Elise Tu

Norovirus (NoV) is highly infectious and is the major cause of outbreak gastroenteritis in adults, with pandemic spread of the virus being reported in 1995 and 2002. The NoV genome is genetically diverse, which has hampered development of sensitive molecular biology-based methods. In this study we report on a nested reverse transcriptase PCR (nRT-PCR) that was designed to amplify the highly conserved 3' end of the polymerase region and the 5' end of the capsid gene of NoV genogroup II (GII). The nRT-PCR was validated with strains isolated from sporadic and outbreak cases between 1997 and 2004 in New South Wales, Australia. Phylogenetic analysis identified six genotypes circulating in New South Wales, GII.1, GII.3, GII.4, GII.6, GII.7, and GII.10, with GII.4 being the predominant genotype. In 2004, there was a marked increase in NoV GII activity in Australia, with a novel GII.4 variant being identified as the etiological agent in 18 outbreaks investigated. This novel GII.4 variant, termed Hunter virus, differed by more than 5% at the amino acid level across the capsid from any other NoV strain in the GenBank and EMBL databases. The Hunter virus was subsequently identified as the etiological agent in large epidemics of gastroenteritis in The Netherlands, Japan, and Taiwan in 2004 and 2005.

BACKGROUND: Acute gastroenteritis is commonly associated with norovirus genogroup II (GII) infection. Norovirus GII has 17 classified genotypes (GII.1-GII.17), but only 1 norovirus genotype (GII.4) is associated with global epidemics of gastroenteritis. In 2006, an increase in global norovirus activity was observed. METHODS: During the period from December 2005 through August 2006, a total of 231 fecal samples were obtained from patients with acute gastroenteritis from Australia and New Zealand. Norovirus RNA was amplified and sequenced to determine norovirus genotype and relatedness to known epidemic norovirus GII.4 variants. RESULTS: Two GII.4 variants, designated 2006a and 2006b, were identified in 61.8% and 11.3%, respectively, of the 186 cases investigated. Norovirus 2006a and 2006b have also been implicated as the predominant causes of norovirus-associated gastroenteritis across Europe in 2006. CONCLUSIONS: The global increase in norovirus-associated gastroenteritis in 2006 was linked to the emergence of 2 novel GII.4 variants, 2006a and 2006b.

Norovirus genogroup II excretion during an outbreak of gastroenteritis was investigated in an aged-care facility. Viral shedding peaked in the acute stage of illness and continued for an average of 28.7 days. The viral decay rate was 0.76 per day, which corresponds to a viral half-life of 2.5 days.

To the Editor: Viral gastroenteritis affects millions of people of all ages worldwide, and some seasonality has been observed in outbreak occurrences (1–3). During early 2006 in New South Wales (NSW), a marked increase in outbreaks of gastroenteritis occurred (Figure): 155 outbreaks were reported during the first 5 months compared with 88 outbreaks during 2005. During the first 5 months of 2006, the Enteric Pathogens Laboratory–South Eastern Area Laboratory Services (EPL-SEALS) recorded an increase in norovirus in stool samples, detected by using an enzyme immunoassay (IDEIA Norovirus, DakoCytomation, Cambridgeshire, UK). From January through May 2006, the proportion of samples positive for norovirus increased successively: 0/47 (0%), 1/73 (1.4%), 5/169 (3.0%), 8/106 (7.5%), and 93/413 (22.5%). This trend followed the increasing reports of outbreaks made to the NSW Department of Health (Figure). In May, the rate of norovirus detection (22.5%) was significantly greater than that of any other pathogen (Fisher exact test, p<0.0001), including intestinal parasites, foodborne bacterial pathogens (Salmonella, Shigella, and Camplylobacter), and enteric viruses (rotavirus, adenovirus, and astrovirus).