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Role of the pseudorabies virus US3 protein kinase in the evasion of antiviral host responses during infection

(2010)
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Abstract
A typical characteristic of herpesviruses is that they achieve lifelong persistence in the infected host by establishing latency from which the virus can reactivate upon specific stimuli. Reactivation may lead to spread of infectious virus and the occurrence of disease symptoms. In order to be able to spread in immune-competent hosts during reactivation periods, herpesviruses have developed diverse strategies to avoid or delay antiviral host responses, thus enabling the virus to replicate, spread, and transmit to other hosts. The aim of this thesis was to study the potential of the multifunctional US3 serine/threonine kinase of the porcine alphaherpesvirus pseudorabies virus (PRV) to interfere with three aspects of the antiviral defense of the host: (i) apoptosis of infected cells, an intrinsic cellular antiviral response, (ii) the antiviral effect of type I interferon (IFN), an innate antiviral response, and (iii) MHC I-mediated antigen presentation, a key component in the adaptive antiviral response.
Keywords
interferon-alpha, apoptosis, immuno-evasion, US3 protein kinase, pseudorabies virus, alphaherpesvirus, MHC I

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Citation

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Chicago
Deruelle, Matthias. 2010. “Role of the Pseudorabies Virus US3 Protein Kinase in the Evasion of Antiviral Host Responses During Infection”. Merelbeke, Belgium: Ghent University. Faculty of Veterinary Medicine.
APA
Deruelle, M. (2010). Role of the pseudorabies virus US3 protein kinase in the evasion of antiviral host responses during infection. Ghent University. Faculty of Veterinary Medicine, Merelbeke, Belgium.
Vancouver
1.
Deruelle M. Role of the pseudorabies virus US3 protein kinase in the evasion of antiviral host responses during infection. [Merelbeke, Belgium]: Ghent University. Faculty of Veterinary Medicine; 2010.
MLA
Deruelle, Matthias. “Role of the Pseudorabies Virus US3 Protein Kinase in the Evasion of Antiviral Host Responses During Infection.” 2010 : n. pag. Print.
@phdthesis{920454,
  abstract     = {A typical characteristic of herpesviruses is that they achieve lifelong persistence in the infected host by establishing latency from which the virus can reactivate upon specific stimuli. Reactivation may lead to spread of infectious virus and the occurrence of disease symptoms. In order to be able to spread in immune-competent hosts during reactivation periods, herpesviruses have developed diverse strategies to avoid or delay antiviral host responses, thus enabling the virus to replicate, spread, and transmit to other hosts.
The aim of this thesis was to study the potential of the multifunctional US3 serine/threonine kinase of the porcine alphaherpesvirus pseudorabies virus (PRV) to interfere with three aspects of the antiviral defense of the host: (i) apoptosis of infected cells, an intrinsic cellular antiviral response, (ii) the antiviral effect of type I interferon (IFN), an innate antiviral response, and (iii) MHC I-mediated antigen presentation, a key component in the adaptive antiviral response.},
  author       = {Deruelle, Matthias},
  isbn         = {9789058642066},
  language     = {eng},
  pages        = {V, 205},
  publisher    = {Ghent University. Faculty of Veterinary Medicine},
  school       = {Ghent University},
  title        = {Role of the pseudorabies virus US3 protein kinase in the evasion of antiviral host responses during infection},
  year         = {2010},
}