Identification of amino acids in highly pathogenic avian influenza H5N1 virus hemagglutinin that determine avian influenza species specificity
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H5N1 genetic structure
4 Abstract: There are four major types of influenza viruses: A, B, C and Thogotovirus. Only influenza A viruses are further classified into subtypes on the basis of the two main surface glycoproteins hemagglutinin (HA) and neuraminidase (NA). Influenza A subtypes and B viruses are further classified by strains. Avian influenza virus can be distinguished as Low Pathogenic Avian Influenza (LPAI) and Highly Pathogenic Avian Influenza (HPAI) forms based on genetic features of the virus and the severity of the illness they cause in poultry. Influenza virus A is usually responsible for bird flu (Avian influenza) but same time also responsible for pandemics of influenza in humans. Out of hundreds of strains of avian influenza A viruses, only four are capable to produce infection in humans: H5N1, H7N3, H7N7 and H9N2. Out of these, highly pathogenic avian influenza, H5N1 strain is of greatest concern for human infection. This virus has affected poultry flocks and other birds in more than 50 countries. Total 309 laboratory-confirmed cases of avian influenza infection in humans have been reported to the World Health Organization between end of December 2003 to end of May 2007; out of which 187 deaths were confirmed. While human cases remain relatively rare and are largely the result of direct virus transmission from infected birds, a few cases of human-to-human transmission have been reported. But still there is a matter of great assurance that, H5N1strain does not easily cross from birds to infect humans. Oseltamivir is the first orally active antiviral drug used in the treatment and prophylaxis of influenza A and B viruses provided that the treatment is started within 48 hours of onset of symptoms. The severity of disease and the potential for human-to-human spread has provided an urgent need to develop a human vaccine for avian influenza. Efforts to produce vaccines are under way.
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The interrelations between H3/73 hemagglutinin of human influenza virus and the other 16 mammalian and avian hemagglutinin subtypes (a total of 50 strains) were studied by the method of radioimmunologic analysis (RIA). The antigenic relations of H3, Hav7 and Heq2 were confirmed, certain common determinants were also found in H3/73 hemagglutinin and avian viral Hav6 and Hav9 hemagglutinins. No interrelations were revealed with previously circulating human influenza viruses H0, H1, H2 as well as with swine influenza virus and avian viruses Hav1-Hav5, Hav8. It has been shown that the H3/73 determinant in some avian viruses evolves similarly to drift-variants of human influenza virus. The method can be recommended for fine analysis of influenza virus antigenic structure as it allows detecting small antigenic quantities.
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In 1997, 18 human infections with H5N1 influenza type A were identified in Hong Kong and six of the patients died. There were concomitant outbreaks of H5N1 infections in poultry. The gene segments of the human H5N1 viruses were derived from avian influenza A viruses and not from circulating human influenza A viruses. In 1999 two cases of human infections caused by avian H9N2 virus were also identified in Hong Kong. These events established that avian influenza viruses can infect humans without passage through an intermediate host and without acquiring gene segments from human influenza viruses. The likely origin of the H5N1 viruses has been deduced from molecular analysis of these and other viruses isolated from the region. The gene sequences of the H5N1 viruses were analysed in order to identify the molecular basis for the ability of these avian viruses to infect humans. Copyright © 2000 John Wiley & Sons, Ltd.
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Influenza A viruses cause natural infections of humans, some other mammals and birds. Few of the 16 haemagglutinin and nine neuraminidase subtype combinations have been isolated from mammals, but all subtypes have been isolated from birds. In the 20th century, there were four pandemics of influenza as a result of the emergence of antigenically different strains in humans: 1918 (H1N1), 1957 (H2N2), 1968 (H3N2) and 1977 (H1N1). Influenza A viruses contain eight distinct RNA genes and reassortment of these can occur in mixed infections with different viruses. The 1957 and 1968 pandemic viruses differed from the preceding viruses in humans by the substitution of genes that came from avian viruses, suggesting they arose by genetic reassortment of viruses of human and avian origin. Up to 1995, there had been only three reports of avian influenza viruses infecting humans, in 1959, 1977 and 1981 (all H7N7), but, since 1996, there have been regular reports of natural infections of humans with avian influenza viruses: in England in 1996 (H7N7), Hong Kong 1997 (H5N1), 1999 (H9N2), and 2003 (H5N1), in The Netherlands 2003 (H7N7), Canada 2004 (H7N3), Vietnam 2004 (H5N1) and Thailand 2004 (H5N1). The H5N1 virus is alarming because 51 (64 %) of the 80 people confirmed as infected since 1997 have died.
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Three antigenic determinants were revealed in H3 hemagglutinin of influenza A viruses isolated from 1968 to 1975. One of them was common for all viruses, and two others specified differences between the viruses possessing H3 hemagglutinin.
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In 2020, several geographically isolated farms in Victoria, Australia, experienced an outbreak of highly pathogenic avian influenza (HPAI) virus H7N7 and low pathogenic avian influenza (LPAI) viruses H5N2 and H7N6. Effective containment and control measures ensured the eradication of these viruses but the event culminated in substantial loss of livestock and significant economic impact. The avian HPAI H7N7 virus generally does not infect humans; however, evidence shows the ocular pathway presents a favourable tissue tropism for human infection. Through antigenic drift, mutations in the H7N7 viral genome may increase virulence and pathogenicity in humans. The Victorian outbreak also detected LPAI H7N6 in emus at a commercial farm. Novel influenza A viruses can emerge by mixing different viral strains in a host susceptible to avian and human influenza strains. Studies show that emus are susceptible to infections from a wide range of influenza viral subtypes, including H5N1 and the pandemic H1N1. The emu's internal organs and tissues express abundant cell surface sialic acid receptors that favour the attachment of avian and human influenza viruses, increasing the potential for internal genetic reassortment and the emergence of novel influenza A viruses. This review summarises the historical context of H7N7 in Australia, considers the potential for increased virulence and pathogenesis through mutations and draws attention to the emu as potentially an unrecognised viral mixing vessel.
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A(H1N1) 09pdm and A(H3N2) influenza viruses are the main cause of occasional influenza pandemics and seasonal influenza epidemics around the world. Unfortunately, the understanding of long-term genetic variation in these viruses remains limited.In this study, hemagglutinin genes from 90 A(H1N1) 09pdm and 48 A(H3N2) influenza viruses in the Beijing area from 2009 to 2014 were sequenced and analyzed.The hemagglutinin genes in A(H1N1) 09pdm and A(H3N2) shared nucleotide similarity that ranged from 93.06% - 99.88% and 98.68% - 99.29%, respectively, compared with current vaccine strains. 10 and 7 amino acid mutations in antigenic sites were identified in these two strains, respectively. In addition, a new site 177 glycosylation, which did not exist in previous circulating strains, was identified in 3 A(H1N1) 09pdm isolates.This study demonstrated the continued evolution of seasonal influenza viruses in the Beijing area, indicating that an update of the vaccine is needed, especially for A(H1N1) 09pdm influenza virus.
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The original article to which this Erratum refers was published in Reviews in Medical Virology 10(4) 2000, 255-277.
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Bangladesh has reported a high number of outbreaks of highly pathogenic avian influenza (HPAI) (H5N1) in poultry. We identified a natural reassortant HPAI (H5N1) virus containing a H9N2-PB1 gene in poultry in Bangladesh. Our findings highlight the risks for prolonged co-circulation of avian influenza viruses and the need to monitor their evolution.
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H5N1 genetic structure
Highly pathogenic
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