Rotavirus Nədir

If your child has rotavirus, it's in their poop before symptoms start and up to 10 days after they taper off. During that time, when your child wipes after using the toilet, rotavirus can spread to their hands. If they don't wash their hands, they might contaminate anything they touch, including:

Although rotavirus infections are unpleasant, you can usually treat this infection at home with extra fluids to prevent dehydration. Occasionally, severe dehydration requires receiving fluids through a vein (intravenously) in the hospital.

Rotavirus Ndir

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A rotavirus infection usually starts within two days of exposure to the virus. Early symptoms are a fever and vomiting, followed by three to seven days of watery diarrhea. The infection can cause abdominal pain as well.

The vaccines are considered safe and effective, and studies show that they prevent thousands of children from developing rotavirus every year. However, rarely, they can cause a part of the intestine to fold back on itself (intussusception), resulting in possibly life-threatening intestinal blockage.

Children who have had intussusception are more likely to have it again after receiving the rotavirus vaccine. The U.S. Food and Drug Administration recommends that the vaccine not be given to children who have a history of intussusception.

For children who don't have a history of intussusception, there is a very small risk that it can develop after the rotavirus vaccine is given. Even so, the benefits of the vaccine far outweigh the risks.

Rotavirus is a virus that causes gastroenteritis. Symptoms include severe diarrhea, vomiting, fever, and dehydration. Almost all children in the U.S. are likely to be infected with rotavirus before their 5th birthday.

There is no medicine to treat it. To prevent dehydration, have your child drink plenty of liquids. Your health care provider may recommend oral rehydration drinks. Some children need to go to the hospital for IV fluids. Two vaccines against rotavirus infections are available.

The Centers for Disease Control and Prevention (CDC) reports that before the rotavirus vaccine was introduced in 2006, the infection led to the following yearly statistics in children 5 years and younger in the United States:

Infants and children under 3 years old are at the highest risk of developing a rotavirus infection. Being in daycare also raises their risk. You might consider taking extra precautions during winter and spring months, as more infections occur this time of year.

Rotavirus is a genus of double-stranded RNA viruses in the family Reoviridae. Rotaviruses are the most common cause of diarrhoeal disease among infants and young children.[1] Nearly every child in the world is infected with a 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 nine species of the genus, referred to as A, B, C, D, F, G, H, I and J. Rotavirus A, the most common species, causes more than 90% of rotavirus infections in humans.[4]

Rotaviral enteritis is usually an easily managed disease of childhood, but among children under 5 years of age rotavirus caused an estimated 151,714 deaths from diarrhoea in 2019.[9] In the United States, before initiation of the rotavirus vaccination programme in the 2000s, 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]

The genome of rotaviruses 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.[30] The RNA is surrounded by a three-layered icosahedral protein capsid. Viral particles are up to 76.5 nm in diameter[31][32] and are not enveloped.[33]

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.[19]

At least six of the twelve proteins encoded by the rotavirus genome bind RNA.[35] The role of these proteins 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.[36]

VP1 is located in the core of the virus particle and is an RNA-dependent RNA polymerase enzyme.[37] 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.[38]

VP4 is on the surface of the virion that protrudes as a spike.[42] It binds to molecules on the surface of cells called receptors and drives the entry of the virus into the cell.[43] 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.[44] VP4 determines how virulent the virus is and it determines the P-type of the virus.[45] In humans there is an association between the blood group (Lewis antigen system, ABO blood group system and 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.[46] This resistance is dependent on the rotavirus genotype.[47]

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.[54] Efficient translation of rotavirus mRNA, which lacks the 3' poly(A) tail, does not require either of these factors.[55]

During the infection, rotaviruses produce 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.[64] 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.[44][65][66]

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.[70] 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.[71]

Rotavirus infections can occur throughout life: the first usually produces symptoms, but subsequent infections are typically mild or asymptomatic,[72][48] as the immune system provides some protection.[73] Consequently, symptomatic infection rates are highest in children under two years of age and decrease progressively towards 45 years of age.[74] 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.[75] There is some evidence to suggest blood group can impact on the susceptibility to infection by rotaviruses.[76]

The diarrhoea is caused by multiple activities of the virus.[80] 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 (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.[56] The elevated concentrations of calcium ions in the cytosol (which are required for the assembly of the progeny viruses) is achieved by NSP4 acting as a viroporin. This increase in calcium ions leads to autophagy (self destruction) of the infected enterocytes.[81]

Healthy enterocytes secrete lactase into the small intestine; milk intolerance due to lactase deficiency is a symptom of rotavirus infection,[84] which can persist for weeks.[85] 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.[86]

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.[87] 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 other animals.[88] Maternal trans-placental IgG might play a role in the protection neonates from rotavirus infections, but on the other hand might reduce vaccine efficacy.[89] 006ab0faaa