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Journal of Virology, August 2008, p. 7578-7590, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00391-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of Interferon in Homologous and Heterologous Rotavirus Infection in the Intestines and Extraintestinal Organs of Suckling Mice{triangledown}

N. Feng, B. Kim,{dagger} M. Fenaux,{ddagger} H. Nguyen, P. Vo, M. B. Omary, and H. B. Greenberg*

Stanford University, Stanford, and Palo Alto VA Health Care System, Palo Alto, California

Received 22 February 2008/ Accepted 12 May 2008

Recent studies demonstrated that viremia and extraintestinal rotavirus infection are common in acutely infected humans and animals, while systemic diseases appear to be rare. Intraperitoneal infection of newborn mice with rhesus rotavirus (RRV) results in biliary atresia (BA), and this condition is influenced by the host interferon response. We studied orally inoculated 5-day-old suckling mice that were deficient in interferon (IFN) signaling to evaluate the role of interferon on the outcome of local and systemic infection after enteric inoculation. We found that systemic replication of RRV, but not murine rotavirus strain EC, was greatly enhanced in IFN-{alpha}/β and IFN-{gamma} receptor double-knockout (KO) or STAT1 KO mice but not in mice deficient in B- or T-cell immunity. The enhanced replication of RRV was associated with a lethal hepatitis, pancreatitis, and BA, while no systemic disease was observed in strain EC-infected interferon-deficient mice. In IFN-{alpha}/β receptor KO mice the extraintestinal infection and systemic disease were only moderately increased, while RRV infection was not augmented and systemic disease was not present in IFN-{gamma} receptor KO mice. The increase of systemic infection in IFN-deficient mice was also observed during simian strain SA11 infection but not following bovine NCDV, porcine OSU, or murine strain EW infection. Our data indicate that the requirements for the interferon system to inhibit intestinal and extraintestinal viral replication in suckling mice vary among different heterologous and homologous rotavirus strains, and this variation is associated with lethal systemic disease.

* Corresponding author. Mailing address: VA Palo Alto Health Care System, 3801 Miranda Ave., MC154C, Palo Alto, CA 94304. Phone: (650) 752-9722. Fax: (650) 852- 3259. E-mail: harry.greenberg{at}stanford.edu

{triangledown} Published ahead of print on 21 May 2008.

{dagger} Present address: College of Veterinary Medicine, Chonbuk National University, Chonju 561-756, Korea.

{ddagger} Present address: Gilead Sciences, Inc., 333 Lakeside Dr., Foster City, CA 94404.

Journal of Virology, August 2008, p. 7578-7590, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00391-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sen, A., Feng, N., Ettayebi, K., Hardy, M. E., Greenberg, H. B. (2009). IRF3 Inhibition by Rotavirus NSP1 Is Host Cell and Virus Strain Dependent but Independent of NSP1 Proteasomal Degradation. J. Virol. 83: 10322-10335 [Abstract] [Full Text]  
  • Feng, N., Sen, A., Nguyen, H., Vo, P., Hoshino, Y., Deal, E. M., Greenberg, H. B. (2009). Variation in Antagonism of the Interferon Response to Rotavirus NSP1 Results in Differential Infectivity in Mouse Embryonic Fibroblasts. J. Virol. 83: 6987-6994 [Abstract] [Full Text]  
  • Holloway, G., Truong, T. T., Coulson, B. S. (2009). Rotavirus Antagonizes Cellular Antiviral Responses by Inhibiting the Nuclear Accumulation of STAT1, STAT2, and NF-{kappa}B. J. Virol. 83: 4942-4951 [Abstract] [Full Text]  


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