Prevalence of “Norwalk-like virus” infections in outbreaks of acute nonbacterial gastroenteritis observed during the 1999–2000 season in Osaka city, Japan
✍ Scribed by Nobuhiro Iritani; Yoshiyuki Seto; Hideyuki Kubo; Kosuke Haruki; Minoru Ayata; Hisashi Ogura
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 186 KB
- Volume
- 66
- Category
- Article
- ISSN
- 0146-6615
- DOI
- 10.1002/jmv.2121
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✦ Synopsis
Abstract
We have investigated the incidence of Norwalk‐like viruses (NLVs) associated with outbreaks of acute nonbacterial gastroenteritis in Osaka City, Japan, since April 1996 using reverse transcription (RT)‐PCR and electron microscopy methods. From the results of the first 3 years, between April 1996 and March 1999, we previously reported that multiple genetic types of NLVs were detected in 71.9% of outbreaks using RT‐PCR with Ando's primers except for one outbreak [Iritani et al., 2000]. However, during the 1999–2000 season, NLV outbreak strains, which could not be detected by RT‐PCR with Ando's primers, were increased. From probe typing and sequence analysis, 76.9% of these undetectable outbreak strains were classified into the P1‐B type and the others were untypeable. These untypeable strains were closely related with Alphatron type strains detected in the Netherlands. The P2‐B probe type of the NLV outbreak strains was predominant (88.2%) in the 1999–2000 season. The phylogram based on the 81 nucleotide sequences from these P2‐B outbreak strains formed 2 clusters closely related with Lordsdale virus. The dominant genetic type of the P2‐B outbreak strains, during the 1996–1997 season in Osaka City, belonged in one of these 2 clusters. These findings of the emergence of NLVs escaping the RT‐PCR method strongly indicated the importance of probe typing and sequence analysis to survey NLV infections. Our surveillance of NLV infection in the outbreaks, for these 4 years, showed that the predominant probe type and dominant genetic type of NLV outbreak strains changed each season. J. Med. Virol. 66:131–138, 2002. © 2002 Wiley‐Liss, Inc.