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Vectors: H5N1 identified in blow flies

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  • Vectors: H5N1 identified in blow flies

    DETECTION AND ISOLATION OF HIGHLY PATHOGENIC H5N1 AVIAN INFLUENZA A VIRUSES FROM BLOW FLIES COLLECTED IN THE VICINITY OF AN INFECTED POULTRY FARM IN KYOTO, JAPAN, 2004 <?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /><o:p></o:p>

    KYOKO SAWABE<SUP>*</SUP>, KEITA HOSHINO, HARUHIKO ISAWA, TOSHINORI SASAKI, TOSHIHIKO HAYASHI, YOSHIO TSUDA, HIROMU KURAHASHI, KIYOSHI TANABAYASHI, AKITOYO HOTTA, TAKEHIKO SAITO, AKIO YAMADA, AND MUTSUO KOBAYASHI <o:p></o:p>
    Am. J. Trop. Med. Hyg., 75(2), 2006, pp. 327-332<o:p></o:p>
    http://www.ajtmh.org/cgi/content/abstract/75/2/327
    Department of Medical Entomology, National Institute of Infectious<SUP> </SUP>Diseases, Shinjuku-ku, Tokyo, Japan; Department of Veterinary<SUP> </SUP>Science, National Institute of Infectious Diseases, Shinjuku-ku,<SUP> </SUP>Tokyo, Japan; Department of Virology III, National Institute<SUP> </SUP>of Infectious Diseases, Shinjuku-ku, Tokyo, Japan<SUP> </SUP><o:p></o:p>

    During the outbreak of highly pathogenic avian influenza that<SUP> </SUP>occurred in Tamba Town, Kyoto Prefecture in 2004, a total of<SUP> </SUP>926 flies were collected from six sites within a radius of 2.3<SUP> </SUP>km from the poultry farm. The H5 influenza A virus genes were<SUP> </SUP>detected from the intestinal organs, crop, and gut of the two<SUP> </SUP>blow fly species, Calliphora nigribarbis and Aldrichina grahami,<SUP> </SUP>by reverse transcription-polymerase chain reaction for the matrix<SUP> </SUP>protein (M) and hemagglutinin (HA) genes. The HA gene encoding<SUP> </SUP>multiple basic amino acids at the HA cleavage site indicated<SUP> </SUP>that this virus is a highly pathogenic strain. Based on the<SUP> </SUP>full-length sequences of the M, HA, and neuraminidase (NA) segments<SUP> </SUP>of virus isolates through embryonated chicken eggs, the virus<SUP> </SUP>from C. nigribarbis (A/blow fly/Kyoto/93/2004) was characterized<SUP> </SUP>as H5N1 subtype influenza A virus and shown to have > 99.9%<SUP> </SUP>identities in all three RNA segments to a strain from chickens<SUP> </SUP>(A/chicken/Kyoto/3/2004) and crows (A/crows/Kyoto/53/2004) derived<SUP> </SUP>during this outbreak period in Kyoto in 2004. Our results suggest<SUP> </SUP>it is possible that blow flies could become a mechanical transmitter<SUP> </SUP>of H5N1 influenza virus.<SUP> </SUP><o:p></o:p>
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  • #2
    Re: Vectors: H5N1 identified in blow flies

    The American Journal of Tropical Medicine and Hygiene, established in 1921, is published monthly by the American Society of Tropical Medicine and Hygiene. It is among the top-ranked tropical medicine journals in the world publishing original scientific articles and the latest science covering new research with an emphasis on population, clinical and laboratory science and the application of technology in the fields of tropical medicine, parasitology, immunology, infectious diseases, epidemiology, basic and molecular biology, virology and international medicine.


    In addition not H5N1, but H5N2 in house flies

    JOURNAL OF VIROLOGY, Apr. 1985, p. 151-160 Vol. 54, No. 1
    0022-538X/85/040151-10$02.00/0
    Copyright &#169; 1985, American Society for Microbiology

    Characterization of Virulent and Avirulent A/Chicken/Pennsylvania/83 Influenza A Viruses: Potential Role of Defective Interfering RNAs in Nature

    W. J. BEAN,'* Y. KAWAOKA,' J. M. WOOD,' J. E. PEARSON,2 AND R. G. WEBSTER'

    Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38101'; and
    National Veterinary Service Laboratory, Ames, Iowa 500102
    Received 27 August 1984/Accepted 21 December 1984

    In April 1983, an influenza virus of low virulence appeared in chickens in Pennsylvania. Subsequently, in
    October 1983, the virus became virulent and caused high mortality in poultry. The causative agent has been
    identified as an influenza virus of the H5N2 serotype. The hemagglutinin is antigenically closely related to
    tern/South Africa/61 (H5N3) and the neuraminidase is similar to that from human 112N2 strains (e.g.,
    A/Japan/305/57) and from some avian influenza virus strains (e.g., A/turkey/Mass/66 [H6N2]). Comparison of
    the genome RNAs of chicken/Penn with other influenza virus isolates by RNA-RNA hybridization indicated that
    ali of the genes of this virus were closely related to those of various other influenza virus isolates from wild
    birds. Chickens infected with the virulent strain shed high concentrations of virus in their feces (107 50&#37; egg
    infective dose per g), and the virus was isolated from the albumin and yolk of eggs layed just before death.
    Virus was also isolated from house flies in chicken houses. Serological and virological studies showed that
    humans are not susceptible to infection with the virus, but can serve as short-term mechanical carriers.
    Analysis of the RNA of the viruses isolated in April and October by gel nmigration and RNA-RNA hybridization
    suggested that these strains were very closely related. Oligonucleotide mapping of the individual genes of
    virulent and avirulent strains showed a limited number of changes in the genome RNAs, but no consistent
    differences between the virulent and avirulent strains that could be correlated with pathogenicity were found.
    Polyacrylamide gel analysis of the early (avirulent) isolates demonstrated the presence of low-molecular-weight
    RNA banlds which is indicative of defective-interfering particles. These RNAs were not present in the virulent
    isolates. Experimental infection of chickens with mixtures of the avirulent and virulent strains demonstrated
    that the avirulent virus interferes with the pathogenicity of the virulent virus. The results suggest that the
    original avirulent virus was probably derived from influenza viruses from wild birds and that the virulent
    strain was derived from the avirulent strain by selective adaptation rather than by recombination or the
    introduction of a new virus into the population. This adaptation may have involved the loss of defective RNAs,as well as mutations, and thus provides a possible model for a role of defective-interfering particles in nature.


    Oops, the paper is already mentioned here

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