Host Factors in Viral Life Cycles

G. Pérez-Vilaró; J. Jungfleisch; V. Saludes; N. Scheller; M. Giménez-Barcons; J. Díez

Mathematical Modelling of Natural Phenomena (2012)

  • Volume: 7, Issue: 5, page 123-132
  • ISSN: 0973-5348

Abstract

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Viruses are obligate intracellular parasites that rely on the host cell for expansion. With the development of global analyses techniques like transcriptomics, proteomics and siRNA library screening of complete cellular gene sets, a large range of host cell factors have been discovered that either support or restrict virus growth. Here we summarize some of the recent findings and focus our discussion on the hepatitis C virus and the human immunodeficiency virus, two major pathogens that threat global health. The identification of cellular proteins affecting multiple viruses points to the existence of central regulation nodes that might be exploited for both, a quantitative description of host-virus interactions within single infected cells and the development of novel, broad-spectrum antiviral drugs.

How to cite

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Pérez-Vilaró, G., et al. "Host Factors in Viral Life Cycles." Mathematical Modelling of Natural Phenomena 7.5 (2012): 123-132. <http://eudml.org/doc/222422>.

@article{Pérez2012,
abstract = {Viruses are obligate intracellular parasites that rely on the host cell for expansion. With the development of global analyses techniques like transcriptomics, proteomics and siRNA library screening of complete cellular gene sets, a large range of host cell factors have been discovered that either support or restrict virus growth. Here we summarize some of the recent findings and focus our discussion on the hepatitis C virus and the human immunodeficiency virus, two major pathogens that threat global health. The identification of cellular proteins affecting multiple viruses points to the existence of central regulation nodes that might be exploited for both, a quantitative description of host-virus interactions within single infected cells and the development of novel, broad-spectrum antiviral drugs. },
author = {Pérez-Vilaró, G., Jungfleisch, J., Saludes, V., Scheller, N., Giménez-Barcons, M., Díez, J.},
journal = {Mathematical Modelling of Natural Phenomena},
keywords = {host factors as central regulation nodes for quantitative models of viral expansion; identification of host-virus interactions; hepatitis C virus; human immunodeficiency virus; host factors as central regulation nodes for quantitative models of viral expansion},
language = {eng},
month = {10},
number = {5},
pages = {123-132},
publisher = {EDP Sciences},
title = {Host Factors in Viral Life Cycles},
url = {http://eudml.org/doc/222422},
volume = {7},
year = {2012},
}

TY - JOUR
AU - Pérez-Vilaró, G.
AU - Jungfleisch, J.
AU - Saludes, V.
AU - Scheller, N.
AU - Giménez-Barcons, M.
AU - Díez, J.
TI - Host Factors in Viral Life Cycles
JO - Mathematical Modelling of Natural Phenomena
DA - 2012/10//
PB - EDP Sciences
VL - 7
IS - 5
SP - 123
EP - 132
AB - Viruses are obligate intracellular parasites that rely on the host cell for expansion. With the development of global analyses techniques like transcriptomics, proteomics and siRNA library screening of complete cellular gene sets, a large range of host cell factors have been discovered that either support or restrict virus growth. Here we summarize some of the recent findings and focus our discussion on the hepatitis C virus and the human immunodeficiency virus, two major pathogens that threat global health. The identification of cellular proteins affecting multiple viruses points to the existence of central regulation nodes that might be exploited for both, a quantitative description of host-virus interactions within single infected cells and the development of novel, broad-spectrum antiviral drugs.
LA - eng
KW - host factors as central regulation nodes for quantitative models of viral expansion; identification of host-virus interactions; hepatitis C virus; human immunodeficiency virus; host factors as central regulation nodes for quantitative models of viral expansion
UR - http://eudml.org/doc/222422
ER -

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