Acute gastroenteritis is one of the most common illnesses, affecting both adults and children . Infectious causes include viral, bacterial and protozoan organisms; in developed countries, the majority are due to viruses. Several groups of viruses are responsible for these infections, including the rotaviruses, enteric adenoviruses, astroviruses, and the human caliciviruses (including the noroviruses and sapoviruses). The caliciviruses are probably the most important cause of gastroenteritis in adults and older children, estimated to cause 23 million illnesses in the United States each year . In the United States, norovirus may be the etiologic agent in up to 7 percent of patients hospitalized for acute gastroenteritis .
The clinical characteristics of illness induced by the human caliciviruses and the astroviruses, as well as methods for their detection in stool samples will be reviewed here. Issues related to the more detailed epidemiology and prevention of norovirus infection and the clinical presentation of rotavirus infection are discussed separately. (See "Epidemiology of viral gastroenteritis in adults" and "Clinical presentation and diagnosis of rotavirus infection".)
The management of acute viral gastroenteritis in adults is discussed in detail separately. (See "Management of acute viral gastroenteritis in adults".)
NOMENCLATURE AND VIROLOGY
The calicivirus family includes pathogens of both human and animals. The human caliciviruses that cause acute gastroenteritis are divided into two genera, the Noroviruses (NoV) and the Sapoviruses (SaV). Noroviruses were first identified as viral causes of gastroenteritis in an outbreak in Norwalk, Ohio, and were previously referred to as the Norwalk-like viruses, or NLV. Similarly, the human caliciviruses that were first identified in Japan were referred to as the Sapporo agent; they are now classified as Sapoviruses.
Caliciviruses contain a single-stranded RNA genome and have a relatively simple structure, containing one major (VP1) and one minor (VP2) capsid protein . Expression of the VP1 in experimental systems leads to formation of empty capsids or virus-like particles (VLPs) that are useful tools to generate immune reagents and investigate pathogenesis. (See 'Diagnosis' below.)