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Journal of Clinical Microbiology, March 2007, p. 990-997, Vol. 45, No. 3
0095-1137/07/$08.00+0     doi:10.1128/JCM.01992-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Mutated G4P[8] Rotavirus Associated with a Nationwide Outbreak of Gastroenteritis in Nicaragua in 2005{triangledown}

Filemon Bucardo,1,2,{dagger} Beatrice Karlsson,2,{dagger} Johan Nordgren,2 Margarita Paniagua,1 Alcides González,3 Juan Jose Amador,3 Felix Espinoza,1 and Lennart Svensson2*

Department of Microbiology, National Autonomous University of Nicaragua, León, Nicaragua,1 Division of Molecular Virology, Medical Faculty, Linköping University, Linköping, Sweden,2 Ministry of Health, Managua, Nicaragua3

Received 26 September 2006/ Returned for modification 29 November 2006/ Accepted 4 January 2007

During February and March 2005, one of the largest national recorded outbreaks of severe acute gastroenteritis occurred in Nicaragua, affecting ≥64,000 individuals and causing ≥56 deaths, predominantly in children under 5 years of age. Through a nationwide laboratory-based study, stool samples were collected and investigated for rotavirus. Of 108 stool samples examined, 72 (67%) were positive for rotavirus. While 69% (50/72) of the positive samples were found in children less than 2 years of age, 50% (6/12) of the adult samples were positive. A mutated G4P[8] strain was the most commonly recognized strain (85%), followed by mixed G strains (8%) and G9P[8] (7%) strains. Phylogenetic analysis of the VP7 gene revealed that the G4 strains belonged to the emerging lineage Ic and was distantly related to the ST3 and VA70 G4 strains. Secondary structure predictions of the VP7 G4 protein revealed an insert of an asparagine residue in position 76, which, combined with additional mutations, surprisingly modified two downstream ß-sheets at amino acid positions 80 to 85 and 115 to 119. The 2005 G4P[8] strain compared to a G4P[8] strain from 2002 had a substitution of an asparagine residue for threonine (Asn->Thr) at position 96 within antigenic region A, thus eliminating a potential glycosylation site. The mutated G4 virus was introduced in Nicaragua after 2002 and probably emerged from Brazil, Argentina, or Uruguay.


* Corresponding author. Mailing address: Division of Molecular Virology, Medical Faculty, University of Linköping, SE-581 85 Linköping, Sweden. Phone: 46 13 228803. Fax: 46 13 221375. E-mail: lensv{at}imk.liu.se.

{triangledown} Published ahead of print on 17 January 2007.

{dagger} F.B. and B.K. contributed equally to this work.


Journal of Clinical Microbiology, March 2007, p. 990-997, Vol. 45, No. 3
0095-1137/07/$08.00+0     doi:10.1128/JCM.01992-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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