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Reye's syndrome is a potentially fatal disease that causes numerous detrimental effects to many organs, especially the brain

and liver, as well as causing hypoglycemia. The exact cause is unknown, and while it has been associated with aspirin consumption by children with viral illness, it also occurs in the absence of aspirin use. The disease causes fatty liver with minimal inflammation and severe encephalopathy (with swelling of the brain). The liver may become slightly enlarged and firm, and there is a change in the appearance of the kidneys. Jaundice is not usually present. Early diagnosis is vital; while most children recover with supportive therapy, severe brain injury or death are potential complications. Reye's syndrome progresses through five stages, explained below: Stage I o rash on palms of hands and feet o Persistent, heavy vomiting that is not relieved by not eating o Generalized lethargy o Confusion o Nightmares o High fever o Headaches Stage II o Stupor caused by encephalitis o Hyperventilation o Fatty liver (found by biopsy) o Hyperactive reflexes Stage III o Continuation of Stage I and II symptoms o Possible coma

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Possible cerebral oedema Rarely, respiratory arrest IV Deepening coma Dilated pupils with minimal response to light Minimal but still present hepatic dysfunction V Very rapid onset following stage IV Deep coma Seizures Multiple organ failure[3] Flaccidity Hyperammonemia (above 300 mg/dL of blood) Death

The precise mechanism by which Reye's syndrome occurs remains unknown. This serious condition is described as a "syndrome" rather than a disease as the clinical features that physicians use to diagnose it are quite broad. Aspirin Some studies have demonstrated an association between aspirin taken for viral illnesses and the development of Reyes syndrome.[4] One small study presented findings that acetaminophen (paracetamol) is a greater risk, [5] but this claim is disputed. The serious symptoms of Reye's syndrome appear to result from damage to cellular mitochondria,[7] at least in the liver, and there are a number of ways that aspirin could cause or exacerbate mitochondrial damage. A potential increased risk of developing Reye's syndrome is one of the main reasons that aspirin has not been recommended for use in children and teenagers, the age group for which the risk of lasting serious effects is highest. No research has found a definitive cause of Reye's syndrome, and association with aspirin has only been shown through epidemological studies. The diagnosis of "Reye's Syndrome" greatly decreased in the 1980s, when genetic testing for inborn errors of metabolism was becoming available in first world countries. A retrospective study of 49 survivors of cases diagnosed as "Reye's Syndrome" showed that the majority of the surviving patients had various metabolic disorders. In some countries, oral mouthcare product Bonjela (not the form specifically designed for teething) has labeling cautioning against its use in children, given its salicylate content. There have been no cases of Reye's secondary to its use, and the measure is a precaution. Other medications containing salicylates are often similarly labeled as a precaution. The Centers for Disease Control and Prevention (CDC), the U.S. Surgeon General, the American Academy of Pediatrics (AAP) and the Food and Drug Administration (FDA) recommend that aspirin and combination products containing aspirin not be given to children under 19 years of age during episodes of fever-causing illnesses. Hence, in the United States, it is advised that the opinion of a doctor or pharmacist be obtained before anyone under 19 years of age is given any medication containing aspirin (also known on some medicine labels as acetylsalicylate, salicylate, acetylsalicylic acid, ASA or salicylic acid). Current advice in the United Kingdom by the Committee on Safety of Medicines is that aspirin should not be given to those under the age of 16 years, unless specifically indicated in Kawasaki disease or in the prevention of blood clot formation. Influenza A virus causes influenza in birds and some mammals and is the only species of Influenzavirus A. Influenzavirus A is a genus of the Orthomyxoviridae family of viruses. Strains of all subtypes of influenza A virus have been isolated from wild birds, although disease is uncommon. Some isolates of influenza A virus cause severe disease both in domestic poultry and, rarely, in humans. Occasionally viruses are transmitted from wild aquatic birds to domestic poultry and this may cause an outbreak or give rise to human influenza pandemics. Influenza A viruses are negative sense, single-stranded, segmented RNA viruses. There are several subtypes, labeled according to an H number (for the type of hemagglutinin) and an N number (for the type of neuraminidase). There are 16 different H antigens (H1 to H16) and nine different N antigens (N1 to N9). The newest H type (H16) was isolated from Blackheaded Gulls caught in Sweden and the Netherlands in 1999 and reported in the literature in 2005. Each virus subtype has mutated into a variety of strains with differing pathogenic profiles; some pathogenic to one species but not others, some pathogenic to multiple species. A filtered and purified Influenza A vaccine for humans was developed and many countries have stockpiled it to allow a quick administration to the population in the event of an Avian influenza pandemic. Avian influenza is sometimes called avian flu, and commonly bird flu.

Variants and subtypes Some Variants are identified and named according to the isolate that they are like and thus are presumed to share lineage (example Fujian flu virus like); according to their typical host (example Human flu virus); according to their subtype (example H3N2); and according to their deadliness (example LP, Low Pathogenic). So a flu from a virus similar to the isolate A/Fujian/411/2002(H3N2) is called Fujian flu, human flu, and H3N2 flu. Variants are sometimes named according to the species (host) the strain is endemic in or adapted to. The main variants named using this convention are: Bird flu Human flu Swine influenza Equine influenza Canine influenza Variants have also sometimes been named according to their deadliness in poultry, especially chickens: Low Pathogenic Avian Influenza (LPAI) Highly Pathogenic Avian Influenza (HPAI), also called: deadly flu or death flu Most known strains are extinct strains. For example, the annual flu subtype H3N2 no longer contains the strain that caused the Hong Kong flu. Structure and genetics "The physical structure of all influenza A viruses is similar. The virions or virus particles are enveloped and can be either spherical or filamentous in form. In clinical isolates that have undergone limited passages in eggs or tissue culture, there are more filamentous than spherical particles, whereas passaged laboratory strains consist mainly of spherical virions. The Influenza A virus genome is contained on eight single (non-paired) RNA strands that code for eleven proteins (HA, NA, NP, M1, M2, NS1, NEP, PA, PB1, PB1-F2, PB2). The total genome size is 13,588 bases. [9] The segmented nature of the genome allows for the exchange of entire genes between different viral strains during cellular cohabitation. The eight RNA segments are: HA encodes hemagglutinin (about 500 molecules of hemagglutinin are needed to make one virion) "The extent of infection into host organism is determined by HA. Influenza viruses bud from the apical surface of polarized epithelial cells (e.g. bronchial epithelial cells) into lumen of lungs and are therefore usually pneumotropic. The reason is that HA is cleaved by tryptase clara which is restricted to lungs. However HAs of H5 and H7 pantropic avian viruses subtypes can be cleaved by furin and subtilisin-type enzymes, allowing the virus to grow in other organs than lungs." [10] NA encodes neuraminidase (about 100 molecules of neuraminidase are needed to make one virion). NP encodes nucleoprotein. M encodes two matrix proteins (the M1 and the M2) by using different reading frames from the same RNA segment (about 3000 matrix protein molecules are needed to make one virion). NS encodes two distinct non-structural proteins (NS1 and NEP) by using different reading frames from the same RNA segment. PA encodes an RNA polymerase. PB1 encodes an RNA polymerase and PB1-F2 protein (induces apoptosis) by using different reading frames from the same RNA segment. PB2 encodes an RNA polymerase. The genome segments have common terminal sequences, and the ends of the RNA strands are partially complementary, allowing them to bond to each other by hydrogen bonds. After transcription from negative-sense to positive-sense RNA the +RNA strands get the cellular 5' cap added by cap snatching, which involves the viral protein NS1 binding to the cellular premRNAs. The cap is then cleaved from the cellular pre-mRNA using a second viral protein, PB2. The short oligo cap is then added to the influenza +RNA strands, allowing its processing as messenger RNA by ribosomes. The +RNA strands also serve for synthesis of -RNA strands for new virions. The RNA synthesis and its assembly with the nucleoprotein takes place in the cell nucleus, the synthesis of proteins takes place in the cytoplasm. The assembled virion cores leave the nucleus and migrate towards the cell membrane, with patches of viral transmembrane proteins (hemagglutinin, neuraminidase and M2 proteins) and an underlying layer of the M1 protein, and bud through these patches, releasing finished enveloped viruses into the extracellular fluid. Influenzavirus B is a genus in the virus family Orthomyxoviridae. The only species in this genus is called "Influenza B virus". Influenza B viruses are only known to infect humans and seals,[1] giving them influenza. This limited host range is apparently responsible for the lack of Influenzavirus B caused influenza pandemics in contrast with those caused by the morphologically similar Influenzavirus A as both mutate by both genetic drift and reassortment.

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