Replication and pathogenic potential of influenza A virus subtypes H3, H7, and H15 from free-range ducks in Bangladesh in mammals

Abstract

Surveillance of wild aquatic birds and free-range domestic ducks in the Tanguar Haor wetlands in Bangladesh has identified influenza virus subtypes H3N6, H7N1, H7N5, H7N9, and H15N9. Molecular characterization of these viruses indicates their contribution to the genesis of new genotypes of H5N1 influenza viruses from clade 2.3.2.1a that are dominant in poultry markets in Bangladesh as well as to the genesis of the highly pathogenic H5N8 virus currently causing disease outbreaks in domestic poultry in Europe and the Middle East. Therefore, we studied the antigenicity, replication, and pathogenicity of influenza viruses isolated from Tanguar Haor in the DBA/2J mouse model. All viruses replicated in the lung without prior mammalian adaptation, and H7N1 and H7N9 viruses caused 100% and 60% mortality, respectively. H7N5 viruses replicated only in the lungs, whereas H7N1 and H7N9 viruses also replicated in the heart, liver, and brain. Replication and transmission studies in mallard ducks showed that H7N1 and H7N9 viruses replicated in ducks without clinical signs of disease and shed at high titers from the cloaca of infected and contact ducks, which could facilitate virus transmission and spread. Our results indicate that H7 avian influenza viruses from free-range ducks can replicate in mammals, cause severe disease, and be efficiently transmitted to contact ducks. Our study highlights the role of free-range ducks in the spread of influenza viruses to other species in live poultry markets and the potential for these viruses to infect and cause disease in mammals.

Genetic characterization and pathogenic potential of H10 avian influenza viruses isolated from live poultry markets in Bangladesh

“…Recently, we described the replication and pathogenic potential of H3, H7, and H15 viruses from free-range ducks in Bangladesh using mice. We observed that H7N1 and H7N9 viruses caused 100% and 60% mortality respectively, and expanded their tissue tropism beyond the pulmonary tissues to heart, liver, and brain 36 . Our current study showed this for both H10N1 and H10N6 AIVs as well as high mortality in mice.…”

Mammalian pathogenicity and transmissibility of low pathogenic avian influenza H7N1 and H7N3 viruses isolated from North America in 2018

“…Two North American LPAI H7N1 viruses isolated during wild bird surveillance efforts were found to cause severe disease in the DBA/2 mouse model [ 16 ], a strain with differential susceptibility to influenza viruses compared with the BALB/c model employed here [ 43 ]. Eurasian-lineage LPAI H7N1 viruses were found to replicate in mice and were capable of severe disease depending on the virus strain and mouse species employed [ 44 , 45 ]. Additionally, an HPAI H7N1 Eurasian-lineage virus was capable of causing severe disease in ferrets and exhibited limited transmission in a direct contact setting; this virus was capable of supporting an airborne transmissible phenotype following serial passage in ferrets [ 46 ].…”

Reverse‐transcription recombinase‐aided amplification assay for H7 subtype avian influenza virus

“…The H7 subtype AIV has spread worldwide and has been detected in China (Wu et al, ), the United States (Olsen et al, ), Korea (Lee et al, ), Bangladesh (El‐Shesheny et al, ), Australia (Scott et al, ), Cambodia (Horwood et al, ) and Belgium (Van Borm et al, ). The pathogenic H7 subtype AIV changed from low pathogenicity in birds to high pathogenicity in both humans and birds (Dhingra et al, ).…”