Journal of Clinical Virology 44 (2009) 1–8
Contents lists available at ScienceDirect
Journal of Clinical Virology journal homepage: www.elsevier.com/locate/jcv
Review
Noroviruses: A comprehensive review夽 Manish M. Patel a,∗ , Aron J. Hall a , Jan Vinjé b , Umesh D. Parashar a a
Epidemiology Branch, Division of Viral Diseases, National Center for Immunizations and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA, United States Gastroenteritis and Respiratory Virus Laboratory Branch, Division of Viral Diseases, National Center for Immunizations and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA, United States b
a r t i c l e
i n f o
Article history: Received 28 August 2008 Received in revised form 10 October 2008 Accepted 14 October 2008 Keywords: Norovirus NoV Calicivirus Review Diarrhea Gastroenteritis
Contents 1. 2. 3. 4. 5. 6. 7.
8.
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Clinical and epidemiologic features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Transmission . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Host susceptibility, immunology, and pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Detection methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Role of NoVs in infection and illness among humans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.1. Antibody prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.2. Sporadic gastroenteritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.3. Epidemic gastroenteritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.4. Clinical management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Prevention and control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.1. Outbreaks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.2. Endemic disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1 2 2 3 3 3 4 4 4 4 5 5 5 6 6
1. Introduction
夽 Disclaimer: The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention. ∗ Corresponding author at: MS-A47, Centers for Disease Control and Prevention, 1600 Clifton Road, NE, Atlanta, GA 30333, United States. Tel.: +1 404 639 2343; fax: +1 404 639 3607. E-mail address:
[email protected] (M.M. Patel). 1386-6532/$ – see front matter. Published by Elsevier B.V. doi:10.1016/j.jcv.2008.10.009
Gastroenteritis, both epidemic and sporadic, is a common cause of morbidity and mortality among persons of all ages, accounting for over 1.8 million deaths in children under 5 years of age worldwide.1 The causes of gastroenteritis include a large variety of bacteria, parasites and viruses, yet in many settings the relative contribution of these agents is unknown. Studies of gastrointestinal disease rarely test for all etiologies comprehensively, and even in those that do, 40–50% of gastroenteritis cases remain of unknown
2
M.M. Patel et al. / Journal of Clinical Virology 44 (2009) 1–8
Fig. 1. Classification of noroviruses in 5 genogroups (GI–V) and 32 genotypes based on sequence diversity in the complete capsid protein VP1. Human strains cluster within GI, GII and GIV.
etiology. However, recent studies employing molecular methods for detection of enteric viruses are closing this diagnostic gap.2,3 Human caliciviruses (i.e., viruses belonging to the genera Norovirus [NoV] and Sapovirus) are now recognized as a leading cause of diarrhea worldwide among persons of all ages. More widespread use of these diagnostics around the world will help elucidate the role of NoVs in different settings and improve targeting of control and treatment measures.4–7 This article reviews the biologic, clinical, and epidemiologic features of NoVs and their role in the etiology of sporadic and epidemic gastroenteritis. 2. History In 1929, Zahorsky first described “Hyperemesis hemis” or “winter vomiting disease,” an illness characterized by the sudden onset of self-limited vomiting and diarrhea that typically peaked during the colder months.8 It was not until 1972, however, that Kapikian and others discovered the etiology of this syndrome. By immune electron microscopic (IEM) examination of stools of volunteers challenged with fecal filtrates from a group of elementary school students affected by an outbreak of gastroenteritis in 1968,9,10 they identified Norwalk virus, the prototype agent of the genus Norovirus (previously denoted as “Norwalk-like viruses”), belonging to the Caliciviridae family. Three other genera are now described in the Caliciviridae family: Sapovirus (previously called “Sapporolike viruses), Lagovirus, and Vesivirus, and a fifth genus (proposed Nebovirus) is pending.11 The molecular cloning of the Norwalk virus genome in 1990 led to dramatic progress in understanding the molecular virology and epidemiology of NoV, development of molecular diagnostic assays, and defining the global burden of NoV disease.12 Although NoVs have not been cultivated and thus direct serotyping using neutralizing antibodies is not possible, reverse transcription-polymerase chain reaction (RT-PCR) and genomic sequencing has demonstrated that NoVs are genetically and antigenically diverse.13 A standardized nomenclature was recently proposed to classify NoVs into
29 genetic clusters that fall within five genogroups.13 Most of the strains relevant to human disease belong to genetic clusters within genogroups I and II (Fig. 1). Since NoV has not been cultivated, developing methods for direct serotyping data will be an important area of future research. Nonetheless, NoV capsid proteins have been expressed in a baculovirus and other expression systems,14 where the capsid proteins self-assemble into virus-like particles (VLP) with morphologic and antigenic properties similar to native NoVs.15,16 Expressed VLPs from several NoV strains have been used as antigens to measure serum antibody responses to infection and as immunogens to generate hyperimmune animal sera. VLPs have also been used to study potential host–cell interactions and identify a cellular receptor for NoV.17,18 Using these VLPs, researchers have recently demonstrated that human histo-blood group antigens (HBGAs) may act as receptors for NoV infection. This finding will have a significant impact on future NoV research with regard to pathogenesis, immunology, and the epidemiology of NoV disease.17,19,20 3. Clinical and epidemiologic features NoVs infect persons of all ages.21 Although NoV disease outbreaks are reported year-round, they peak during months with cold weather in temperate climates.22 However, recent studies have demonstrated spring and summer peaks in NoV outbreaks and diarrheal hospitalizations among children
