Molecular epidemiology of caliciviruses detected in sporadic and outbreak cases of gastroenteritis in France from December 1998 to February 2004
|Author(s)||Bon Fabienne1, Ambert Balay K1, Giraudon H1, Kaplon J1, Le Guyader Soizick2, Pommepuy Monique2, Gallay A3, Vaillant V3, de Valk H3, Chikhi Brachet R4, Flahaut A4, Pothier P1, Kohli E1|
|Affiliation(s)||1 : CHU Dijon, Virol Lab, Dijon, France.
2 : IFREMER, Microbiol Lab, Nantes, France.
3 : Inst Natl Veille Sanitaire, Paris, France.
4 : INSERM, U444, Paris, France.
|Source||European Journal of Clinical Microbiology & Infectious Diseases (0095-1137) (Springer), 2005-09 , Vol. 43 , N. 9 , P. 4659-4664|
|WOS© Times Cited||83|
|Keyword(s)||Genogroup, Cocirculation, Gastroenteritis, Caliciviruses, Epidemiological|
|Abstract||We compiled sequence and epidemiological data from 172 caliciviruses detected in France from December 1998 to February 2004 in sporadic and outbreak cases. The results showed a cocirculation of strains with a majority of genogroup II (GII) noroviruses. Three groups of noroviruses, not detected before in our laboratory, emerged and spread during the period: the recombinant GGIIb and Norwalk-related strains not amplified in the polymerase gene in 2000 and a new Lordsdale variant in 2002. We observed that (I) GII4 noroviruses were predominant in nursing home and hospital outbreaks but rare in oyster- and water-related outbreaks despite continuous circulation in the population; (ii) at the opposite, genogroup I strains were detected in the majority of environmental outbreaks; (iii) several strains were frequently found in oyster- and water-linked outbreaks (up to seven), whereas one single strain was detected when transmission was from person to person; and (iv) whereas GII noroviruses were predominant in sporadic cases where patients were under 15 years of age, GI strains were more frequent in outbreaks occurring in this age group. Finally, from a methodology point of view, this compilation shows that detection and characterization in the polymerase gene are not adequate in a significant number of cases and should be completed by amplification and sequencing in the capsid gene.|