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Role of Pattern Recognition Receptors in KSHV Infection

Kaposi’s sarcoma-associated herpesvirus or Human herpesvirus-8 (KSHV/HHV-8), an oncogenic human herpesvirus and the leading cause of cancer in HIV-infected individuals, is a major public health concern with recurring reports of epidemics on a global level. The early detection of KSHV virus and subse...

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Autores principales: Uppal, Timsy, Sarkar, Roni, Dhelaria, Ranjit, Verma, Subhash C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5876660/
https://www.ncbi.nlm.nih.gov/pubmed/29558453
http://dx.doi.org/10.3390/cancers10030085
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author Uppal, Timsy
Sarkar, Roni
Dhelaria, Ranjit
Verma, Subhash C.
author_facet Uppal, Timsy
Sarkar, Roni
Dhelaria, Ranjit
Verma, Subhash C.
author_sort Uppal, Timsy
collection PubMed
description Kaposi’s sarcoma-associated herpesvirus or Human herpesvirus-8 (KSHV/HHV-8), an oncogenic human herpesvirus and the leading cause of cancer in HIV-infected individuals, is a major public health concern with recurring reports of epidemics on a global level. The early detection of KSHV virus and subsequent activation of the antiviral immune response by the host’s immune system are crucial to prevent KSHV infection. The host’s immune system is an evolutionary conserved system that provides the most important line of defense against invading microbial pathogens, including viruses. Viruses are initially detected by the cells of the host innate immune system, which evoke concerted antiviral responses via the secretion of interferons (IFNs) and inflammatory cytokines/chemokines for elimination of the invaders. Type I IFN and cytokine gene expression are regulated by multiple intracellular signaling pathways that are activated by germline-encoded host sensors, i.e., pattern recognition receptors (PRRs) that recognize a conserved set of ligands, known as ‘pathogen-associated molecular patterns (PAMPs)’. On the contrary, persistent and dysregulated signaling of PRRs promotes numerous tumor-causing inflammatory events in various human cancers. Being an integral component of the mammalian innate immune response and due to their constitutive activation in tumor cells, targeting PRRs appears to be an effective strategy for tumor prevention and/or treatment. Cellular PRRs are known to respond to KSHV infection, and KSHV has been shown to be armed with an array of strategies to selectively inhibit cellular PRR-based immune sensing to its benefit. In particular, KSHV has acquired specific immunomodulatory genes to effectively subvert PRR responses during the early stages of primary infection, lytic reactivation and latency, for a successful establishment of a life-long persistent infection. The current review aims to comprehensively summarize the latest advances in our knowledge of role of PRRs in KSHV infections.
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spelling pubmed-58766602018-04-09 Role of Pattern Recognition Receptors in KSHV Infection Uppal, Timsy Sarkar, Roni Dhelaria, Ranjit Verma, Subhash C. Cancers (Basel) Review Kaposi’s sarcoma-associated herpesvirus or Human herpesvirus-8 (KSHV/HHV-8), an oncogenic human herpesvirus and the leading cause of cancer in HIV-infected individuals, is a major public health concern with recurring reports of epidemics on a global level. The early detection of KSHV virus and subsequent activation of the antiviral immune response by the host’s immune system are crucial to prevent KSHV infection. The host’s immune system is an evolutionary conserved system that provides the most important line of defense against invading microbial pathogens, including viruses. Viruses are initially detected by the cells of the host innate immune system, which evoke concerted antiviral responses via the secretion of interferons (IFNs) and inflammatory cytokines/chemokines for elimination of the invaders. Type I IFN and cytokine gene expression are regulated by multiple intracellular signaling pathways that are activated by germline-encoded host sensors, i.e., pattern recognition receptors (PRRs) that recognize a conserved set of ligands, known as ‘pathogen-associated molecular patterns (PAMPs)’. On the contrary, persistent and dysregulated signaling of PRRs promotes numerous tumor-causing inflammatory events in various human cancers. Being an integral component of the mammalian innate immune response and due to their constitutive activation in tumor cells, targeting PRRs appears to be an effective strategy for tumor prevention and/or treatment. Cellular PRRs are known to respond to KSHV infection, and KSHV has been shown to be armed with an array of strategies to selectively inhibit cellular PRR-based immune sensing to its benefit. In particular, KSHV has acquired specific immunomodulatory genes to effectively subvert PRR responses during the early stages of primary infection, lytic reactivation and latency, for a successful establishment of a life-long persistent infection. The current review aims to comprehensively summarize the latest advances in our knowledge of role of PRRs in KSHV infections. MDPI 2018-03-20 /pmc/articles/PMC5876660/ /pubmed/29558453 http://dx.doi.org/10.3390/cancers10030085 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Uppal, Timsy
Sarkar, Roni
Dhelaria, Ranjit
Verma, Subhash C.
Role of Pattern Recognition Receptors in KSHV Infection
title Role of Pattern Recognition Receptors in KSHV Infection
title_full Role of Pattern Recognition Receptors in KSHV Infection
title_fullStr Role of Pattern Recognition Receptors in KSHV Infection
title_full_unstemmed Role of Pattern Recognition Receptors in KSHV Infection
title_short Role of Pattern Recognition Receptors in KSHV Infection
title_sort role of pattern recognition receptors in kshv infection
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5876660/
https://www.ncbi.nlm.nih.gov/pubmed/29558453
http://dx.doi.org/10.3390/cancers10030085
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