TY - JOUR
T1 - The zoonotic potential of avian influenza viruses isolated from wild waterfowl in Zambia
AU - Simulundu, Edgar
AU - Nao, Naganori
AU - Yabe, John
AU - Muto, Nilton A.
AU - Sithebe, Thami
AU - Sawa, Hirofumi
AU - Manzoor, Rashid
AU - Kajihara, Masahiro
AU - Muramatsu, Mieko
AU - Ishii, Akihiro
AU - Ogawa, Hirohito
AU - Mweene, Aaron S.
AU - Takada, Ayato
N1 - Funding Information:
We thank Hiroko Miyamoto and Mari Ishijima (Hokkaido University Research Center for Zoonosis Control) for excellent technical assistance. We are also grateful to Dr. Mathew Nyirenda and Dr. Collins Ateba (North West University, Mafikeng Campus) for proofreading the manuscript, and Dr. Yuji Sunden (Graduate School of Veterinary Medicine, Hokkaido University) for kindly supporting pathological studies. This work was supported by the Japan Initiative for Global Research Network on Infectious Diseases (J-GRID) and the Global COE Program ‘Establishment of International Collaboration Centers for Zoonosis Control’ from the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan, as well as the Japan Science and Technology Agency (JST)/Japan International Cooperation Agency (JICA) within the framework of the Science and Technology Research Partnership for Sustainable Development (SATREPS).
Publisher Copyright:
© 2014, Springer-Verlag Wien.
PY - 2014/9/1
Y1 - 2014/9/1
N2 - Whilst remarkable progress in elucidating the mechanisms governing interspecies transmission and pathogenicity of highly pathogenic avian influenza viruses (AIVs) has been made, similar studies focusing on low-pathogenic AIVs isolated from the wild waterfowl reservoir are limited. We previously reported that two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues preferentially associated with human influenza virus proteins (so-called human signatures) and replicated better in the lungs of infected mice and caused more morbidity than a strain lacking such residues. To further substantiate these observations, we infected chickens and mice intranasally with AIV strains of various subtypes (H3N6, H3N8, H4N6, H6N2, H9N1 and H11N9) isolated from wild waterfowl in Zambia. Although some strains induced seroconversion, all of the tested strains replicated poorly and were nonpathogenic for chickens. In contrast, most of the strains having human signatures replicated well in the lungs of mice, and one of these strains caused severe illness in mice and induced lung injury that was characterized by a severe accumulation of polymorphonuclear leukocytes. These results suggest that some strains tested in this study may have the potential to infect mammalian hosts directly without adaptation, which might possibly be associated with the possession of human signature residues. Close monitoring and evaluation of host-associated signatures may help to elucidate the prevalence and emergence of AIVs with potential for causing zoonotic infections.
AB - Whilst remarkable progress in elucidating the mechanisms governing interspecies transmission and pathogenicity of highly pathogenic avian influenza viruses (AIVs) has been made, similar studies focusing on low-pathogenic AIVs isolated from the wild waterfowl reservoir are limited. We previously reported that two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues preferentially associated with human influenza virus proteins (so-called human signatures) and replicated better in the lungs of infected mice and caused more morbidity than a strain lacking such residues. To further substantiate these observations, we infected chickens and mice intranasally with AIV strains of various subtypes (H3N6, H3N8, H4N6, H6N2, H9N1 and H11N9) isolated from wild waterfowl in Zambia. Although some strains induced seroconversion, all of the tested strains replicated poorly and were nonpathogenic for chickens. In contrast, most of the strains having human signatures replicated well in the lungs of mice, and one of these strains caused severe illness in mice and induced lung injury that was characterized by a severe accumulation of polymorphonuclear leukocytes. These results suggest that some strains tested in this study may have the potential to infect mammalian hosts directly without adaptation, which might possibly be associated with the possession of human signature residues. Close monitoring and evaluation of host-associated signatures may help to elucidate the prevalence and emergence of AIVs with potential for causing zoonotic infections.
UR - http://www.scopus.com/inward/record.url?scp=84907690434&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84907690434&partnerID=8YFLogxK
U2 - 10.1007/s00705-014-2124-1
DO - 10.1007/s00705-014-2124-1
M3 - Article
C2 - 24862188
AN - SCOPUS:84907690434
VL - 159
SP - 2633
EP - 2640
JO - Archives of Virology
JF - Archives of Virology
SN - 0304-8608
IS - 10
ER -