Giuseppe
Emeritus
[Source: Science, full text: (LINK). Abstract, edited.]
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<CITE><ABBR>Science</ABBR> 14 October 2011:
Vol. 334 no. 6053 pp. 249-252
DOI: 10.1126/science.1211057 </CITE>
<CITE></CITE>
<CITE></CITE>Report
Intestinal Microbiota Promote Enteric Virus Replication and Systemic Pathogenesis
Abstract
Intestinal bacteria aid host health and limit bacterial pathogen colonization. However, the influence of bacteria on enteric viruses is largely unknown. We depleted the intestinal microbiota of mice with antibiotics before inoculation with poliovirus, an enteric virus. Antibiotic-treated mice were less susceptible to poliovirus disease and supported minimal viral replication in the intestine. Exposure to bacteria or their N-acetylglucosamine–containing surface polysaccharides, including lipopolysaccharide and peptidoglycan, enhanced poliovirus infectivity. We found that poliovirus binds lipopolysaccharide, and exposure of poliovirus to bacteria enhanced host cell association and infection. The pathogenesis of reovirus, an unrelated enteric virus, also was more severe in the presence of intestinal microbes. These results suggest that antibiotic-mediated microbiota depletion diminishes enteric virus infection and that enteric viruses exploit intestinal microbes for replication and transmission.
Received for publication 12 July 2011.
Accepted for publication 7 September 2011.
-Vol. 334 no. 6053 pp. 249-252
DOI: 10.1126/science.1211057 </CITE>
<CITE></CITE>
<CITE></CITE>Report
Intestinal Microbiota Promote Enteric Virus Replication and Systemic Pathogenesis
- Sharon K. Kuss<SUP>1</SUP>, Gavin T. Best<SUP>1</SUP>, Chris A. Etheredge<SUP>1</SUP>,*, Andrea J. Pruijssers<SUP>2</SUP>,<SUP>3</SUP>, Johnna M. Frierson<SUP>3</SUP>,<SUP>4</SUP>, Lora V. Hooper<SUP>1</SUP>,<SUP>5</SUP>,<SUP>6</SUP>, Terence S. Dermody<SUP>2</SUP>,<SUP>3</SUP>,<SUP>4</SUP>, Julie K. Pfeiffer<SUP>1</SUP>,†
- <SUP>1</SUP>Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
- <SUP>2</SUP>Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37240, USA.
- <SUP>3</SUP>Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN 37240, USA.
- <SUP>4</SUP>Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37240, USA.
- <SUP>5</SUP>Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA,
- <SUP>6</SUP>Howard Hughes Medical Institute.
- ↵* Present address: Neurosciences Department, Medical University of South Carolina, Charleston, SC 29425, USA.
- ↵†To whom correspondence should be addressed. E-mail: julie.pfeiffer@utsouthwestern.edu
Abstract
Intestinal bacteria aid host health and limit bacterial pathogen colonization. However, the influence of bacteria on enteric viruses is largely unknown. We depleted the intestinal microbiota of mice with antibiotics before inoculation with poliovirus, an enteric virus. Antibiotic-treated mice were less susceptible to poliovirus disease and supported minimal viral replication in the intestine. Exposure to bacteria or their N-acetylglucosamine–containing surface polysaccharides, including lipopolysaccharide and peptidoglycan, enhanced poliovirus infectivity. We found that poliovirus binds lipopolysaccharide, and exposure of poliovirus to bacteria enhanced host cell association and infection. The pathogenesis of reovirus, an unrelated enteric virus, also was more severe in the presence of intestinal microbes. These results suggest that antibiotic-mediated microbiota depletion diminishes enteric virus infection and that enteric viruses exploit intestinal microbes for replication and transmission.
Received for publication 12 July 2011.
Accepted for publication 7 September 2011.
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