Seasonal influenza a virus in feces of hospitalized adults

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Emerg Infect Dis. 2011 Nov;17(11):2038-42.
Seasonal influenza a virus in feces of hospitalized adults.
Chan MC, Lee N, Chan PK, To KF, Wong RY, Ho WS, Ngai KL, Sung JJ.
Source

The Chinese University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China.
Abstract

In a cohort of hospitalized adults with seasonal influenza A in Hong Kong, viral RNA was frequently (47%) detected in stool specimens. Viable virus was rarely isolated. Viral RNA positivity had little correlation with gastrointestinal symptoms and outcomes. In vitro studies suggested low potential for seasonal influenza viruses to cause direct intestinal infections.

PMID:
22099092
[PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/22099092

 

[tetano]

Re: Seasonal influenza a virus in feces of hospitalized adults

Conclusions:

Direct intestinal infection by seasonal influenza viruses seems an unlikely explanation for the frequent fecal detection of viral RNA in the patients reported here. No clinical correlation was shown for RNA positivity (but was shown with lymphopenia and positive virus isolation in NPA, indicating higher virus load), and culture positivity is rare (4,5,10,11). Human-like influenza virus receptor is not found to express on normal intestinal epithelial cells (12). These findings agree with reports which showed that intestinal cells and tissues do not support efficient replication of seasonal viruses (12,13), thus their low potential to cause direct intestinal infection. Alternatively, swallowing of virus-containing nasopharyngeal secretions (although it seems inadequate to explain the higher rate of detecting fecal viral RNA than RSV or PIV) and hematogenous dissemination to organs through infected lymphocytes or macrophages in severe influenza cases with high virus load (spillover) are possible explanations for fecal viral RNA detection (2,14). Our findings on virus receptor distribution and in vitro virus binding to intestinal lamina propria leukocytes lends support to the latter hypothesis. Notably, viral RNA positivity in nonpulmonary tissues infiltrating mononuclear cells without detectable viral particles or antigens or tissue damage has been reported (15). Our study does not reject the possibility of seasonal influenza viruses causing occasional, disseminated infection in profoundly immunosuppressed persons because receptor affinity is not absolute (2). Conversely, highly pathogenic avian influenza (H5N1) and pandemic (H1N1) 2009 viruses have the ability to bind to avian-like influenza virus receptors on colonic epithelium and to replicate efficiently in intestinal cells and tissues (12). Their enhanced potential to cause direct intestinal infections and fecal–oral transmission deserve further investigation.

Dr Chan is a postdoctoral fellow at the Institute of Digestive Disease, The Chinese University of Hong Kong. His research focuses on respiratory and gastrointestinal infections, especially those caused by influenza viruses and noroviruses, respectively.

http://wwwnc.cdc.gov/eid/article/17/11/11-0205_article.htm

 

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Re: Seasonal influenza a virus in feces of hospitalized adults

Copyright © 2010, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
J. Virol. doi:10.1128/JVI.01568-10
JVI Accepts, published online ahead of print on 3 November 2010

The 2009 pandemic H1N1 and triple ressortant swine H1N1 influenza
viruses replicate efficiently but elicit an attenuated inflammatory
response in polarized human bronchial epithelial cells
Hui Zeng, Claudia Pappas, Jacqueline M. Katz, and Terrence M Tumpey*


We compared the growth characteristics of 2009 H1N1 (Mexico/4482) virus with seasonal H1N1 virus in intestinal epithelial cells in attempts to understand the tissue tropism of this pandemic virus. Replication of seasonal H1N1 (45) and pandemic H1N1 influenza virus (18) was previously studied in non-differentiated CaCO-2 cells. In these
studies we used differentiated polarized CaCO-2 cells and found that the 2009 H1N1 virus replicated more efficiently than the seasonal H1N1 virus. This is consistent with the detection of infectious virus in rectal swabs and intestinal tissues of 2009 H1N1-infected ferrets (21), and detection of virus in stool of H1N1-infected patients (35). Furthermore we show that H1N1 virus could be detected at higher titers in both the apical and basolateral compartments of CaCO-2 cultures and transport of infectious virus fro apical to basolateral chambers (and vice versa) was more pronounced with the 2009 H1N1 virus compared to the seasonal H1N1 virus. Compared to infected Calu-3 cells, much less apoptosis and necrosis was observed in infected CaCO-2 cells, suggesting different host responses to influenza virus infection between the two cell types
Currently, it is not clear how the virus reaches the GI tract and this mechanism requires further investigation.

http://jvi.asm.org/content/early/2010/11/03/JVI.01568-10.short