The cellular SUMOylation system as a novel target for antiinfl ue | 901
Journal of Antivirals & Antiretrovirals

Journal of Antivirals & Antiretrovirals
Open Access

ISSN: 1948-5964

The cellular SUMOylation system as a novel target for antiinfl uenza therapies

International Conference and Exhibition on VIROLOGY

5-7 September 2011 Baltimore, USA

Germ�n Rosas-Acosta

Scientific Tracks Abstracts: JAA

Abstract :

The recent emergence of the so-called swine origin H1N1 2009 infl uenza virus, which exhibits high genetic compatibility with H5N1 avian infl uenza viruses, has provided more favorable conditions for the potential appearance of a new highly pathogenic H5N1 human pandemic virus. Considering the known speed at which mutations conferring resistance to current antivirals get introduced into viral populations, and the likelihood of those mutations being present in a new pandemic strains, it is imperative to develop new broad-spectrum antiinfl uenza therapies that could be rapidly implemented in the event of such new pandemic. To this end, the targeting of cellular components required for viral replication has gained attention as one of the most promising approaches. Here, we characterize the cellular SUMOylation system as a valuable target for the development of novel anti-infl uenza therapies. Briefl y, through a combination of in vitro and tissue culture studies using diff erent cell lines and viral strains, our studies have demonstrated that i) several infl uenza viral proteins are SUMOylated during infection, ii) modulating the activity of the cellular SUMOylation system before infection aff ects the normal progression of the infl uenza life cycle, and iii) infl uenza infection triggers a global increase in cellular SUMOylation. Altogether, these fi ndings indicate that SUMOylation may regulate the activity of various viral proteins and play an important role for viral fi tness and pathogenesis. Th is is supported by our recent data indicating that SUMOylation aff ects the activity of both, the viral RNA-dependent RNA-Polymerase and the non-structural protein NS1. In consequence, compounds capable of either, deregulating the SUMOylation of specifi c viral proteins, or blocking the global increase in cellular SUMOylation observed during viral infection, may prove eff ective in blocking infl uenza viral multiplication.

Biography :

Dr. Rosas-Acosta obtained a BSc in Microbiology at the Universidad de Los Andes, in Bogota, Colombia, in 1989. After working as a research assistant for 4 years, he performed doctoral studies in Biomedical Sciences at New York University and postdoctoral work in Virology at Texas A&M University and the Texas A&M Health Science Center ? College of Medicine. Dr. Rosas-Acosta joined the University of Texas at El Paso as an Assistant Professor in Biological Sciences and member of the Border Biomedical Research Center in 2007. Dr. Rosas-Acosta?s lab was the fi rst to report on the relevance of the SUMOylation system for infl uenza virus infection.