The complete genomes of three human H5N1 influenza isolates were characterized, together with the haemagglutinin (HA) and neuraminidase (NA) genes from two additional human isolates and one chicken isolate. These six influenza isolates were obtained from four different provinces of Thailand during the avian influenza outbreak in Asia from late 2003 to May 2004. All six Thailand isolates contained multiple basic amino acids at the cleavage site in the HA gene. Amino acid residues at the receptor-binding site of the five human viruses were similar to those of the chicken virus and other H5N1 viruses from Hong Kong. The presence of amantadine resistance in the Thailand viruses isolated during this outbreak was suggested by a fixed mutation in M2 and confirmed by a phenotypic assay. All genomic segments of the Thailand viruses clustered with the recently described genotype Z. The Thailand viruses contained more avian-specific residues than the 1997 Hong Kong H5N1 viruses, suggesting that the virus may have adapted to allow a more efficient spread in avian species.
Disease OutbreaksInfluenza A Virus, H5N1 SubtypeAmantadineAnimalsAntiviral AgentsChickensDrug Resistance, ViralHemagglutinin Glycoproteins, Influenza VirusHumansInfluenza A virusInfluenza in BirdsInfluenza, HumanMolecular EpidemiologyMolecular Sequence DataMutationNeuraminidasePhylogenyReceptors, Virus
Structured evidence records
Evidence records
7 total
Molecular Adaptation4 records
Molecular AdaptationExtraction confidence 0.95
Key finding
H5N1 viruses from Thailand possessed a polybasic HA cleavage site associated with high pathogenicity and host adaptation.
Amino acid residues at the receptor-binding site of the five human viruses were similar to those of the chicken virus and other H5N1 viruses from Hong Kong.
Genes or proteins
HA
Receptors
virus receptor
Mechanism types
receptor_binding; host_range
Molecular AdaptationExtraction confidence 0.95
Key finding
Thailand H5N1 isolates exhibited amantadine resistance linked to a fixed mutation in M2 viroporin.
The presence of amantadine resistance in the Thailand viruses isolated during this outbreak was suggested by a fixed mutation in M2 and confirmed by a phenotypic assay.
Genes or proteins
M2
Mutations
M2 mutation conferring amantadine resistance
Mechanism types
drug_resistance
Molecular AdaptationExtraction confidence 0.90
Key finding
Thailand H5N1 viruses displayed avian-specific amino acid residues, indicating adaptation optimizing replication and transmission in avian hosts.
The Thailand viruses contained more avian-specific residues than the 1997 Hong Kong H5N1 viruses, suggesting that the virus may have adapted to allow a more efficient spread in avian species.
Mechanism types
host_adaptation; transmission_fitness
Genomic Evolution2 records
Genomic EvolutionExtraction confidence 0.90
Key finding
Genomic sequencing and phylogenetic analysis of human and chicken H5N1 influenza isolates from Thailand showed that all segments belong to genotype Z, with avian-like residues indicating adaptive evolution toward avian hosts.
The complete genomes of three human H5N1 influenza isolates were characterized, together with the haemagglutinin (HA) and neuraminidase (NA) genes from two additional human isolates and one chicken isolate ... All genomic segments of the Thailand viruses clustered with the recently described genotype Z.
Comparative genomic analysis revealed that human H5N1 viruses shared receptor-binding site residues with chicken H5N1 viruses, supporting close evolutionary relatedness between avian and human isolates.
The complete genomes of three human H5N1 influenza isolates were characterized ... and one chicken isolate ... Amino acid residues at the receptor-binding site of the five human viruses were similar to those of the chicken virus and other H5N1 viruses from Hong Kong.
Genes or proteins
HA; NA
Analysis methods
comparative genomics; sequence alignment
Spillover Event1 records
Spillover EventExtraction confidence 0.85
Key finding
Human H5N1 influenza infections in Thailand were caused by viruses closely related to avian H5N1 from chickens, providing direct evidence of bird-to-human spillover during the 2003–2004 outbreak.
The complete genomes of three human H5N1 influenza isolates were characterized, together with the HA and NA genes from two additional human isolates and one chicken isolate. These six influenza isolates were obtained during the avian influenza outbreak in Asia from late 2003 to May 2004, and the human viruses were similar to the chicken virus.
