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      Characterization of avian influenza viruses isolated from domestic ducks in Vietnam in 2009 and 2010

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          Abstract

          In the surveillance of avian influenza in Vietnam, 26 H9N2, 1 H3N2, 1 H3N8, 7 H4N6, 3 H11N3, and 1 H11N9 viruses were isolated from tracheal and cloacal swab samples of 300 domestic ducks in April 2009, and 1 H9N6 virus from 300 bird samples in March 2010. Out of the 27 H9 virus isolates, the hemagglutinins of 18 strains were genetically classified as belonging to the sublineage G1, and the other nine belonged to the Korean sublineage. Phylogenetic analysis revealed that one of the 27 H9 viruses was a reassortant in which the PB2 gene belonged to the Korean sublineage and the other seven genes belonged to the G1 sublineage. Three representative H9N2 viruses were intranasally inoculated into ducks, chickens, pigs, and mice. On the basis of experimental infection studies, it was found that each of the three viruses readily infected pigs and replicated in their upper respiratory tracts, and they infected chickens with slight replication. Viruses were recovered from the lungs of mice inoculated with two of the three isolates. The present results reveal that H9 avian influenza viruses are prevailing and genetic reassortment occurs among domestic ducks in Vietnam. It is recommended that careful surveillance of swine influenza with H9 viruses should be performed to prepare for pandemic influenza.

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          Most cited references32

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          A review of avian influenza in different bird species.

          Only type A influenza viruses are known to cause natural infections in birds, but viruses of all 15 haemagglutinin and all nine neuraminidase influenza A subtypes in the majority of possible combinations have been isolated from avian species. Influenza A viruses infecting poultry can be divided into two distinct groups on the basis of their ability to cause disease. The very virulent viruses cause highly pathogenic avian influenza (HPAI), in which mortality may be as high as 100%. These viruses have been restricted to subtypes H5 and H7, although not all viruses of these subtypes cause HPAI. All other viruses cause a much milder, primarily respiratory disease, which may be exacerbated by other infections or environmental conditions. Since 1959, primary outbreaks of HPAI in poultry have been reported 17 times (eight since 1990), five in turkeys and 12 in chickens. HPAI viruses are rarely isolated from wild birds, but extremely high isolation rates of viruses of low virulence for poultry have been recorded in surveillance studies, giving overall figures of about 15% for ducks and geese and around 2% for all other species. Influenza viruses have been shown to affect all types of domestic or captive birds in all areas of the world, but the frequency with which primary infections occur in any type of bird depends on the degree of contact there is with feral birds. Secondary spread is usually associated with human involvement, probably by transferring infective faeces from infected to susceptible birds.
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            Avian-to-human transmission of H9N2 subtype influenza A viruses: relationship between H9N2 and H5N1 human isolates.

            In 1997, 18 cases of influenza in Hong Kong (bird flu) caused by a novel H5N1 (chicken) virus resulted in the deaths of six individuals and once again raised the specter of a potentially devastating influenza pandemic. Slaughter of the poultry in the live bird markets removed the source of infection and no further human cases of H5N1 infection have occurred. In March 1999, however, a new pandemic threat appeared when influenza A H9N2 viruses infected two children in Hong Kong. These two virus isolates are similar to an H9N2 virus isolated from a quail in Hong Kong in late 1997. Although differing in their surface hemagglutinin and neuraminidase components, a notable feature of these H9N2 viruses is that the six genes encoding the internal components of the virus are similar to those of the 1997 H5N1 human and avian isolates. This common feature emphasizes the apparent propensity of avian viruses with this genetic complement to infect humans and highlights the potential for the emergence of a novel human pathogen.
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              Potential for transmission of avian influenza viruses to pigs.

              Pandemic strains of influenza A virus arise by genetic reassortment between avian and human viruses. Pigs have been suggested to generate such reassortants as intermediate hosts. In order for pigs to serve as 'mixing vessels' in genetic reassortment events, they must be susceptible to both human and avian influenza viruses. The ability of avian influenza viruses to replicate in pigs, however, has not been examined comprehensively. In this study, we assessed the growth potential of 42 strains of influenza virus in pigs. Of these, 38 were avian strains, including 27 with non-human-type haemagglutinins (HA; H4 to H13). At least one strain of each HA subtype replicated in the respiratory tract of pigs for 5 to 7 days to a level equivalent to that of swine and human viruses. These results indicate that avian influenza viruses with or without non-human-type HAs can be transmitted to pigs, thus raising the possibility of introduction of their genes into humans. Sera from pigs infected with avian viruses showed high titres of antibodies in ELISA and neutralization tests, but did not inhibit haemagglutination of homologous viruses, cautioning against the use of haemagglutination-inhibition tests to identify pigs infected with avian influenza viruses. Co-infection of pigs with a swine virus and with an avian virus unable to replicate in this animal generated reassortant viruses, whose polymerase and HA genes were entirely of avian origin, that could be passaged in pigs. This finding indicates that even avian viruses that do not replicate in pigs can contribute genes in the generation of reassortants.
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                Author and article information

                Contributors
                +81-11-7065207 , +81-11-7065273 , kida@vetmed.hokudai.ac.jp
                Journal
                Arch Virol
                Arch. Virol
                Archives of Virology
                Springer Vienna (Vienna )
                0304-8608
                1432-8798
                9 November 2011
                2012
                : 157
                : 2
                : 247-257
                Affiliations
                [1 ]GRID grid.39158.36, ISNI 0000000121737691, Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, , Hokkaido University, ; Kita 18 Nishi 9, Kita-ku, Sapporo, 060-0818 Japan
                [2 ]GRID grid.26999.3d, ISNI 000000012151536X, OIE Regional Representation for Asia and the Pacific, Food Science Building 5F, , The University of Tokyo, ; 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-8657 Japan
                [3 ]GRID grid.467776.3, Ministry of Agriculture and Rural Development, ; 15/78 Giaiphong, Phuongmai, Dongda, Hanoi, Vietnam
                [4 ]GRID grid.39158.36, ISNI 0000000121737691, Research Center for Zoonosis Control, , Hokkaido University, ; Kita 20 Nishi 10, Kita-ku, Sapporo, 001-0020 Japan
                [5 ]GRID grid.419082.6, ISNI 0000000417549200, Japan Science and Technology Agency Basic Research Programs, ; 4-1-8, Honcho Kawaguchi, Saitama, 332-0012 Japan
                Article
                1152
                10.1007/s00705-011-1152-3
                7086777
                22068881
                81d16f4c-dbce-44a6-a004-d76ef1ad1412
                © Springer-Verlag 2011

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                : 23 June 2011
                : 15 October 2011
                Categories
                Original Article
                Custom metadata
                © Springer-Verlag 2012

                Microbiology & Virology
                influenza,influenza virus,avian influenza,h9n2 virus,avian influenza virus
                Microbiology & Virology
                influenza, influenza virus, avian influenza, h9n2 virus, avian influenza virus

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