From low to high pathogenicity-Characterization of H7N7 avian influenza viruses in two epidemiologically linked outbreaks

2018 ◽  
Vol 65 (6) ◽  
pp. 1576-1587 ◽  
Author(s):  
Klaas Dietze ◽  
Annika Graaf ◽  
Timo Homeier-Bachmann ◽  
Christian Grund ◽  
Leonie Forth ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
High Pathogenicity

scholarly journals Ecology of H3 avian influenza viruses in Korea and assessment of their pathogenic potentials

2008 ◽  
Vol 89 (4) ◽  
pp. 949-957 ◽  
Author(s):  
Min-Suk Song ◽  
Taek-Kyu Oh ◽  
Ho Jin Moon ◽  
Dai-Woon Yoo ◽  
Eun Ho Lee ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Wild Bird ◽  
Migratory Birds ◽  
Influenza Viruses ◽  
Interspecies Transmission ◽  
Avian Influenza Viruses ◽  
Backyard Poultry ◽  
Live Poultry ◽  
Live Poultry Markets

To determine the genetic origins of novel H3 avian influenza viruses of chickens and ducks in Korea, genetic characterization of H3 avian influenza viruses isolated from live poultry markets and migratory aquatic birds in South Korea during 2004–2006 was conducted. Phylogenetic analysis revealed that at least four novel genotypes of H3N2 and two genotypes of H3N6 avian influenza viruses were co-circulating in backyard poultry of Korea. The viruses were reassortants between H9N2 viruses of Korean chickens and unknown influenza viruses of migratory birds. Genetic comparison of H3 viruses from live bird markets with those from wild bird isolates revealed that certain gene segments of wild bird isolates are related closely to those of Korean group H9N2 viruses isolated from live poultry markets in 2003. Furthermore, animal-challenge studies demonstrated that the pathogenicity of certain avian H3 influenza viruses was altered due to reassortment, leading to H3 avian influenza viruses in Korea that can potentially expand their host range to include mammals. These studies emphasize the continuing need to monitor backyard poultry at live poultry markets to better understand interspecies transmission and the emergence of novel influenza viruses that have the potential to infect humans.

scholarly journals Erratum: Characterization of the Pathogenesis of H10N3, H10N7, and H10N8 Subtype Avian Influenza Viruses Circulating in Ducks

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Miaomiao Zhang ◽  
Xingxing Zhang ◽  
Kaidi Xu ◽  
Qiaoyang Teng ◽  
Qinfang Liu ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Influenza Viruses ◽  
Avian Influenza Viruses

scholarly journals Amino Acid Residue 217 in the Hemagglutinin Glycoprotein Is a Key Mediator of Avian Influenza H7N9 Virus Antigenicity

2018 ◽  
Vol 93 (1) ◽  
Author(s):  
Pengxiang Chang ◽  
Joshua E. Sealy ◽  
Jean-Remy Sadeyen ◽  
Munir Iqbal
Keyword(s):  
Amino Acid ◽  
Avian Influenza ◽  
Immune Escape ◽  
Influenza Viruses ◽  
Single Mutation ◽  
H7n9 Virus ◽  
Avian Influenza Viruses ◽  
Antigenic Analysis ◽  
Neutralizing Capacity ◽  
High Pathogenicity

ABSTRACTAvian influenza viruses continue to evolve and acquire mutations that facilitate antigenic drift and virulence change. In 2017, low-pathogenicity H7N9 avian influenza viruses evolved to a high-pathogenicity phenotype in China. Comparative antigenic analysis of the low- and high-pathogenicity virus strains showed marked variability. In order to identify residues that may be linked to the antigenic change among the H7N9 viruses, we serially passaged the viruses in the presence of homologous ferret antiserum. Progeny viruses able to overcome the neutralizing capacity of the antiserum were sequenced. The analysis showed that the emergent immune escape viruses contained mutations A125T, A151T, and L217Q in the hemagglutinin (HA) glycoprotein as early as passage 5 and that these mutations persisted until passage 10. The results revealed that a single mutation, L217Q, in the HA of H7N9 virus led to 23- and 8-fold reductions in hemagglutination inhibition (HI) titer with ferret and chicken antisera, respectively. Further analysis showed that this change also contributed to antigenic differences between the low- and high-pathogenicity H7N9 viruses, thus playing a major role in their antigenic diversification. Therefore, evolutionary changes at amino acid position 217 in the H7N9 viruses can serve as a genetic marker for virus antigenic diversity during vaccine seed matching and selection. Thein vitroimmune escape mutant selection method used in this study could also aid in the prediction of emerging antigenic variants in naturally infected or immunized animals.IMPORTANCEAvian influenza H7N9 viruses circulating in poultry and wild birds continue to evolve and acquire important phenotypic changes. Mutations to the virus hemagglutinin (HA) glycoprotein can modulate virus antigenicity and facilitate virus escape from natural or vaccine-induced immunity. The focus of this study was to identify evolutionary markers in the HA of H7N9 that drive escape from antibody-based immunity. To achieve this, we propagated low-pathogenicity H7N9 virus in the presence of polyclonal antiserum derived from ferrets infected with the same strain of virus (homologous antiserum). This selection process was repeated 10 times. The HA gene sequences of viruses recovered after the fifth passage showed that the viruses readily acquired mutations at three different amino acid positions (A125T, A151T, and L217Q). Further functional analysis of these mutations confirmed that the mutation at residue 217 in the HA was responsible for mediating changes to the immunological properties of the H7N9 virus.

scholarly journals Insights into the Acquisition of Virulence of Avian Influenza Viruses during a Single Passage in Ferrets

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 915
Author(s):  
Butler ◽  
Middleton ◽  
Haining ◽  
Layton ◽  
Rockman ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Respiratory Tract ◽  
Severe Disease ◽  
Influenza Viruses ◽  
Mammalian Host ◽  
Upper Respiratory Tract ◽  
Avian Influenza Viruses ◽  
Single Passage ◽  
H5n1 Isolate ◽  
High Pathogenicity

Circulating avian influenza viruses pose a significant threat, with human infections occurring infrequently but with potentially severe consequences. To examine the dynamics and locale of the adaptation process of avian influenza viruses when introduced to a mammalian host, we infected ferrets with H5N1 viruses. As expected, all ferrets infected with the human H5N1 isolate A/Vietnam/1203/2004 showed severe disease and virus replication outside the respiratory tract in multiple organs including the brain. In contrast infection of ferrets with the avian H5N1 virus A/Chicken/Laos/Xaythiani26/2006 showed a different collective pattern of infection; many ferrets developed and cleared a mild respiratory infection but a subset (25–50%), showed extended replication in the upper respiratory tract and developed infection in distal sites. Virus from these severely infected ferrets was commonly found in tissues that included liver and small intestine. In most instances the virus had acquired the common virulence substitution PB2 E627K but, in one case, a previously unidentified combination of two amino acid substitutions at PB2 S489P and NP V408I, which enhanced polymerase activity, was found. We noted that virus with high pathogenicity adaptations could be dominant in an extra-respiratory site without being equally represented in the nasal wash. Further ferret passage of these mutated viruses resulted in high pathogenicity in all ferrets. These findings illustrate the remarkable ability of avian influenza viruses that avoid clearance in the respiratory tract, to mutate towards a high pathogenicity phenotype during just a single passage in ferrets and also indicate a window of less than 5 days in which treatment may curtail systemic infection.

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