Early and Delayed Shut-off of Host Protein Synthesis in Cells Infected with Herpes Simplex Virus

Fenwick, M. L.; Clark, J. C. D.

doi:10.1099/0022-1317-61-1-121

Cited by 87 publications

(57 citation statements)

References 9 publications

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“…The requirement for viable BHV-1 suggests that a mechanism similar to the secondary phase of HSV-1 shutoff of host cells may be involved (Fenwick & Clark, 1982;Kwong et al, 1988). This would imply that limited expression of viral genes, at least, was essential for BTL lysis.…”

Section: Discussionmentioning

confidence: 99%

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

Griebel

Ohmann²,

Lawman³

et al. 1990

Journal of General Virology

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The interaction between activated bovine T lymphocytes (BTLs) and bovine herpesvirus type 1 (BHV-1) was investigated. BHV-1 infection of BTLs reduced the amplitude of recombinant bovine interleukin 2-induced proliferative responses. This decreased proliferation was caused by a virus-induced lymphocytolysis which was dependent on viable virus and was not inhibited by recombinant bovine interferon-~xl. Furthermore, lymphocytolysis was not associated with virus replication or with the synthesis of detectable levels of viral proteins. Electron microscopic examination of virusinfected cells revealed that lymphocytolysis was characterized by early nuclear disintegration resembling apoptosis. These observations suggest that activated T cells, localized at the site of BHV-1 infection, may be susceptible to virus-induced cytolysis.

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Section: Discussionmentioning

confidence: 99%

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

Griebel

Ohmann²,

Lawman³

et al. 1990

Journal of General Virology

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“…Total inhibition occurred within 4 h of infection, before the appearance of cytopathic changes, cell lysis, or production of intact virus particles (22). This inhibition ofCSA synthesis occurs at a time when HSV-I is known to inhibit the synthesis of many host proteins (47,48). We investigated the possibility that live herpes virus was present in supernatants ofsome ofthese cultures.…”

Section: Discussionmentioning

confidence: 99%

Viral infection of vascular endothelial cells alters production of colony-stimulating activity.

Gerson¹,

Friedman

Cines

1985

J. Clin. Invest.

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Viral infections in humans are frequently associated with granulocytopenia and/or granulocytosis. Such changes in myelopoiesis could result from infection of the granulocyte-macrophage colony-forming cell (CFC-GM) or changes in the production of colony-stimulating activity (CSA). Endothelial cells are a known source of CSA and may be transiently or persistently infected during a number of viral infections, including infection with herpes simplex virus type I (HSV-I) and measles virus. Therefore, we examined the effect of

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“…Contribution of vhs to the RNA accumulation during PRV infection: Many research groups have reported that the shutoff of protein synthesis is mediated by the ribonuclease (RNase) activity of vhs at early stages in the HSV replication cycle [7,12]. However, the role that vhs plays in RNA accumulation during PRV infection remains unclear.…”

Section: Construction Of the Vhs-deletion Mutant Prvmentioning

confidence: 99%

Role of the UL41 Protein of Pseudorabies Virus in Host Shutoff, Pathogenesis and Induction of TNF-.ALPHA. Expression

Lin

Hsu

Chang

et al. 2010

The Journal of Veterinary Medical Science

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ABSTRACT. The vhs (virion host shutoff) is highly conserved in alphaherpesvirus, including pseudorabies virus (PRV). In an attempt to explore the function of vhs of PRV, we constructed and characterized a mutant virus (41). In the absence of vhs activity, 41 mutant is highly attenuated in mice model and the lethality is correlated with the virus dissemination in neural tissues. As with herpes simplex virus type 1 (HSV-1), the prototype virus of alphaherpesvirus, the pronounced decrease in cellular protein synthesis triggered by wild type PRV was largely restored in cells infected with 41 virus. Furthermore, tumor necrosis factor- (TNF-) protein expression was elevated significantly in spleen of mice infected with vhs mutant virus. Since TNF- has been indicated to be an important cytokine in the innate immune response against various infections, our results implicate vhs may contribute to the protection against PRV lethality via the action of TNF-. Overall, we confirm the shutoff function of vhs protein in PRV, and demonstrate the role that vhs protein plays in virulence, and regulation of cytokine production.KEY WORDS: pseudorabies virus (PRV), tumor necrosis factor- (TNF-), UL41, virion host shutoff (vhs) protein.J. Vet. Med. Sci. 72(9): 1179-1187, 2010 Pseudorabies virus (PRV) is a swine herpesvirus belonging to the Alphaherpesvirinae, the best characterized virus of this family being herpes simplex virus type 1 (HSV-1) [21]. One of the hallmarks of productive HSV-1 infection is the shutoff of host protein synthesis that helps redirect the cellular translation machinery to viral protein synthesis. The decrease in host protein synthesis is achieved mainly through the actions of the virion host shutoff (vhs) protein encoded by UL41 gene and ICP27 [10,11]. Earlier reports showed that vhs harbors mRNA-specific ribonuclease activities via disruption of preexisting polyribosomes leading to the shutoff of protein synthesis [8,22,24]. Very recently, a number of cellular mRNAs have been demonstrated to be the targets of vhs [3][4][5]29]. Not only destabilizing cellular mRNA, the ribonuclease activity of vhs also accelerates the turnover of viral mRNAs which is hypothesized to facilitate the sequential expression of the three kinetic classes of viral genes [16,27].The endonuclease activity of vhs has been demonstrated with purified protein expressed in prokaryotic system [30]. Recently, selective targeting of vhs was observed in several distinct sequence contexts. It was demonstrated that vhs specifically destabilizes regions of AU-rich elements at the 3' end of IEX-1 mRNA [30], although the mechanism of IEX-1 transcript decay in the course of HSV-1 infection remains unclear [4,13]. Several lines of evidence have indicated a role for vhs protein in the regulation of the immune response. Gopinath et al. revealed that down-regulation of MHC class I expression by bovine herpesvirus 1 is mediated by vhs activity [9,15]. Furthermore, the production of several proinflammatory chemokines and cytokines, including inter...

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Early and Delayed Shut-off of Host Protein Synthesis in Cells Infected with Herpes Simplex Virus

Cited by 87 publications

References 9 publications

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

Viral infection of vascular endothelial cells alters production of colony-stimulating activity.

Role of the UL41 Protein of Pseudorabies Virus in Host Shutoff, Pathogenesis and Induction of TNF-.ALPHA. Expression

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