|Senne, Dennis - NVSL, AMES,IA|
|Pedersen, J - NVSL, AMES,IA|
|Panigrahy, B - NVSL, AMES,IA|
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 4, 2002
Publication Date: September 1, 2003
Citation: Senne, D.A., Suarez, D.L., Pedersen, J.C., Panigrahy, B. 2003. Molecular And Biological Characteristics Of H5 and H7 Avian Influenza Viruses Found In Live-Bird Markets Of Northeastern United States During 1994-2001. Avian Diseases 2003, 47:898-904. Interpretive Summary: Avian influenza virus can infect a number of different types of birds including chickens and turkeys. The virus can cause mild disease or it can cause a serious deadly disease in poultry. The deadly form of the disease is called highly pathogenic avian influenza, and it has only been associated with two subtypes of avian influenza, H5 and H7. Because of the concern for these two subtypes of virus, any outbreak of H5 or H7 influenza in poultry is examined by testing representative viruses by experimental chicken inoculation and by sequencing of certain parts of the influenza virus known to be related to disease. Evidence of multiple outbreaks of H5 and H7 were reported in the last five years, but all isolates tested were not highly pathogenic. Most H7 influenza viruses from live bird markets in the Northeast U.S. were found to be related, which shows that current eradication efforts were unsuccessful.
Technical Abstract: Surveillance for H5 and H7 subtypes of avian influenza virus AIV) in the live-bird markets (LBMs) of the northeastern U.S. has been in effect since 1986 when the markets were first recognized as a potential reservoir for the AIV. Long-term maintenance of AIV in the LBM system has been documented but little is known about the influence of prolonged replication in unnatural avian hosts on the genetics of the virus, especially in the region of the hemagglutinin gene that can influence pathogenicity. Isolation of low pathogenic H5 AIVs from the LBMs have been sporadic; however, in 1994 a low pathogenic H7N2 virus was isolated that has persisted in the LBMs for over seven years. Efforts to eliminate the H7 virus from the markets have been unsuccessful. During the seven-year period, several molecular changes have been detected at the hemagglutinin cleavage site of the H7 virus. These changes include the substitution of proline for threonine and lysine for asparagine, respectively at the -2 and -5 positions of the HA1. In addition, there has been a 24 base-pair deletion in the receptor binding region of the HA. The accumulation of an additional basic amino acid at the cleavage site is a cause for concern to regulatory authorities, and efforts to eliminate the virus from the LBM system have been intensified.