RNA-Dependent Protein Kinase Is Required for Alpha-1 Interferon Transgene-Induced Resistance to Genital Herpes Simplex Virus Type 2

Carr, Daniel J.J.; Tomanek, Lisa; Silverman, Robert H.; Campbell, Iain L.; Williams, Bryan R.G.

doi:10.1128/jvi.79.14.9341-9345.2005

Cited by 18 publications

(15 citation statements)

References 32 publications

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“…Unlike the present results using PKR –/– mice, another group reported no difference in sensitivity to genital HSV‐2 infection in PKR –/– mice 10 . We have previously reported the absolute requirement for PKR expression in IFN‐α1 resistance to genital HSV‐2 infection 27 . The discrepancy of our results to those previously reported may reside with the difference in the strain of PKR –/– mouse employed (C57BL/6 versus B6/129) or virus strain and inoculum.…”

Section: Discussioncontrasting

confidence: 99%

The lack of RNA‐dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infection

Carr

Wuest²,

Tomanek

et al. 2006

Immunology

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Summary Mice deficient in RNA‐dependent protein kinase (PKR–/–) or deficient in PKR and a functional 2′,5′‐oligoadenylate synthetase (OAS) pathway (PKR/RL–/–) are more susceptible to genital herpes simplex virus type 2 (HSV‐2) infection than wild‐type mice or mice that are deficient only in a functional OAS pathway (RL–/–) as measured by survival over 30 days. The increase in susceptibility correlated with an increase in virus titre recovered from vaginal tissue or brainstem of infected mice during acute infection. There was also an increase in CD45+ cells and CD8+ T cells residing in the central nervous system of HSV‐2‐infected PKR/RL–/– mice in comparison with RL–/– or wild‐type control animals. In contrast, there was a reduction in the HSV‐specific CD8+ T cells within the draining lymph node of the PKR/RL–/– mice. Collectively, activation of PKR, but not of OAS, contributes significantly to the local control and spread of HSV‐2 following genital infection.

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Section: Discussioncontrasting

confidence: 99%

The lack of RNA‐dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infection

Carr

Wuest²,

Tomanek

et al. 2006

Immunology

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“…The importance of type I IFNs in resistance to HSV-2 infection is also suggested by the fact that topical application of IFN-␣1-expressing plasmids to the vaginal epithelium increases the resistance of mice to HSV-2 challenge and spread (26). The resistance to HSV-2 that is induced by exogenous type I IFN is dependent on RNA-dependent protein kinase (PKR) and CD8 ϩ T cells and thus involves both the innate and adaptive immune responses to viral infection (6,10).…”

mentioning

confidence: 99%

Loss of the Type I Interferon Pathway Increases Vulnerability of Mice to Genital Herpes Simplex Virus 2 Infection

Conrady

Halford

Carr

2011

J Virol

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The mouse model of genital herpes relies on medoxyprogesterone treatment of female mice to render the vaginal lumen susceptible to inoculation with herpes simplex virus 2 (HSV-2). In the present study, we report that mice deficient in the A1 chain of the type I interferon receptor (CD118 ؊/؊ ) are susceptible to HSV-2 in the absence of medroxyprogesterone preconditioning. In the absence of hormone pretreatment, 2,000 PFU of a clinical isolate of HSV-2 was sufficient to establish a productive infection in the vagina of 75% ؎ 17% and in the spinal cord of 71% ؎ 14% of CD118 ؊/؊ mice, whereas the same dose of HSV-2 replicated to detectable levels in only 13% ؎ 13% of vaginal samples and 0% of spinal cord samples from wild-type mice, as determined at day 5 postinfection. The susceptibility to HSV-2 infection in the CD118 ؊/؊ mice was associated with a significant reduction in the infiltration of HSV-specific cytotoxic T lymphocytes into the vaginal tissue, the local production of gamma interferon (IFN-␥), and the expression of T cell-recruiting chemokines CCL5, CXCL9, and CXCL10. Collectively, the results underscore the significant contribution of type I IFNs in resistance to genital HSV-2 infection.

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“…Se ha demostrado que esta proteína juega un rol importante en el control de la replicación de VHS, tanto in vivo como in vitro 99,100 . Para evadir la función de esta proteína del hospedero, los genes tardíos γ34.5 y U S 11 de VHS-1 inhiben la actividad de PKR 101,102 (Figura 2, panel izquierdo).…”

Section: Evasión De La Respuesta Inmune Innataunclassified

Evasión de la respuesta inmune por virus herpes simplex

Retamal-Díaz

Suazo

Garrido

et al. 2015

Rev. chil. infectol.

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RNA-Dependent Protein Kinase Is Required for Alpha-1 Interferon Transgene-Induced Resistance to Genital Herpes Simplex Virus Type 2

Cited by 18 publications

References 32 publications

The lack of RNA‐dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infection

The lack of RNA‐dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infection

Loss of the Type I Interferon Pathway Increases Vulnerability of Mice to Genital Herpes Simplex Virus 2 Infection

Evasión de la respuesta inmune por virus herpes simplex

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