Wikiversity

WikiJournal of Medicine/Rotavirus

< WikiJournal of Medicine

WikiJournal of Medicine
Open access • Publication charge free • Public peer review • Wikipedia-integrated

WikiJournal of Medicine is an open-access, free-to-publish, Wikipedia-integrated academic journal for Medical and Biomedical topics. <seo title=" WJM, WikiJMed, Wiki.J.Med., WikiJMed, Wikiversity Journal of Medicine, WikiJournal Medicine, Wikipedia Medicine, Wikipedia medical journal, WikiMed, Wikimedicine, Wikimedical, Medicine, Biomedicine, Free to publish, Open access, Open-access, Non-profit, online journal, Public peer review "/>

<meta name='citation_doi' value='10.15347/wjm/2017.007'>

Article information

Abstract

Rotavirus is the most common cause of diarrhoeal disease among infants and young children.[1] It is a genus of double-stranded RNA viruses in the family Reoviridae. Nearly every child in the world is infected with rotavirus at least once by the age of five.[2] Immunity develops with each infection, so subsequent infections are less severe; adults are rarely affected.[3] There are eight species of this virus, referred to as A, B, C, D, E, F, G and H. Rotavirus A, the most common species, causes more than 90% of rotavirus 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 (which is often called "stomach flu" despite having no relation to influenza). Although rotavirus was discovered in 1973 by Ruth Bishop and her colleagues by electron micrograph images[4] and accounts for approximately one third of hospitalisations for severe diarrhoea in infants and children,[5] its importance has historically been underestimated within the public health community, particularly in developing countries.[6] In addition to its impact on human health, rotavirus also infects animals, and is a pathogen of livestock.[7]

Rotavirus is usually an easily managed disease of childhood, but in 2013, rotavirus caused 37 percent of deaths of children from diarrhoea and 215,000 deaths worldwide,[8] and almost two million more become severely ill.[6] Most of these deaths occurred in developing countries.[9] 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.[10] Following rotavirus vaccine introduction in the United States, hospitalisation rates have fallen significantly.[11][12] Public health campaigns to combat rotavirus focus on providing oral rehydration therapy for infected children and vaccination to prevent the disease.[13] The incidence and severity of rotavirus infections has declined significantly in countries that have added rotavirus vaccine to their routine childhood immunisation policies.[14][15][16]



Virology

 

 Computer–aided reconstruction of a rotavirus based on several electron micrographs


Types of rotavirus

There are eight species of rotavirus, referred to as groups A, B, C, D, E, F, G, and H.[17] Humans are primarily infected by species A, B and C, most commonly by species A. A–E species cause disease in other animals,[18] species E and H in pigs, and D, F and G in birds.[19][20] Within rotavirus A there are different strains, called serotypes.[21] As with influenza virus, a dual classification system is used based on two proteins on the surface of the virus. The glycoprotein VP7 defines the G serotypes and the protease-sensitive protein VP4 defines P serotypes.[22] Because the two genes that determine G-types and P-types can be passed on separately to progeny viruses, different combinations are found.[22] A whole genome genotyping system has been established for group A rotaviruses, which has been used to determine the origin of atypical strains.[23] The prevalence of rotavirus the individual G-types and P-types varies between, and within, countries and years.[24]

Structure

The genome of rotavirus consists of 11 unique double helix molecules of RNA (dsRNA) which are 18,555 nucleotides in total. Each helix, or segment, is a gene, numbered 1 to 11 by decreasing size. Each gene codes for one protein, except genes 9, which codes for two.[25] The RNA is surrounded by a three-layered icosahedral protein capsid. Viral particles are up to 76.5 nm in diameter[26][27] and are not enveloped. Figure 1 shows a computer reconstructed image of a rotavirus particle based on electron micrographs of actual particles.

 

 A simplified diagram of the location of rotavirus structural proteins


Proteins

There are six viral proteins (VPs) that form the virus particle (virion). These structural proteins are called VP1, VP2, VP3, VP4, VP6 and VP7. In addition to the VPs, there are six nonstructural proteins (NSPs), that are only produced in cells infected by rotavirus. These are called NSP1, NSP2, NSP3, NSP4, NSP5 and NSP6.[18]

At least six of the twelve proteins encoded by the rotavirus genome bind RNA.[28] The role of these proteins play in rotavirus replication is not entirely understood; their functions are thought to be related to RNA synthesis and packaging in the virion, mRNA transport to the site of genome replication, and mRNA translation and regulation of gene expression.[29]

Structural proteins

 

 Electron micrograph of gold nanoparticles attached to rotavirus. The small dark circular objects are gold nanoparticles coated with a monoclonal antibody specific for rotavirus protein VP6.


Figure 2 shows the location of the proteins and RNA in a rotavirus virion. VP1 is located in the core of the virus particle and is an RNA polymerase enzyme.[30] In an infected cell this enzyme produces mRNA transcripts for the synthesis of viral proteins and produces copies of the rotavirus genome RNA segments for newly produced virus particles.[31]

VP2 forms the core layer of the virion and binds the RNA genome.[32]

VP3 is part of the inner core of the virion and is an enzyme called guanylyl transferase. This is a capping enzyme that catalyses the formation of the 5' cap in the post-transcriptional modification of mRNA.[33] The cap stabilises viral mRNA by protecting it from nucleic acid degrading enzymes called nucleases.[34]

VP4 is on the surface of the virion that protrudes as a spike.[35] It binds to molecules on the surface of cells called receptors and drives the entry of the virus into the cell.[36] VP4 has to be modified by the protease enzyme trypsin, which is found in the gut, into VP5* and VP8* before the virus is infectious.[37] VP4 determines how virulent the virus is and it determines the P-type of the virus.[38] In humans there is an association between the blood group secretor status and susceptibility to infection. Non-secretors seem resistant to infection by types P[4] and P[8], indicating that blood group antigens are the receptors for these genotypes.[39]

VP6 forms the bulk of the capsid. It is highly antigenic and can be used to identify rotavirus species.[40] This protein is used in laboratory tests for rotavirus A infections.[41] Figure 3 shows VP6-specific monoclonal antibodies, which have been attached to particles of gold, reacting with VP6 on the virus capsid.

VP7 is a glycoprotein that forms the outer surface of the virion. Apart from its structural functions, it determines the G-type of the strain and, along with VP4, is involved in immunity to infection.[26]

Nonstructural viral proteins

NSP1, the product of gene 5, is a nonstructural RNA-binding protein.[42] NSP1 also blocks the interferon response, the part of the innate immune system that protects cells from viral infection. NSP1 causes the proteosome to degrade key signaling components required to stimulate production of interferon in an infected cell and to respond to interferon secreted by adjacent cells. Targets for degradation include several IRF transcription factors required for interferon gene transcription.[43]

NSP2 is an RNA-binding protein that accumulates in cytoplasmic inclusions (viroplasms) and is required for genome replication.[44][32]

NSP3 is bound to viral mRNAs in infected cells and it is responsible for the shutdown of cellular protein synthesis.[45] NSP3 inactivates two translation initiation factors essential for synthesis of proteins from host mRNA. First, NSP3 ejects poly(A)-binding protein (PABP) from the translation initiation factor eIF4F. PABP is required for efficient translation of transcripts with a 3' poly(A) tail, which is found on most host cell transcripts. Second, NSP3 inactivates eIF2 by stimulating its phosphorylation.[46] Efficient translation of rotavirus mRNA, which lacks the 3' poly(A) tail, does not require either of these factors.[47]

NSP4 is a viral enterotoxin that induces diarrhoea and was the first viral enterotoxin discovered.[48]

NSP5 is encoded by genome segment 11 of rotavirus A. In virus-infected cells NSP5 accumulates in the viroplasm.[49]

NSP6 is a nucleic acid binding protein[50] and is encoded by gene 11 from an out-of-phase open reading frame.[51]

Table 1 | Rotavirus genes and proteins
RNA Segment (Gene) Size (base pairs) Protein Molecular weight (kDa) Location Copies per particle Function
1 3302 VP1 125 At the vertices of the core 12 RNA-dependent RNA polymerase
2 2690 VP2 102 Forms inner shell of the core 120 RNA binding
3 2591 VP3 88 At the vertices of the core 12 methyltransferase mRNA capping enzyme
4 2362 VP4 87 Surface spike 180 Cell attachment, virulence
5 1611 NSP1 59 Nonstructural 0 5'RNA binding, interferon antagonist
6 1356 VP6 45 Inner Capsid 780 Structural and species-specific antigen
7 1104 NSP3 37 Nonstructural 0 Enhances viral mRNA activity and shut-offs cellular protein synthesis
8 1059 NSP2 35 Nonstructural 0 NTPase involved in RNA packaging
9 1062 VP71 VP72 38 and 34 Surface 780 Structural and neutralisation antigen
10 751 NSP4 20 Nonstructural 0 Enterotoxin
11 667 NSP5 NSP6 22 Nonstructural 0 ssRNA and dsRNA binding modulator of NSP2, phosphoprotein

This table is based on the simian rotavirus strain SA11. RNA-protein coding assignments differ in some strains.

Replication

 

 A simplified drawing of the rotavirus replication cycle. The stages are (1) attachment of the virus to the host cells, which is mediated by VP4 and VP7 (2) penetration of the cell by the virus and uncoating of the viral capsid (3) plus strand ssRNA synthesis ( this acts as the mRNA) synthesis, which is mediated by VP1, VP3 and VP2 (4) formation of the viroplasm , viral RNA packaging and minus strand RNA synthesis and formation of the double-layered virus particles (5) virus particle maturation and release of progeny virions.


The virus enter cells by receptor mediated endocytosis and form a vesicle known as an endosome. Proteins in the third layer (VP7 and the VP4 spike) disrupt the membrane of the endosome, creating a difference in the calcium concentration. This causes the breakdown of VP7 trimers into single protein subunits, leaving the VP2 and VP6 protein coats around the viral dsRNA, forming a double-layered particle (DLP).[52]

The eleven dsRNA strands remain within the protection of the two protein shells and the viral RNA-dependent RNA polymerase creates mRNA transcripts of the double-stranded viral genome. By remaining in the core, the viral RNA evades innate host immune responses including RNA interference that are triggered by the presence of double-stranded RNA (Figure 4).[53]

During the infection, rotavirus produces mRNA for both protein biosynthesis and gene replication. Most of the rotavirus proteins accumulate in viroplasm, where the RNA is replicated and the DLPs are assembled. In the viroplasm the positive sense viral RNAs that are used as templates for the synthesis of viral genomic dsRNA are protected from siRNA-induced RNase degradation.[54] Viroplasm is formed around the cell nucleus as early as two hours after virus infection, and consists of viral factories thought to be made by two viral nonstructural proteins: NSP5 and NSP2. Inhibition of NSP5 by RNA interference in vitro results in a sharp decrease in rotavirus replication. The DLPs migrate to the endoplasmic reticulum where they obtain their third, outer layer (formed by VP7 and VP4). The progeny viruses are released from the cell by lysis.[37][55][56]

Transmission

 

 Rotaviruses in the faeces of an infected child


Rotavirus is transmitted by the fæcal-oral route, via contact with contaminated hands, surfaces and objects,[57] and possibly by the respiratory route.[58] Viral diarrhoea is highly contagious. The faeces of an infected person can contain more than 10 trillion infectious particles per gram (Figure 5);[40] fewer than 100 of these are required to transmit infection to another person.[3]

Rotaviruses are stable in the environment and have been found in estuary samples at levels up to 1–5 infectious particles per US gallon, the viruses survive between 9 and 19 days.[59] 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.[58]

Signs and symptoms

Main resource: w:rotaviral enteritis

Rotaviral enteritis is a mild to severe disease characterised by nausea, 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.[60] The period of illness is acute. 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.[61]

Rotavirus A infections can occur throughout life: the first usually produces symptoms, but subsequent infections are typically mild or asymptomatic,[62][40] as the immune system provides some protection.[63] Consequently, symptomatic infection rates are highest in children under two years of age and decrease progressively towards 45 years of age.[64] The most severe symptoms tend to occur in children six months to two years of age, the elderly, and those with immunodeficiency. 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.[65] There is some to evidence to suggest blood group secretor status and the predominant bacteria in the gut can impact on the susceptibility to infection by rotavirus.[66]

Disease mechanisms

 

 Electron micrograph of a rotavirus infected enterocyte (top) compared to an uninfected cell (bottom). The bar = approx. 500 nm


Rotaviruses replicate mainly in the gut,[67] and infect enterocytes of the villi of the small intestine, leading to structural and functional changes of the epithelium (Figure 6).[68] There is evidence in humans, and particularly in animal models of extraintestinal dissemination of infectious virus to other organs and macrophages.[69]

The diarrhoea is caused by multiple activities of the virus.[70] Malabsorption occurs because of the destruction of gut cells called enterocytes (Figure 3). The toxic rotavirus protein NSP4 induces age- and calcium ion-dependent chloride secretion, disrupts SGLT1 (sodium/glucose cotransporter 2) transporter-mediated reabsorption of water, apparently reduces activity of brush-border membrane disaccharidases, and activates the calcium ion-dependent secretory reflexes of the enteric nervous system.[48] The elevated concentrations of calcium ions in the cytosol (which are required for the assembly of the progeny viruses) is achived by NSP4 acting as a viroporin. This increase in calcium ions leads to autophagy (self destruction) of the infected enterocytes.[71]

NSP4 is also secreted. This extracellular form, which is modified by protease enzymes in the gut, is an enterotoxin which acts on uninfected cells via integrin receptors, which in turn cause and increase in intracellular calcium ion concentrations, secretory diarrhoea and autophagy.[72]

The vomiting, which is a characteristic of rotaviral enteritis, is caused by the virus infecting the enterochromaffin cells on the lining of the digestive tract. The infection stimulates the production of 5' hydroxytryptamine (serotonin). This activates vagal afferent nerves, which in turn activates the cells of the brain stem that control the vomiting reflex.[73]

Healthy enterocytes secrete lactase into the small intestine; milk intolerance due to lactase deficiency is a symptom of rotavirus infection,[74] which can persist for weeks.[75] A recurrence of mild diarrhoea often follows the reintroduction of milk into the child's diet, due to bacterial fermentation of the disaccharide lactose in the gut.[76]

Immune responses

Specific responses

Rotaviruses elicit both B and T cell immune responses. Antibodies to the rotavirus VP4 and VP7 proteins neutralise viral infectivity in vitro and in vivo.[77] Specific antibodies of the classes IgM, IgA and IgG are produced, which have been shown to protect against rotavirus infection by the passive transfer of the antibodies in animals.[78] Maternal trans-placental IgG might play a role in the protection neonates from rotavirus infections, but on the other hand might reduce vaccine efficacy.[79]

Innate responses

Following infection by rotaviruses there is a rapid innate immune response involving types I and III interferons and other cytokines (particularly Th1 and Th2 [80]) which inhibit the replication of the virus and recruit macophages, and natural killer cells to the rotavirus infected cells.[81] The rotavirus dsRNA activates pattern recognition receptors such toll-like receptors that stimulate the production of interferons.[82] The rotavirus protein NSP1 counteracts the effects of type 1 interferons by suppressing the activity of the interferon regulatory proteins IRF3, IRF5 and IRF7.[82]

Markers of protection

The levels of IgG and IgA in the blood, and IgA in the gut correlate with protection from infection.[83] Rotavirus specific serum IgG and IgA at high titres (e.g. >1:200) have been claimed to be protective and there is a significant correlation between IgA titres and rotavirus vaccine efficacy.[84]

Diagnosis and detection

Diagnosis of infection with rotavirus normally follows diagnosis of gastroenteritis as the cause of severe diarrhoea. Most children admitted to hospital with gastroenteritis are tested for rotavirus A.[85][86] Specific diagnosis of infection with rotavirus A is made by finding the virus in the child's stool by enzyme immunoassay. There are several licensed test kits on the market which are sensitive, specific and detect all serotypes of rotavirus A.[87] Other methods, such as electron microscopy and PCR (polymerase chain reaction), are used in research laboratories.[88] Reverse transcription-polymerase chain reaction (RT-PCR) can detect and identify all species and serotypes of human rotavirus.[89]

Treatment and prognosis

Treatment of acute rotavirus infection is nonspecific and involves management of symptoms and, most importantly, management of dehydration.[13] If untreated, children can die from the resulting severe dehydration.[90] Depending on the severity of diarrhoea, treatment consists of oral rehydration therapy, during which the child is given extra water to drink that contains specific amounts of salt and sugar.[91] In 2004, the World Health Organisation (WHO) and UNICEF recommended the use of low-osmolarity oral rehydration solution and zinc supplementation as a two-pronged treatment of acute diarrhoea.[92] Some infections are serious enough to warrant hospitalisation where fluids are given by intravenous therapy or nasogastric intubation, and the child's electrolytes and blood sugar are monitored.[85] Probiotics have been shown to reduce the duration of rotavirus diarrhoea,[93] and according to the European Society for Pediatric Gastroenterology "effective interventions include administration of specific probiotics such as Lactobacillus rhamnosus or Saccharomyces boulardii, diosmectite or racecadotril."[94] Rotavirus infections rarely cause other complications and for a well managed child the prognosis is excellent.[95]

Prevention

Main resource: w:Rotavirus vaccine

Rotavirus is highly contagious and cannot be treated with antibiotics or other drugs. Because improved sanitation does not decrease the prevalence of rotaviral disease, and the rate of hospitalisations remains high despite the use of oral rehydrating medicines, the primary public health intervention is vaccination.[2]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.[96][97] 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.[98] The experience provoked intense debate about the relative risks and benefits of a rotavirus vaccine.[99] In 2006, two new vaccines against rotavirus A infection were shown to be safe and effective in children,[100] and in 2009, the WHO recommended that rotavirus vaccine be included in all national immunisation programmes.[101]

The incidence and severity of rotavirus infections has declined significantly in countries that have acted on this recommendation.[14][15][16] A 2014 review of available clinical trial data from countries routinely using rotavirus vaccines in their national immunisation programs found that rotavirus vaccines have reduced rotavirus hospitalisations by 49-92 percent and all cause diarrhoea hospitalisations by 17-55 percent.[102] In Mexico, which in 2006 was among the first countries in the world to introduce rotavirus vaccine, diarrhoeal disease death rates dropped during the 2009 rotavirus season by more than 65 percent among children age two and under.[103] In Nicaragua, which in 2006 became the first developing country to introduce a rotavirus vaccine, severe rotavirus infections were reduced by 40 percent and emergency room visits by a half.[104] In the United States, rotavirus vaccination since 2006 has led to drops in rotavirus-related hospitalisations by as much as 86 percent. The vaccines may also have prevented illness in non-vaccinated children by limiting the number of circulating infections.[105] In developing countries in Africa and Asia, where the majority of rotavirus deaths occur, a large number of safety and efficacy trials as well as recent post-introduction impact and effectiveness studies of Rotarix and RotaTeq have found that vaccines dramatically reduced severe disease among infants.[16][106][107][108] In September 2013, the vaccine was offered to all children in the UK, aged between two and three months, and it is expected to halve the cases of severe infection and reduce the number of children admitted to hospital because of the infection by 70 percent.[109] In Europe, hospitalisation rates following infection by rotavirus have decreased by 65% to 84% following the introduction of the vaccine.[110] Globally, vaccination has reduced hospital admissions and emergency department visits by a median of 67%.[111]

Rotavirus vaccines are licensed in over 100 countries, and more than 80 countries have introduced routine rotavirus vaccination, almost half with the support of Gavi, the Vaccine Alliance.[112] To make rotavirus vaccines available, accessible, and affordable in all countries—particularly low- and middle-income countries in Africa and Asia where the majority of rotavirus deaths occur, PATH (formerly Program for Appropriate Technology in Health), the WHO, the U.S. Centers for Disease Control and Prevention, and Gavi have partnered with research institutions and governments to generate and disseminate evidence, lower prices, and accelerate introduction.[113]

Epidemiology

 

 The seasonal variation of rotavirus A infections in England: rates of infection peak during the winter months.[114]


Rotavirus A, which accounts for more than 90% of rotavirus gastroenteritis in humans,[115] is endemic worldwide. Each year rotavirus causes millions of cases of diarrhoea in developing countries, almost 2 million of which result in hospitalisation.[6] In 2013, an estimated 215,000 children younger than five died from rotavirus, 90 percent of whom were in developing countries.[6] Almost every child has been infected with rotavirus by age five.[116] Rotavirus is the leading single cause of severe diarrhoea among infants and children, is responsible for about a third of the cases requiring hospitalisation,[11] and causes 37% of deaths attributable to diarrhoea and 5% of all deaths in children younger than five.[117] Boys are twice as likely as girls to be admitted to hospital for rotavirus.[118][119] In the pre-vaccination era, rotavirus infections occurred primarily during cool, dry seasons (Figure 7).[120][121] The number attributable to food contamination is unknown.[122]

Outbreaks of rotavirus A diarrhoea are common among hospitalised infants, young children attending day care centres, and elderly people in nursing homes.[65][123] An outbreak caused by contaminated municipal water occurred in Colorado in 1981.[124] During 2005, the largest recorded epidemic of diarrhoea occurred in Nicaragua. This unusually large and severe outbreak was associated with mutations in the rotavirus A genome, possibly helping the virus escape the prevalent immunity in the population.[125] A similar large outbreak occurred in Brazil in 1977.[126]

Rotavirus B, also called adult diarrhoea rotavirus or ADRV, has caused major epidemics of severe diarrhoea affecting thousands of people of all ages in China. These epidemics occurred as a result of sewage contamination of drinking water.[127][128] Rotavirus B infections also occurred in India in 1998; the causative strain was named CAL. Unlike ADRV, the CAL strain is endemic.[129][130] To date, epidemics caused by rotavirus B have been confined to mainland China, and surveys indicate a lack of immunity to this species in the United States.[131] Rotavirus C has been associated with rare and sporadic cases of diarrhoea in children, and small outbreaks have occurred in families.[132]

Other animals

Rotaviruses infect the young of many species of animals and they are a major cause of diarrhoea in wild and reared animals worldwide.[7] As a pathogen of livestock, notably in young calves and piglets, rotaviruses cause economic loss to farmers because of costs of treatment associated with high morbidity and mortality rates.[133] These rotaviruses are a potential reservoir for genetic exchange with human rotaviruses.[133] There is evidence that animal rotaviruses can infect humans, either by direct transmission of the virus or by contributing one or several RNA segments to reassortants with human strains.[134][135][136]

History

 

 One of Flewett's original electron micrographs showing a single rotavirus particle. When examined by negative stained electron microscopy, rotaviruses often resemble wheels.


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.[137] Three decades later, preserved samples of the agent were shown to be rotavirus.[138] In the intervening years, a virus in mice[139] was shown to be related to the virus causing scours.[140] In 1973, Ruth Bishop and colleagues described related viruses found in children with gastroenteritis.[4]

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) (Figure 8);[141][142] the name was officially recognised by the International Committee on Taxonomy of Viruses four years later.[143] In 1976, related viruses were described in several other species of animals.[140] These viruses, all causing acute gastroenteritis, were recognised as a collective pathogen affecting humans and animals worldwide.[141] Rotavirus serotypes were first described in 1980,[144] 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.[145] The ability to grow rotavirus in culture accelerated the pace of research, and by the mid-1980s the first candidate vaccines were being evaluated.[146]

References

  1. ↑ Dennehy PH (2015). "Rotavirus Infection: A Disease of the Past?". Infectious Disease Clinics of North America 29 (4): 617–35. doi:10.1016/j.idc.2015.07.002. PMID 26337738. 
  2. ↑ 2.0 2.1 Bernstein DI (2009). "Rotavirus overview". The Pediatric Infectious Disease Journal 28 (Suppl 3): S50–3. doi:10.1097/INF.0b013e3181967bee. PMID 19252423. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0891-3668&volume=28&issue=3&spage=S50. 
  3. ↑ 3.0 3.1 Grimwood K; Lambert SB (2009). "Rotavirus vaccines: opportunities and challenges". Human Vaccines 5 (2): 57–69. doi:10.4161/hv.5.2.6924. PMID 18838873. http://www.landesbioscience.com/journals/hv/abstract.php?id=6924. 
  4. ↑ 4.0 4.1 Bishop R (2009). "Discovery of rotavirus: Implications for child health". Journal of Gastroenterology and Hepatology 24 (Suppl 3): S81–5. doi:10.1111/j.1440-1746.2009.06076.x. PMID 19799704. 
  5. ↑ World Health Organization (2015). "Global Rotavirus Sentinel Hospital Surveillance Network" (PDF).
  6. ↑ 6.0 6.1 6.2 6.3 Simpson E; Wittet S; Bonilla J; Gamazina K; Cooley L; Winkler JL (2007). "Use of formative research in developing a knowledge translation approach to rotavirus vaccine introduction in developing countries". BMC Public Health 7: 281. doi:10.1186/1471-2458-7-281. PMID 17919334. PMC 2173895. http://www.biomedcentral.com/1471-2458/7/281. 
  7. ↑ 7.0 7.1 Dubovi EJ; MacLachlan NJ (2010). Fenner's Veterinary Virology (4th ed.). Boston: Academic Press. p. 288. ISBN 0-12-375158-6. 
  8. ↑ Tate JE; Burton AH; Boschi-Pinto C; Parashar UD (2016). "Global, Regional, and National Estimates of Rotavirus Mortality in Children <5 Years of Age, 2000-2013". Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 62 (Suppl 2): S96–105. doi:10.1093/cid/civ1013. PMID 27059362. 
  9. ↑ World Health Organization (2008). "Global networks for surveillance of rotavirus gastroenteritis, 2001–2008". Weekly Epidemiological Record 83 (47): 421–8. http://www.who.int/wer/2008/wer8347.pdf. Retrieved 3 May 2012. 
  10. ↑ Fischer TK; Viboud C; Parashar U; Malek M; Steiner C; Glass R; Simonsen L (2007). "Hospitalizations and deaths from diarrhea and rotavirus among children <5 years of age in the United States, 1993–2003". Journal of Infectious Diseases 195 (8): 1117–25. doi:10.1086/512863. PMID 17357047. 
  11. ↑ 11.0 11.1 Leshem E; Moritz RE; Curns AT; Zhou F; Tate JE; Lopman BA; Parashar UD (2014). "Rotavirus Vaccines and Health Care Utilization for Diarrhea in the United States (2007–2011)". Pediatrics 134 (1): 15–23. doi:10.1542/peds.2013-3849. PMID 24913793. http://pediatrics.aappublications.org/content/134/1/15. 
  12. ↑ Tate JE; Cortese MM; Payne DC; Curns AT; Yen C; Esposito DH; Cortes JE; Lopman BA et al. (2011). "Uptake, impact, and effectiveness of rotavirus vaccination in the United States: review of the first 3 years of postlicensure data". The Pediatric Infectious Disease Journal 30 (Suppl 1): S56–60. doi:10.1097/INF.0b013e3181fefdc0. PMID 21183842. 
  13. ↑ 13.0 13.1 Diggle L (2007). "Rotavirus diarrhea and future prospects for prevention". British Journal of Nursing 16 (16): 970–4. doi:10.12968/bjon.2007.16.16.27074. PMID 18026034. 
  14. ↑ 14.0 14.1 Giaquinto C; Dominiak-Felden G; Van Damme P; Myint TT; Maldonado YA; Spoulou V; Mast TC; Staat MA (2011). "Summary of effectiveness and impact of rotavirus vaccination with the oral pentavalent rotavirus vaccine: a systematic review of the experience in industrialized countries". Human Vaccines 7 (7): 734–48. doi:10.4161/hv.7.7.15511. PMID 21734466. http://www.landesbioscience.com/journals/hv/abstract.php?id=15511. 
  15. ↑ 15.0 15.1 Jiang V; Jiang B; Tate J; Parashar UD; Patel MM (2010). "Performance of rotavirus vaccines in developed and developing countries". Human Vaccines 6 (7): 532–42. doi:10.4161/hv.6.7.11278. PMID 20622508. PMC 3322519. http://www.landesbioscience.com/journals/hv/abstract.php?id=11278. 
  16. ↑ 16.0 16.1 16.2 Parashar UD, Tate JE, ed (2016). "Health Benefits of Rotavirus Vaccination in Developing Countries". Clinical Infectious Diseases 62 (Suppl 2): S91-228. http://cid.oxfordjournals.org/content/62/suppl_2.toc. 
  17. ↑ "Virus Taxonomy: 2014 Release". International Committee on Taxonomy of Viruses (ICTV).
  18. ↑ 18.0 18.1 Kirkwood CD (2010). "Genetic and antigenic diversity of human rotaviruses: potential impact on vaccination programs". The Journal of Infectious Diseases 202 (Suppl 1): S43–8. doi:10.1086/653548. PMID 20684716. 
  19. ↑ Wakuda M; Ide T; Sasaki J; Komoto S; Ishii J; Sanekata T; Taniguchi K (2011). "Porcine rotavirus closely related to novel group of human rotaviruses". Emerging Infectious Diseases 17 (8): 1491–3. doi:10.3201/eid1708.101466. PMID 21801631. PMC 3381553. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3381553/. 
  20. ↑ Marthaler D; Rossow K; Culhane M; Goyal S; Collins J; Matthijnssens J; Nelson M; Ciarlet M (2014). "Widespread rotavirus H in commercially raised pigs, United States". Emerging Infectious Diseases 20 (7): 1195–8. doi:10.3201/eid2007.140034. PMID 24960190. PMC 4073875. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4073875/. 
  21. ↑ O'Ryan M (2009). "The ever-changing landscape of rotavirus serotypes". The Pediatric Infectious Disease Journal 28 (Suppl 3): S60–2. doi:10.1097/INF.0b013e3181967c29. PMID 19252426. 
  22. ↑ 22.0 22.1 Patton JT (2012). "Rotavirus diversity and evolution in the post-vaccine world". Discovery Medicine 13 (68): 85–97. PMID 22284787. PMC 3738915. http://www.discoverymedicine.com/John-T-Patton/2012/01/26/rotavirus-diversity-and-evolution-in-the-post-vaccine-world/. 
  23. ↑ Phan MVT; Anh PH; Cuong NV; Munnink BBO; van der Hoek L; My PT; Tri TN; Bryant JE et al. (2016). "Unbiased whole-genome deep sequencing of human and porcine stool samples reveals circulation of multiple groups of rotaviruses and a putative zoonotic infection". Virus Evolution 2 (2). doi:10.1093/ve/vew027. PMID 28748110. PMC 5522372. //www.ncbi.nlm.nih.gov/pmc/articles/PMC5522372/. 
  24. ↑ Beards GM; Desselberger U; Flewett TH (1989). "Temporal and geographical distributions of human rotavirus serotypes, 1983 to 1988". Journal of Clinical Microbiology 27 (12): 2827–33. doi:10.1128/jcm.27.12.2827-2833.1989. PMID 2556435. PMC 267135. //www.ncbi.nlm.nih.gov/pmc/articles/PMC267135/. 
  25. ↑ Estes MK; Cohen J (1989). "Rotavirus gene structure and function". Microbiological Reviews 53 (4): 410–49. doi:10.1128/mr.53.4.410-449.1989. PMID 2556635. PMC 372748. //www.ncbi.nlm.nih.gov/pmc/articles/PMC372748/. 
  26. ↑ 26.0 26.1 Pesavento JB; Crawford SE; Estes MK; Prasad BV (2006). "Rotavirus proteins: structure and assembly". In Roy P (ed.). Reoviruses: Entry, Assembly and Morphogenesis. Current Topics in Microbiology and Immunology. 309. New York: Springer. pp. 189–219. doi:10.1007/3-540-30773-7_7. ISBN 978-3-540-30772-3. PMID 16913048. 
  27. ↑ Prasad BV; Chiu W (1994). "Structure of rotavirus". In Ramig RF (ed.). Rotaviruses. Current Topics in Microbiology and Immunology. 185. New York: Springer. pp. 9–29. doi:10.1007/978-3-642-78256-5_2. ISBN 9783540567615. 
  28. ↑ Patton JT (1995). "Structure and function of the rotavirus RNA-binding proteins". The Journal of General Virology 76 (11): 2633–44. doi:10.1099/0022-1317-76-11-2633. PMID 7595370. 
  29. ↑ Patton JT (2001). "Rotavirus RNA replication and gene expression". Novartis Foundation Symposium. Novartis Foundation Symposia 238: 64–77; discussion 77–81. doi:10.1002/0470846534.ch5. ISBN 9780470846537. PMID 11444036. 
  30. ↑ Vásquez-del Carpió R; Morales JL; Barro M; Ricardo A; Spencer E (2006). "Bioinformatic prediction of polymerase elements in the rotavirus VP1 protein". Biological Research 39 (4): 649–59. doi:10.4067/S0716-97602006000500008. PMID 17657346. 
  31. ↑ Trask SD; Ogden KM; Patton JT (2012). "Interactions among capsid proteins orchestrate rotavirus particle functions". Current Opinion in Virology 2 (4): 373–9. doi:10.1016/j.coviro.2012.04.005. PMID 22595300. PMC 3422376. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3422376/. 
  32. ↑ 32.0 32.1 Taraporewala ZF; Patton JT (2004). "Nonstructural proteins involved in genome packaging and replication of rotaviruses and other members of the Reoviridae". Virus Research 101 (1): 57–66. doi:10.1016/j.virusres.2003.12.006. PMID 15010217. 
  33. ↑ Angel J; Franco MA; Greenberg HB (2009). Desk Encyclopedia of Human and Medical Virology. Boston: Academic Press. p. 277. ISBN 0-12-375147-0. 
  34. ↑ Cowling VH (2009). "Regulation of mRNA cap methylation". The Biochemical Journal 425 (2): 295–302. doi:10.1042/BJ20091352. PMID 20025612. PMC 2825737. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2825737/. 
  35. ↑ Gardet A; Breton M; Fontanges P; Trugnan G; Chwetzoff S (2006). "Rotavirus spike protein VP4 binds to and remodels actin bundles of the epithelial brush border into actin bodies". Journal of Virology 80 (8): 3947–56. doi:10.1128/JVI.80.8.3947-3956.2006. PMID 16571811. PMC 1440440. http://jvi.asm.org/cgi/content/full/80/8/3947. 
  36. ↑ Arias CF; Isa P; Guerrero CA; Méndez E; Zárate S; López T; Espinosa R; Romero P et al. (2002). "Molecular biology of rotavirus cell entry". Archives of Medical Research 33 (4): 356–61. doi:10.1016/S0188-4409(02)00374-0. PMID 12234525. 
  37. ↑ 37.0 37.1 Jayaram H; Estes MK; Prasad BV (2004). "Emerging themes in rotavirus cell entry, genome organization, transcription and replication". Virus Research 101 (1): 67–81. doi:10.1016/j.virusres.2003.12.007. PMID 15010218. 
  38. ↑ Hoshino Y; Jones RW; Kapikian AZ (2002). "Characterization of neutralization specificities of outer capsid spike protein VP4 of selected murine, lapine, and human rotavirus strains". Virology 299 (1): 64–71. doi:10.1006/viro.2002.1474. PMID 12167342. 
  39. ↑ Van Trang N; Vu HT; Le NT; Huang P; Jiang X; Anh DD (2014). "Association between norovirus and rotavirus infection and histo-blood group antigen types in Vietnamese children". Journal of Clinical Microbiology 52 (5): 1366–74. doi:10.1128/JCM.02927-13. PMID 24523471. PMC 3993640. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3993640/. 
  40. ↑ 40.0 40.1 40.2 Bishop RF (1996). "Natural history of human rotavirus infection". Archives of Virology 12: 119–28. doi:10.1007/978-3-7091-6553-9_14. PMID 9015109. 
  41. ↑ Beards GM; Campbell AD; Cottrell NR; Peiris JS; Rees N; Sanders RC; Shirley JA; Wood HC et al. (1984). "Enzyme-linked immunosorbent assays based on polyclonal and monoclonal antibodies for rotavirus detection" (PDF). Journal of Clinical Microbiology 19 (2): 248–54. doi:10.1128/jcm.19.2.248-254.1984. PMID 6321549. PMC 271031. http://jcm.asm.org/cgi/reprint/19/2/248. 
  42. ↑ Hua J; Mansell EA; Patton JT (1993). "Comparative analysis of the rotavirus NS53 gene: conservation of basic and cysteine-rich regions in the protein and possible stem-loop structures in the RNA". Virology 196 (1): 372–8. doi:10.1006/viro.1993.1492. PMID 8395125. 
  43. ↑ Arnold MM (2016). "The Rotavirus Interferon Antagonist NSP1: Many Targets, Many Questions". Journal of Virology 90 (11): 5212–5. doi:10.1128/JVI.03068-15. PMID 27009959. 
  44. ↑ Kattoura MD; Chen X; Patton JT (1994). "The rotavirus RNA-binding protein NS35 (NSP2) forms 10S multimers and interacts with the viral RNA polymerase". Virology 202 (2): 803–13. doi:10.1006/viro.1994.1402. PMID 8030243. 
  45. ↑ Poncet D, Aponte C, Cohen J (1993). "Rotavirus protein NSP3 (NS34) is bound to the 3' end consensus sequence of viral mRNAs in infected cells" (PDF). Journal of Virology 67 (6): 3159–65. doi:10.1128/jvi.67.6.3159-3165.1993. PMID 8388495. PMC 237654. http://jvi.asm.org/cgi/reprint/67/6/3159. 
  46. ↑ Gratia M; Vende P; Charpilienne A; Baron HC; Laroche C; Sarot E; Pyronnet S; Duarte M et al. (2016). "Challenging the Roles of NSP3 and Untranslated Regions in Rotavirus mRNA Translation". Plos One 11 (1): e0145998. doi:10.1371/journal.pone.0145998. PMID 26727111. PMC 4699793. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4699793/. 
  47. ↑ López S; Arias CF (2012). "Rotavirus-host cell interactions: an arms race". Current Opinion in Virology 2 (4): 389–98. doi:10.1016/j.coviro.2012.05.001. PMID 22658208. 
  48. ↑ 48.0 48.1 Hyser JM; Estes MK (2009). "Rotavirus vaccines and pathogenesis: 2008". Current Opinion in Gastroenterology 25 (1): 36–43. doi:10.1097/MOG.0b013e328317c897. PMID 19114772. PMC 2673536. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0267-1379&volume=25&issue=1&spage=36. 
  49. ↑ Afrikanova I; Miozzo MC; Giambiagi S; Burrone O (1996). "Phosphorylation generates different forms of rotavirus NSP5". Journal of General Virology 77 (9): 2059–65. doi:10.1099/0022-1317-77-9-2059. PMID 8811003. http://vir.sgmjournals.org/cgi/reprint/77/9/2059. 
  50. ↑ Rainsford EW; McCrae MA (2007). "Characterization of the NSP6 protein product of rotavirus gene 11". Virus Research 130 (1–2): 193–201. doi:10.1016/j.virusres.2007.06.011. PMID 17658646. 
  51. ↑ Mohan KV; Atreya CD (2001). "Nucleotide sequence analysis of rotavirus gene 11 from two tissue culture-adapted ATCC strains, RRV and Wa". Virus Genes 23 (3): 321–9. doi:10.1023/A:1012577407824. PMID 11778700. 
  52. ↑ Baker M; Prasad BVV (2010). "Rotavirus cell entry". In Johnson J (ed.). Cell Entry by Non-Enveloped Viruses. Current Topics in Microbiology and Immunology. 343. pp. 121–48. doi:10.1007/82_2010_34. ISBN 978-3-642-13331-2. PMID 20397068. 
  53. ↑ Arnold MM (2016). "The Rotavirus Interferon Antagonist NSP1: Many Targets, Many Questions". Journal of Virology 90 (11): 5212–5. doi:10.1128/JVI.03068-15. PMID 27009959. PMC 4934742. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4934742/. 
  54. ↑ Silvestri LS; Taraporewala ZF; Patton JT (2004). "Rotavirus replication: plus-sense templates for double-stranded RNA synthesis are made in viroplasms". Journal of Virology 78 (14): 7763–74. doi:10.1128/JVI.78.14.7763-7774.2004. PMID 15220450. PMC 434085. //www.ncbi.nlm.nih.gov/pmc/articles/PMC434085/. 
  55. ↑ Patton JT, Vasquez-Del Carpio R, Spencer E (2004). "Replication and transcription of the rotavirus genome". Current Pharmaceutical Design 10 (30): 3769–77. doi:10.2174/1381612043382620. PMID 15579070. 
  56. ↑ Ruiz MC; Leon T; Diaz Y; Michelangeli F (2009). "Molecular biology of rotavirus entry and replication". The Scientific World Journal 9: 1476–97. doi:10.1100/tsw.2009.158. PMID 20024520. 
  57. ↑ Butz AM; Fosarelli P; Dick J; Cusack T; Yolken R (1993). "Prevalence of rotavirus on high-risk fomites in day-care facilities". Pediatrics 92 (2): 202–5. doi:10.1542/peds.92.2.202. PMID 8393172. 
  58. ↑ 58.0 58.1 Dennehy PH (2000). "Transmission of rotavirus and other enteric pathogens in the home". Pediatric Infectious Disease Journal 19 (Suppl 10): S103–5. doi:10.1097/00006454-200010001-00003. PMID 11052397. 
  59. ↑ Rao VC; Seidel KM; Goyal SM; Metcalf TG; Melnick JL (1984). "Isolation of enteroviruses from water, suspended solids, and sediments from Galveston Bay: survival of poliovirus and rotavirus adsorbed to sediments" (PDF). Applied Environmental Microbiology 48 (2): 404–9. doi:10.1128/aem.48.2.404-409.1984. PMID 6091548. PMC 241526. http://aem.asm.org/cgi/reprint/48/2/404. 
  60. ↑ Hochwald C; Kivela L (1999). "Rotavirus vaccine, live, oral, tetravalent (RotaShield)". Pediatric Nursing 25 (2): 203–4, 207. PMID 10532018. 
  61. ↑ Maldonado YA; Yolken RH (1990). "Rotavirus". Baillière's Clinical Gastroenterology 4 (3): 609–25. doi:10.1016/0950-3528(90)90052-I. PMID 1962726. 
  62. ↑ Glass RI; Parashar UD; Bresee JS; Turcios R; Fischer TK; Widdowson MA; Jiang B; Gentsch JR (2006). "Rotavirus vaccines: current prospects and future challenges". The Lancet 368 (9532): 323–32. doi:10.1016/S0140-6736(06)68815-6. PMID 16860702. 
  63. ↑ Offit PA (2001). Gastroenteritis viruses. New York: Wiley. pp. 106–124. ISBN 0-471-49663-4. 
  64. ↑ Ramsay M; Brown D (2000). "Epidemiology of Group A Rotaviruses: Surveillance and Burden of Disease Studies". In Desselberger U, Gray J (eds.). Rotaviruses: Methods and Protocols. Methods in Molecular Medicine. 34. Totowa, NJ: Humana Press. p. 217. doi:10.1385/1-59259-078-0:217. ISBN 0-89603-736-3. PMID 21318862. 
  65. ↑ 65.0 65.1 Anderson EJ; Weber SG (2004). "Rotavirus infection in adults". The Lancet Infectious Diseases 4 (2): 91–9. doi:10.1016/S1473-3099(04)00928-4. PMID 14871633. 
  66. ↑ Rodríguez-Díaz J; García-Mantrana I; Vila-Vicent S; Gozalbo-Rovira R; Buesa J; Monedero V; Collado MC (2017). "Relevance of secretor status genotype and microbiota composition in susceptibility to rotavirus and norovirus infections in humans". Scientific Reports 7: 45559. doi:10.1038/srep45559. PMID 28358023. PMC 5372083. //www.ncbi.nlm.nih.gov/pmc/articles/PMC5372083/. 
  67. ↑ Greenberg HB; Estes MK (2009). "Rotaviruses: from pathogenesis to vaccination". Gastroenterology 136 (6): 1939–51. doi:10.1053/j.gastro.2009.02.076. PMID 19457420. PMC 3690811. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3690811/. 
  68. ↑ Greenberg HB; Clark HF; Offit PA (1994). "Rotavirus pathology and pathophysiology". In Ramig RF (ed.). Rotaviruses. Current Topics in Microbiology and Immunology. 185. New York: Springer. pp. 255–83. doi:10.1007/978-3-642-78256-5_9. ISBN 9783540567615. 
  69. ↑ Crawford SE; Patel DG; Cheng E; Berkova Z; Hyser JM; Ciarlet M; Finegold MJ; Conner ME et al. (2006). "Rotavirus viremia and extraintestinal viral infection in the neonatal rat model". Journal of Virology 80 (10): 4820–32. doi:10.1128/JVI.80.10.4820-4832.2006. PMID 16641274. PMC 1472071. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1472071/. 
  70. ↑ Ramig RF (2004). "Pathogenesis of intestinal and systemic rotavirus infection". Journal of Virology 78 (19): 10213–20. doi:10.1128/JVI.78.19.10213-10220.2004. PMID 15367586. PMC 516399. //www.ncbi.nlm.nih.gov/pmc/articles/PMC516399/. 
  71. ↑ Hyser JM; Collinson-Pautz MR; Utama B; Estes MK (2010). "Rotavirus disrupts calcium homeostasis by NSP4 viroporin activity". mBio 1 (5). doi:10.1128/mBio.00265-10. PMID 21151776. PMC 2999940. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2999940/. 
  72. ↑ Berkova Z; Crawford SE; Trugnan G; Yoshimori T; Morris AP; Estes MK (2006). "Rotavirus NSP4 induces a novel vesicular compartment regulated by calcium and associated with viroplasms". Journal of Virology 80 (12): 6061–71. doi:10.1128/JVI.02167-05. PMID 16731945. PMC 1472611. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1472611/. 
  73. ↑ Hagbom M; Sharma S; Lundgren O; Svensson L (2012). "Towards a human rotavirus disease model". Current Opinion in Virology 2 (4): 408–18. doi:10.1016/j.coviro.2012.05.006. PMID 22722079. 
  74. ↑ Farnworth ER (2008). "The evidence to support health claims for probiotics". The Journal of Nutrition 138 (6): 1250S–4S. doi:10.1093/jn/138.6.1250S. PMID 18492865. http://jn.nutrition.org/cgi/pmidlookup?view=long&pmid=18492865. 
  75. ↑ Ouwehand A; Vesterlund S (2003). "Health aspects of probiotics". IDrugs : the Investigational Drugs Journal 6 (6): 573–80. PMID 12811680. 
  76. ↑ Arya SC (1984). "Rotaviral infection and intestinal lactase level". Journal of Infectious Diseases 150 (5): 791. doi:10.1093/infdis/150.5.791. PMID 6436397. 
  77. ↑ Ward R (2009). "Mechanisms of protection against rotavirus infection and disease". The Pediatric Infectious Disease Journal 28 (Suppl 3): S57–9. doi:10.1097/INF.0b013e3181967c16. PMID 19252425. 
  78. ↑ Vega CG; Bok M; Vlasova AN; Chattha KS; Fernández FM; Wigdorovitz A; Parreño VG; Saif LJ (2012). "IgY antibodies protect against human Rotavirus induced diarrhea in the neonatal gnotobiotic piglet disease model". Plos One 7 (8): e42788. doi:10.1371/journal.pone.0042788. PMID 22880110. PMC 3411843. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3411843/. 
  79. ↑ Mwila K; Chilengi R; Simuyandi M; Permar SR; Becker-Dreps S (2017). "Contribution of Maternal Immunity to Decreased Rotavirus Vaccine Performance in Low- and Middle-Income Countries". Clinical and Vaccine Immunology : CVI 24 (1). doi:10.1128/CVI.00405-16. PMID 27847365. PMC 5216432. //www.ncbi.nlm.nih.gov/pmc/articles/PMC5216432/. 
  80. ↑ Gandhi GR; Santos VS; Denadai M; da Silva Calisto VK; de Souza Siqueira Quintans J; de Oliveira e Silva AM; de Souza Araújo AA; Narain N et al. (2017). "Cytokines in the management of rotavirus infection: A systematic review of in vivo studies". Cytokine 96: 152–60. doi:10.1016/j.cyto.2017.04.013. PMID 28414969. 
  81. ↑ Holloway G; Coulson BS (2013). "Innate cellular responses to rotavirus infection". The Journal of General Virology 94 (6): 1151–60. doi:10.1099/vir.0.051276-0. PMID 23486667. 
  82. ↑ 82.0 82.1 Villena J; Vizoso-Pinto MG; Kitazawa H (2016). "Intestinal Innate Antiviral Immunity and Immunobiotics: Beneficial Effects against Rotavirus Infection". Frontiers in Immunology 7: 563. doi:10.3389/fimmu.2016.00563. PMID 27994593. PMC 5136547. //www.ncbi.nlm.nih.gov/pmc/articles/PMC5136547/. 
  83. ↑ Offit PA (1994). "Rotaviruses: immunological determinants of protection against infection and disease". Advances in Virus Research 44: 161–202. doi:10.1016/S0065-3527(08)60329-2. PMID 7817873. 
  84. ↑ Patel M; Glass RI; Jiang B; Santosham M; Lopman B; Parashar U (2013). "A systematic review of anti-rotavirus serum IgA antibody titer as a potential correlate of rotavirus vaccine efficacy". The Journal of Infectious Diseases 208 (2): 284–94. doi:10.1093/infdis/jit166. PMID 23596320. 
  85. ↑ 85.0 85.1 Patel MM; Tate JE; Selvarangan R; Daskalaki I; Jackson MA; Curns AT; Coffin S; Watson B et al. (2007). "Routine laboratory testing data for surveillance of rotavirus hospitalizations to evaluate the impact of vaccination". The Pediatric Infectious Disease Journal 26 (10): 914–9. doi:10.1097/INF.0b013e31812e52fd. PMID 17901797. 
  86. ↑ The Pediatric ROTavirus European CommitTee (PROTECT) (2006). "The paediatric burden of rotavirus disease in Europe". Epidemiology and Infection 134 (5): 908–16. doi:10.1017/S0950268806006091. PMID 16650331. PMC 2870494. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2870494/. 
  87. ↑ Angel J; Franco MA; Greenberg HB (2009). Desk Encyclopedia of Human and Medical Virology. Boston: Academic Press. p. 278. ISBN 0-12-375147-0. 
  88. ↑ Goode J; Chadwick D (2001). Gastroenteritis viruses. New York: Wiley. p. 14. ISBN 0-471-49663-4. 
  89. ↑ Fischer TK; Gentsch JR (2004). "Rotavirus typing methods and algorithms". Reviews in Medical Virology 14 (2): 71–82. doi:10.1002/rmv.411. PMID 15027000. 
  90. ↑ Alam NH; Ashraf H (2003). "Treatment of infectious diarrhea in children". Paediatric Drugs 5 (3): 151–65. doi:10.2165/00128072-200305030-00002. PMID 12608880. 
  91. ↑ Sachdev HP (1996). "Oral rehydration therapy". Journal of the Indian Medical Association 94 (8): 298–305. PMID 8855579. 
  92. ↑ World Health Organization, UNICEF. "Joint Statement: Clinical Management of Acute Diarrhoea" (PDF). Retrieved 3 May 2012.
  93. ↑ Ahmadi E; Alizadeh-Navaei R; Rezai MS (2015). "Efficacy of probiotic use in acute rotavirus diarrhea in children: A systematic review and meta-analysis". Caspian Journal of Internal Medicine 6 (4): 187–95. PMID 26644891. PMC 4649266. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4649266/. 
  94. ↑ Guarino A; Ashkenazi S; Gendrel D; Lo Vecchio A; Shamir R; Szajewska H (2014). "European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/European Society for Pediatric Infectious Diseases evidence-based guidelines for the management of acute gastroenteritis in children in Europe: update 2014". Journal of Pediatric Gastroenterology and Nutrition 59 (1): 132–52. doi:10.1097/MPG.0000000000000375. PMID 24739189. 
  95. ↑ Ramig RF (2007). "Systemic rotavirus infection". Expert Review of Anti-infective Therapy 5 (4): 591–612. doi:10.1586/14787210.5.4.591. PMID 17678424. 
  96. ↑ "Rotavirus vaccine for the prevention of rotavirus gastroenteritis among children. Recommendations of the Advisory Committee on Immunization Practices (ACIP)". MMWR. Recommendations and Reports : Morbidity and Mortality Weekly Report. Recommendations and Reports 48 (RR-2): 1–20. 1999. PMID 10219046. 
  97. ↑ Kapikian AZ (2001). "A rotavirus vaccine for prevention of severe diarrhoea of infants and young children: development, utilization and withdrawal". Novartis Foundation Symposium. Novartis Foundation Symposia 238: 153–71; discussion 171–9. doi:10.1002/0470846534.ch10. ISBN 9780470846537. PMID 11444025. 
  98. ↑ Bines JE (2005). "Rotavirus vaccines and intussusception risk". Current Opinions in Gastroenterology 21 (1): 20–5. PMID 15687880. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0267-1379&volume=21&issue=1&spage=20. 
  99. ↑ Bines J (2006). "Intussusception and rotavirus vaccines". Vaccine 24 (18): 3772–6. doi:10.1016/j.vaccine.2005.07.031. PMID 16099078. 
  100. ↑ Dennehy PH (2008). "Rotavirus vaccines: an overview". Clinical Microbiology Reviews 21 (1): 198–208. doi:10.1128/CMR.00029-07. PMID 18202442. PMC 2223838. http://cmr.asm.org/cgi/content/full/21/1/198?view=long&pmid=18202442. 
  101. ↑ Tate JE; Patel MM; Steele AD; Gentsch JR; Payne DC; Cortese MM; Nakagomi O; Cunliffe NA et al. (2010). "Global impact of rotavirus vaccines". Expert Review of Vaccines 9 (4): 395–407. doi:10.1586/erv.10.17. PMID 20370550. 
  102. ↑ Tate JE; Parashar UD (2014). "Rotavirus Vaccines in Routine Use". Clinical Infectious Diseases 59 (9): 1291–1301. doi:10.1093/cid/ciu564. PMID 25048849. http://cid.oxfordjournals.org/content/59/9/1291. 
  103. ↑ Richardson V; Hernandez-Pichardo J; Quintanar-Solares M; Esparza-Aguilar M; Johnson B; Gomez-Altamirano CM; Parashar U; Patel M (2010). "Effect of Rotavirus Vaccination on Death From Childhood Diarrhea in Mexico". The New England Journal of Medicine 362 (4): 299–305. doi:10.1056/NEJMoa0905211. PMID 20107215. 
  104. ↑ Patel M; Pedreira C; De Oliveira LH; Umaña J; Tate J; Lopman B; Sanchez E; Reyes M et al. (2012). "Duration of protection of pentavalent rotavirus vaccination in Nicaragua". Pediatrics 130 (2): e365–72. doi:10.1542/peds.2011-3478. PMID 22753550. 
  105. ↑ Patel MM; Parashar UD; eds. (2011). "Real World Impact of Rotavirus Vaccination". Pediatric Infectious Disease Journal 30 (1): S1. doi:10.1097/INF.0b013e3181fefa1f. PMID 21183833. http://journals.lww.com/pidj/toc/2011/01001. Retrieved 8 May 2012. 
  106. ↑ Steele AD, Armah GE, Page NA, Cunliffe NA, ed (2010). "Rotavirus Infection in Africa: Epidemiology, Burden of Disease, and Strain Diversity". Journal of Infectious Diseases 202 (Suppl 1): S1-S265. http://jid.oxfordjournals.org/content/202/Supplement_1.toc. 
  107. ↑ Nelson EAS, Widdowson MA, Kilgore PE, Steele D, Parashar UD, ed (2009). "Rotavirus in Asia: Updates on Disease Burden, Genotypes and Vaccine Introduction". Vaccine 27 (Suppl 5): F1-F138. http://www.sciencedirect.com/science/journal/0264410X/27/supp/S5. 
  108. ↑ World Health Organization (2009). "Rotavirus vaccines: an update". Weekly Epidemiological Record 51–52 (84): 533–40. http://www.who.int/wer/2009/wer8451_52.pdf. Retrieved 8 May 2012. 
  109. ↑ "New vaccine to help protect babies against rotavirus". UK Department of Health. 10 November 2012. Retrieved 10 November 2012.
  110. ↑ Karafillakis E; Hassounah S; Atchison C (2015). "Effectiveness and impact of rotavirus vaccines in Europe, 2006-2014". Vaccine 33 (18): 2097–107. doi:10.1016/j.vaccine.2015.03.016. PMID 25795258. 
  111. ↑ Burnett E; Jonesteller CL; Tate JE; Yen C; Parashar UD (2017). "Global Impact of Rotavirus Vaccination on Childhood Hospitalizations and Mortality from Diarrhea". The Journal of Infectious Diseases 215 (11): 1666–72. doi:10.1093/infdis/jix186. PMID 28430997. 
  112. ↑ "Rotavirus Deaths & Rotavirus Vaccine Introduction Maps – ROTA Council". rotacouncil.org. Retrieved 29 July 2016.
  113. ↑ Moszynski P (2011). "GAVI rolls out vaccines against child killers to more countries". BMJ 343: d6217. doi:10.1136/bmj.d6217. PMID 21957215. http://www.bmj.com/cgi/pmidlookup?view=long&pmid=21957215. 
  114. ↑ "Rotavirus vaccination programme for infants". www.gov.uk. Public Health England. 2013-07-26.
  115. ↑ Leung AKC; Kellner JD; Davies HD (2005). "Rotavirus gastroenteritis". Advances in Therapy 22 (5): 476–87. doi:10.1007/BF02849868. PMID 16418157. 
  116. ↑ Parashar UD; Gibson CJ; Bresse JS; Glass RI (2006). "Rotavirus and severe childhood diarrhea". Emerging Infectious Diseases 12 (2): 304–6. doi:10.3201/eid1202.050006. PMID 16494759. PMC 3373114. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3373114/. 
  117. ↑ Tate JE; Burton AH; Boschi-Pinto C; Steele AD; Duque J; Parashar UD (2012). "2008 estimate of worldwide rotavirus-associated mortality in children younger than 5 years before the introduction of universal rotavirus vaccination programmes: a systematic review and meta-analysis". The Lancet Infectious Diseases 12 (2): 136–41. doi:10.1016/S1473-3099(11)70253-5. PMID 22030330. 
  118. ↑ Rheingans RD; Heylen J; Giaquinto C (2006). "Economics of rotavirus gastroenteritis and vaccination in Europe: what makes sense?". Pediatric Infectious Diseases Journal 25 (Suppl 1): S48–55. doi:10.1097/01.inf.0000197566.47750.3d. PMID 16397429. 
  119. ↑ Ryan MJ; Ramsay M; Brown D; Gay NJ; Farrington CP; Wall PG (1996). "Hospital admissions attributable to rotavirus infection in England and Wales". Journal of Infectious Diseases 174 (Suppl 1): S12–8. doi:10.1093/infdis/174.Supplement_1.S12. PMID 8752285. 
  120. ↑ Atchison CJ; Tam CC; Hajat S; van Pelt W; Cowden JM; Lopman BA (2010). "Temperature-dependent transmission of rotavirus in Great Britain and The Netherlands". Proceedings of the Royal Society B: Biological Sciences 277 (1683): 933–42. doi:10.1098/rspb.2009.1755. PMID 19939844. PMC 2842727. http://rspb.royalsocietypublishing.org/cgi/pmidlookup?view=long&pmid=19939844. 
  121. ↑ Levy K; Hubbard AE; Eisenberg JN (2009). "Seasonality of rotavirus disease in the tropics: a systematic review and meta-analysis". International Journal of Epidemiology 38 (6): 1487–96. doi:10.1093/ije/dyn260. PMID 19056806. PMC 2800782. http://ije.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=19056806. 
  122. ↑ Koopmans M; Brown D (1999). "Seasonality and diversity of Group A rotaviruses in Europe". Acta Paediatrica 88 (Suppl 426): 14–9. doi:10.1111/j.1651-2227.1999.tb14320.x. PMID 10088906. 
  123. ↑ Sassi HP; Sifuentes LY; Koenig DW; Nichols E; Clark-Greuel J; Wong LF; McGrath K; Gerba CP et al. (2015). "Control of the spread of viruses in a long-term care facility using hygiene protocols". American Journal of Infection Control 43 (7): 702–6. doi:10.1016/j.ajic.2015.03.012. PMID 25944726. 
  124. ↑ Hopkins RS; Gaspard GB; Williams FP; Karlin RJ; Cukor G; Blacklow NR (1984). "A community waterborne gastroenteritis outbreak: evidence for rotavirus as the agent". American Journal of Public Health 74 (3): 263–5. doi:10.2105/AJPH.74.3.263. PMID 6320684. PMC 1651463. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1651463/. 
  125. ↑ Bucardo F; Karlsson B; Nordgren J; Paniagua M; González A; Amador JJ; Espinoza F; Svensson L (2007). "Mutated G4P[8] rotavirus associated with a nationwide outbreak of gastroenteritis in Nicaragua in 2005". Journal of Clinical Microbiology 45 (3): 990–7. doi:10.1128/JCM.01992-06. PMID 17229854. PMC 1829148. http://jcm.asm.org/cgi/content/full/45/3/990. 
  126. ↑ Linhares AC; Pinheiro FP; Freitas RB; Gabbay YB; Shirley JA; Beards GM (1981). "An outbreak of rotavirus diarrhea among a non-immune, isolated South American Indian community". American Journal of Epidemiology 113 (6): 703–10. doi:10.1093/oxfordjournals.aje.a113151. PMID 6263087. 
  127. ↑ Hung T; Wang C; Fang Z; Chou Z; Chang X; Liong X; Chen G; Yao H et al. (1984). "Waterborne outbreak of rotavirus diarrhea in adults in China caused by a novel rotavirus". The Lancet 323 (8387): 1139–42. doi:10.1016/S0140-6736(84)91391-6. PMID 6144874. 
  128. ↑ Fang ZY; Ye Q; Ho MS; Dong H; Qing S; Penaranda ME; Hung T; Wen L et al. (1989). "Investigation of an outbreak of adult diarrhea rotavirus in China". Journal of Infectious Diseases 160 (6): 948–53. doi:10.1093/infdis/160.6.948. PMID 2555422. 
  129. ↑ Kelkar SD; Zade JK (2004). "Group B rotaviruses similar to strain CAL-1, have been circulating in Western India since 1993". Epidemiology and Infection 132 (4): 745–9. doi:10.1017/S0950268804002171. PMID 15310177. PMC 2870156. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2870156/. 
  130. ↑ Ahmed MU; Kobayashi N; Wakuda M; Sanekata T; Taniguchi K; Kader A; Naik TN; Ishino M et al. (2004). "Genetic analysis of group B human rotaviruses detected in Bangladesh in 2000 and 2001". Journal of Medical Virology 72 (1): 149–55. doi:10.1002/jmv.10546. PMID 14635024. 
  131. ↑ Penaranda ME; Ho MS; Fang ZY; Dong H; Bai XS; Duan SC; Ye WW; Estes MK et al. (1989). "Seroepidemiology of adult diarrhea rotavirus in China, 1977 to 1987". Journal of Clinical Microbiology 27 (10): 2180–3. doi:10.1128/jcm.27.10.2180-2183.1989. PMID 2479654. PMC 266989. //www.ncbi.nlm.nih.gov/pmc/articles/PMC266989/. 
  132. ↑ Moon S; Humphrey CD; Kim JS; Baek LJ; Song JW; Song KJ; Jiang B (2011). "First detection of group C rotavirus in children with acute gastroenteritis in South Korea". Clinical Microbiology and Infection 17 (2): 244–7. doi:10.1111/j.1469-0691.2010.03270.x. PMID 20491826. 
  133. ↑ 133.0 133.1 Martella V; Bányai K; Matthijnssens J; Buonavoglia C; Ciarlet M (2010). "Zoonotic aspects of rotaviruses". Veterinary Microbiology 140 (3–4): 246–55. doi:10.1016/j.vetmic.2009.08.028. PMID 19781872. 
  134. ↑ Müller H; Johne R (2007). "Rotaviruses: diversity and zoonotic potential--a brief review". Berliner Und Munchener Tierarztliche Wochenschrift 120 (3-4): 108–12. PMID 17416132. 
  135. ↑ Cook N; Bridger J; Kendall K; Gomara MI; El-Attar L; Gray J (2004). "The zoonotic potential of rotavirus". The Journal of Infection 48 (4): 289–302. doi:10.1016/j.jinf.2004.01.018. PMID 15066329. 
  136. ↑ Dóró R; Farkas SL; Martella V; Bányai K (2015). "Zoonotic transmission of rotavirus: surveillance and control". Expert Review of Anti-infective Therapy 13 (11): 1337–50. doi:10.1586/14787210.2015.1089171. PMID 26428261. 
  137. ↑ Light JS; Hodes HL (1943). "Studies on Epidemic Diarrhea of the New-born: Isolation of a Filtrable Agent Causing Diarrhea in Calves". American Journal of Public Health and the Nation's Health 33 (12): 1451–4. doi:10.2105/AJPH.33.12.1451. PMID 18015921. PMC 1527675. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1527675/. 
  138. ↑ Mebus CA; Wyatt RG; Sharpee RL; Sereno MM; Kalica AR; Kapikian AZ; Twiehaus MJ (1976). "Diarrhea in gnotobiotic calves caused by the reovirus-like agent of human infantile gastroenteritis" (PDF). Infection and Immunity 14 (2): 471–4. doi:10.1128/iai.14.2.471-474.1976. PMID 184047. PMC 420908. http://iai.asm.org/cgi/reprint/14/2/471. 
  139. ↑ Rubenstein D; Milne RG; Buckland R; Tyrrell DA (1971). "The growth of the virus of epidemic diarrhoea of infant mice (EDIM) in organ cultures of intestinal epithelium". British Journal of Experimental Pathology 52 (4): 442–5. PMID 4998842. PMC 2072337. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2072337/. 
  140. ↑ 140.0 140.1 Woode GN; Bridger JC; Jones JM; Flewett TH; Davies HA; Davis HA; White GB (1976). "Morphological and antigenic relationships between viruses (rotaviruses) from acute gastroenteritis in children, calves, piglets, mice, and foals" (PDF). Infection and Immunity 14 (3): 804–10. doi:10.1128/iai.14.3.804-810.1976. PMID 965097. PMC 420956. http://iai.asm.org/cgi/reprint/14/3/804. 
  141. ↑ 141.0 141.1 Flewett TH; Woode GN (1978). "The rotaviruses". Archives of Virology 57 (1): 1–23. doi:10.1007/BF01315633. PMID 77663. 
  142. ↑ Flewett TH; Bryden AS; Davies H; Woode GN; Bridger JC; Derrick JM (1974). "Relation between viruses from acute gastroenteritis of children and newborn calves". The Lancet 304 (7872): 61–3. doi:10.1016/S0140-6736(74)91631-6. PMID 4137164. 
  143. ↑ Matthews RE (1979). "Third report of the International Committee on Taxonomy of Viruses. Classification and nomenclature of viruses". Intervirology 12 (3–5): 129–296. doi:10.1159/000149081. PMID 43850. 
  144. ↑ Beards GM; Brown DW (1988). "The antigenic diversity of rotaviruses: significance to epidemiology and vaccine strategies". European Journal of Epidemiology 4 (1): 1–11. doi:10.1007/BF00152685. PMID 2833405. 
  145. ↑ Urasawa T; Urasawa S; Taniguchi K (1981). "Sequential passages of human rotavirus in MA-104 cells". Microbiology and Immunology 25 (10): 1025–35. doi:10.1111/j.1348-0421.1981.tb00109.x. PMID 6273696. 
  146. ↑ Ward RL, Bernstein DI (2009). "Rotarix: a rotavirus vaccine for the world". Clinical Infectious Diseases 48 (2): 222–8. doi:10.1086/595702. PMID 19072246. http://www.cid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=19072246. 
Retrieved from "https://en.wikiversity.org/w/index.php?title=WikiJournal_of_Medicine/Rotavirus&oldid=2405076"