi:10.1016/0092-8674(88)90154-7

Cited by 226 publications

(144 citation statements)

References 28 publications

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“…The HAd E3 19kDa glycoprotein, an integral membrane glycoprotein, protects the virus-infected cell from lysis by cytotoxic T lymphocyte (CTL) attack by forming a complex with newly synthesized major histocompatibility complex class I antigens in the endoplasmic reticulum and thus inhibits their transport to the surface of infected cells (Burgert & Kvist, 1987). The E3 14.7 kDa protein prevents lysis of virus-infected mouse cells by tumour necrosis factor ~ (TNF-00 (Gooding et al, 1988). The E3 14.5 kDa and E3 10.4 kDa proteins together prevent cytolysis by TNF-~ and also down-regulate the expression of the epidermal growth factor receptor in virusinfected cells (Carlin et al, 1989;Tollefson et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

“…BAd3-based expression vectors have the potential to provide an excellent alternative to conventional vaccines for the protection of cattle against infectious respiratory diseases. However, since HAd E3 gene products are involved in modulating host immune responses to virus infection (Burgert & Kvist, 1987;Gooding et al, 1988;Carlin et al, 1989;Tollefson et al, 1991;Wold et aI., 1994) and HAd E3-deletion mutants have been shown to have an increased pathogenic potential in cotton rats (Sigmodon hispidus) compared to their wild-type (wt) counterpart (Ginsberg et al, 1989), there is a need to evaluate the pathogenic potential of and immune responses to a BAd3-based recombinant virus. Previously, we established that the cotton rat is a useful small-animal model to study BAd3 pneumonia (Mittal et al, 1995 c).…”

confidence: 99%

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Pathology and immunogenicity in the cotton rat (Sigmodon hispidus) model after infection with a bovine adenovirus type 3 recombinant virus expressing the firefly luciferase gene

Mittal

Middleton²,

Tikoo³

et al. 1996

Journal of General Virology

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Section: Discussionmentioning

confidence: 99%

Pathology and immunogenicity in the cotton rat (Sigmodon hispidus) model after infection with a bovine adenovirus type 3 recombinant virus expressing the firefly luciferase gene

Mittal

Middleton²,

Tikoo³

et al. 1996

Journal of General Virology

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“…A second mechanism involves the E3 14.7K, 14.5K and 10.4K products. All these proteins protect adenovirusinfected mouse cells from cytolysis by tumour necrosis factor (TNF) with the 14-7K product playing the dominant role in this process (Gooding et al, 1988(Gooding et al, , 1991a. In human cells however, complete protection from TNF also appears to require the 19K product encoded in the Elb transcription unit (Gooding et aI., 1991 b).…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of human adenovirus E1a by E3 gene products: evidence for translational control of E1a by E3 14{middle dot}5K and/or E3 10{middle dot}4K products

Zhang

Bellett²,

Hla³

et al. 1994

Journal of General Virology

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The mechanism for down-regulation of Ela expression by products encoded in the E3 transcription unit of human adenovirus types 2 and 5, that occurs in infected L929 cells, has been investigated further. We show that the phenomenon occurs in different mouse cells and also in some human cells suggesting that the observations have relevance to natural human infections. We also provide evidence that probably all viral proteins are down-regulated by E3 products, although to different extents, but that host proteins are unaffected. Whereas Ela protein levels and synthesis are reduced in the presence of E3 products, Ela protein half-life and polysomal Ela RNA levels and size distribution are not. These data suggest that E3 products down-regulate Ela protein levels by interfering with the translation of Elaspecific mRNA. Studies were additionally carried out with mutant adenoviruses containing different defects in the E3 transcription unit. Based on these studies it seems likely that the E3 14.5K and 10.4K proteins are crucially involved in E 1 a down-regulation. Our data are discussed in terms of strategies for immune evasion by group C human adenoviruses.

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“…TNFa is a known activator of NF-kB signalling and is considered to be inhibitory to virus infection (McFadden et al, 2009). Ad5 infection can stimulate NF-kB signalling in several ways (Higginbotham et al, 2002;Pahl et al, 1996;Schmitz et al, 1996) while several viral E3 gene products counteract TNFa activity (Gooding et al, 1988), suggesting NF-kB activation might be inhibitory to Ad5 infection. We therefore tested whether elevated HSP70 in HelaDII cells enhanced Ad5 infection by inhibiting NF- kB.…”

Section: Possible Roles Of Hsp70 During Ad5 Infectionmentioning

confidence: 99%

Promyelocytic leukemia protein isoform II inhibits infection by human adenovirus type 5 through effects on HSP70 and the interferon response

Atwan

Wright

Woodman

et al. 2016

Journal of General Virology

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Promyelocytic leukemia (PML) proteins have been implicated in antiviral responses but PML and associated proteins are also suggested to support virus replication. One isoform, PML-II, is required for efficient transcription of interferon and interferon-responsive genes. We therefore investigated the PML-II contribution to human adenovirus 5 (Ad5) infection, using shRNAmediated knockdown. HelaDII cells showed a 2-3-fold elevation in Ad5 yield, reflecting an increase in late gene expression. This increase was found to be due in part to the reduced innate immune response consequent upon PML-II depletion. However, the effect was minor because the viral E4 Orf3 protein targets and inactivates this PML-II function. The major benefit to Ad5 in HelaDII cells was exerted via an increase in HSP70; depletion of HSP70 completely reversed this replicative advantage. Increased Ad5 late gene expression was not due either to the previously described inhibition of inflammatory responses by HSP70 or to effects of HSP70 on major late promoter or L4 promoter activity, but might be linked to an observed increase in E1B 55K, as this protein is known to be required for efficient late gene expression. The induction of HSP70 by PML-II removal was specific for the HSPA1B gene among the HSP70 gene family and thus was not the consequence of a general stress response. Taken together, these data show that PML-II, through its various actions, has an overall negative effect on the Ad5 lifecycle.

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A 14,700 MW protein from the E3 region of adenovirus inhibits cytolysis by tumor necrosis factor

Cited by 226 publications

References 28 publications

Pathology and immunogenicity in the cotton rat (Sigmodon hispidus) model after infection with a bovine adenovirus type 3 recombinant virus expressing the firefly luciferase gene

Pathology and immunogenicity in the cotton rat (Sigmodon hispidus) model after infection with a bovine adenovirus type 3 recombinant virus expressing the firefly luciferase gene

Down-regulation of human adenovirus E1a by E3 gene products: evidence for translational control of E1a by E3 14{middle dot}5K and/or E3 10{middle dot}4K products

Promyelocytic leukemia protein isoform II inhibits infection by human adenovirus type 5 through effects on HSP70 and the interferon response

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