Rotavirus
Rotavirus is the most common cause of severe diarrhoea among infants and young children,[1] and is one of several viruses that cause infections often called stomach flu, despite having no relation to influenza. It is a genus of double-stranded RNA virus in the family Reoviridae. By the age of five, nearly every child in the world has been infected with rotavirus at least once.[2] However, with each infection, immunity develops, and subsequent infections are less severe;[3] adults are rarely affected.[4] There are five species of this virus, referred to as A, B, C, D, and E.[5] Rotavirus A, the most common, causes more than 90% of infections in humans.
The virus is transmitted by the faecal-oral route. It infects and damages the cells that line the small intestine and causes gastroenteritis. Although rotavirus was discovered in 1973[6] and accounts for up to 50% of hospitalisations for severe diarrhoea in infants and children,[7] its importance is still not widely known within the public health community, particularly in developing countries.[8] In addition to its impact on human health, rotavirus also infects animals, and is a pathogen of livestock.[9]
Rotavirus is usually an easily managed disease of childhood, but worldwide more than 500,000 children under five years of age still die from rotavirus infection each year[10] and almost two million more become severely ill.[8] In the United States, before initiation of the rotavirus vaccination programme, rotavirus caused about 2.7 million cases of severe gastroenteritis in children, almost 60,000 hospitalisations, and around 37 deaths each year.[11] Public health campaigns to combat rotavirus focus on providing oral rehydration therapy for infected children and vaccination to prevent the disease.[12]
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[edit] History
One of Flewett's original electron micrographs
Computer–aided reconstruction of a rotavirus based on several electron micrographs
In 1943, Jacob Light and Horace Hodes proved that a filterable agent in the faeces of children with infectious diarrhoea also caused scours (livestock diarrhoea) in cattle.[13] Three decades later, preserved samples of the agent were shown to be rotavirus.[14] In the intervening years, a virus in mice[15] was shown to be related to the virus causing scours.[16] In 1973, Ruth Bishop described related viruses found in children with gastroenteritis.[6][17]
In 1974, Thomas Henry Flewett suggested the name rotavirus after observing that, when viewed through an electron microscope, a rotavirus particle looks like a wheel (rota in Latin);[18][19] the name was officially recognised by the International Committee on Taxonomy of Viruses four years later.[20] In 1976, related viruses were described in several other species of animals.[16] These viruses, all causing acute gastroenteritis, were recognised as a collective pathogen affecting humans and animals worldwide.[18] Rotavirus serotypes were first described in 1980,[21] and in the following year, rotavirus from humans was first grown in cell cultures derived from monkey kidneys, by adding trypsin (an enzyme found in the duodenum of mammals and now known to be essential for rotavirus to replicate) to the culture medium.[22] The ability to grow rotavirus in culture accelerated the pace of research, and by the mid-1980s the first candidate vaccines were being evaluated.[23]
In 1998, a rotavirus vaccine was licensed for use in the United States. Clinical trials in the United States, Finland, and Venezuela had found it to be 80 to 100% effective at preventing severe diarrhoea caused by rotavirus A, and researchers had detected no statistically significant serious adverse effects.[24][25] The manufacturer, however, withdrew it from the market in 1999, after it was discovered that the vaccine may have contributed to an increased risk for intussusception, a type of bowel obstruction, in one of every 12,000 vaccinated infants.[26] The experience provoked intense debate about the relative risks and benefits of a rotavirus vaccine.[27] In 2006, two new vaccines against rotavirus A infection were shown to be safe and effective in children,[28] and in June 2009 the World Health Organization recommended that rotavirus vaccination be included in all national immunisation programmes to provide protection against this virus.[29]
[edit] Signs and symptoms
Rotavirus gastroenteritis is a mild to severe disease characterised by vomiting, watery diarrhoea, and low-grade fever. Once a child is infected by the virus, there is an incubation period of about two days before symptoms appear.[30] Symptoms often start with vomiting followed by four to eight days of profuse diarrhoea. Dehydration is more common in rotavirus infection than in most of those caused by bacterial pathogens, and is the most common cause of death related to rotavirus infection.[31]
Rotavirus A infections can occur throughout life: the first usually produces symptoms, but subsequent infections are typically asymptomatic,[4] as the immune system provides some protection.[2] Consequently, symptomatic infection rates are highest in children under two years of age and decrease progressively towards 45 years of age.[32][33] Infection in newborn children, although common, is often associated with mild or asymptomatic disease;[34][35] the most severe symptoms tend to occur in children six months to two years of age, the elderly, and those with compromised or absent immune system functions. Due to immunity acquired in childhood, most adults are not susceptible to rotavirus; gastroenteritis in adults usually has a cause other than rotavirus, but asymptomatic infections in adults may maintain the transmission of infection in the community.[36] Symptomatic reinfections are often due to a different rotavirus A serotype.[3][37]
[edit] Transmission
Rotavirus A from the faeces of an infected child
Rotavirus is transmitted by the faecal-oral route, via contact with contaminated hands, surfaces and objects,[38] and possibly by the respiratory route.[1] The faeces of an infected person can contain more than 10 trillion infectious particles per gram;[4] only 10–100 of these are required to transmit infection to another person.[39]
Rotaviruses are stable in the environment and have been found in estuary samples at levels as high as 1–5 infectious particles per US gallon.[40] Sanitary measures adequate for eliminating bacteria and parasites seem to be ineffective in control of rotavirus, as the incidence of rotavirus infection in countries with high and low health standards is similar.[1]
[edit] Disease mechanisms
Electron micrograph of a rotavirus infected enterocyte (top) compared to an uninfected cell (bottom). The bar = approx. 500 nm
The diarrhoea is caused by multiple activities of the virus. Malabsorption occurs because of the destruction of gut cells called enterocytes. The toxic rotavirus protein NSP4 induces age- and calcium ion-dependent chloride secretion, disrupts SGLT1 transporter-mediated reabsorption of water, apparently reduces activity of brush-border membrane disaccharidases, and possibly activates the calcium ion-dependent secretory reflexes of the enteric nervous system.[41][42] Healthy enterocytes secrete lactase into the small intestine; milk intolerance due to lactase deficiency is a particular symptom of rotavirus infection,[43][44] which can persist for weeks.[45] A
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