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Mollett, B.

Publications and source records attributed to Mollett, B..

3 recordsLinked to original sources

Detection and spread of high pathogenicity avian influenza virus H5N1 in the Antarctic Region

Until recent events, the Antarctic was the only major geographical region in which high pathogenicity avian influenza virus (HPAIV) had never previously been detected. The current panzootic of H5N1 HPAIV has decimated wild bird populations across Europe, North America, and South America. Here we report on the detection of clade 2.3.4.4b H5N1 HPAIV in the Antarctic and sub-Antarctic regions of South Georgia and the Falkland Islands, respectively. We initially detected H5N1 HPAIV in samples collected from brown skuas at Bird Island, South Georgia on 8th October 2023. Since this detection, mortalities were observed in brown skuas, kelp gulls, South Georgia shag, Antarctic tern, elephant seals and fur seals at multiple sites across South Georgia. Subsequent testing confirmed H5N1 HPAIV across several sampling locations in multiple avian species and two seal species. Simultaneously, we also confirmed H5N1 HPAIV in southern fulmar and black-browed albatross in the Falkland Islands. Genetic assessment of the virus indicates spread from South America, likely through movement of migratory birds. Critically, genetic assessment of sequences from mammalian species demonstrates no increased risk to human populations. Here we describe the detection, species impact and genetic composition of the virus and propose both introductory routes and potential long-term impact on avian and mammalian species across the Antarctic region. We also speculate on the threat to specific populations following recent reports in the area.

microbiology↗

The origin of internal genes contributes to the replication and transmission fitness of H7N9 avian influenza virus

H9N2 avian influenza viruses (AIVs) have donated internal gene segments during the emergence of zoonotic AIVs, including H7N9. We used reverse genetics to generate three reassortant viruses (2:6 H7N9) which contained the Haemagglutinin and Neuraminidase from Anhui/13 (H7N9) and the six internal gene segments from H9N2 AIVs of G1-like or BJ94-like lineages enzootic in different geographic regions in Asia. Infection of chickens with the 2:6 H7N9 containing internal gene segments from G1-like H9N2 conferred attenuation in vivo, with lower shedding and reduced transmission to contact chickens. However, possession of BJ94-like H9N2 internal gene segments resulted in more rapid transmission and significantly elevated cloacal shedding compared to the parental Anhui/13 H7N9. In vitro analysis also showed that the 2:6 H7N9 having BJ94-like internal genes had significantly increased replication compared to the Anhui/13 H7N9 in chicken cells. In vivo co-infection experiments followed, where chickens were co-infected with pairs of Anhui/13 H7N9 and one of each of the three 2:6 H7N9 reassortants. During ensuing transmission events, the Anhui/13 H7N9 virus outcompeted 2:6 H7N9 with internal gene segments of BJ94-like or G1-like H9N2 viruses. Co-infection did lead to the emergence of novel reassortant genotypes that were transmitted to contact chickens. Some of the reassortant viruses had a greater replication in chicken and human cells compared to the progenitors. We demonstrated that the internal gene cassette determines the transmission fitness of H7N9 viruses in chickens and the reassortment events can generate novel H7N9 genotypes with increased virulence in chickens and enhanced zoonotic potential. ImportanceH9N2 avian influenza viruses (AIVs) are enzootic in poultry in different geographical regions. The internal genes of these viruses can be exchanged with other zoonotic AIVs, most notably the China-origin H7N9 that can give rise to new virus genotypes with increased veterinary, economic and public health threats to both poultry and humans. We investigated the propensity of the internal genes of H9N2 viruses (G1 or BJ94) in the generation of novel reassortant H7N9 AIVs. We observed that the internal genes of H7N9 which were derivative of BJ94-like H9N2 virus have a fitness advantage compared to those from the G1-like H9N2 viruses for efficient transmission among chickens. We also observed the generation of novel reassortant viruses during chicken transmission which infected and replicated efficiently in human cells. Therefore, such emergent reassortant genotypes may pose an elevated zoonotic threat.

microbiology↗

Co-infection of chickens with H9N2 and H7N9 avian influenza viruses leads to emergence of reassortant H9N9 virus with increased fitness for poultry and enhanced zoonotic potential

An H7N9 low pathogenicity avian influenza virus (LPAIV) emerged through genetic reassortment between H9N2 and other LPAIVs circulating in birds in China. This virus causes inapparent clinical disease in chickens, but zoonotic transmission results in severe and fatal disease in humans. We evaluated the consequences of reassortment between the H7N9 and the contemporary H9N2 viruses of G1 lineage that are enzootic in poultry across the Indian sub-continent and the Middle East. Co-infection of chickens with these viruses resulted in emergence of novel reassortant H9N9 viruses carrying genes derived from both H9N2 and H7N9 viruses. These reassortant H9N9 viruses showed significantly increased replication fitness, enhanced pathogenicity in chicken embryos and the potential to transmit via contact among ferrets. Our study highlights that the co-circulation of H7N9 and H9N2 viruses could represent a threat for the generation of novel reassortant viruses with greater virulence in poultry and an increased zoonotic potential. O_FIG O_LINKSMALLFIG WIDTH=197 HEIGHT=200 SRC="FIGDIR/small/438444v1_ufig1.gif" ALT="Figure 1"> View larger version (96K): org.highwire.dtl.DTLVardef@1f425cborg.highwire.dtl.DTLVardef@1dd3ba2org.highwire.dtl.DTLVardef@1762348org.highwire.dtl.DTLVardef@1064cb7_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract C_FIG In BriefH9N2 viruses have a high propensity to reassort with other avian influenza viruses. We found that co-infection of chickens with H9N2 and H7N9 led to the emergence of reassortant viruses including the H9N9 subtype. Some reassortant H9N9 viruses exhibited increased replication fitness, increased pathogenicity in the chicken embryo, greater avidity for human and avian cell receptors, lower pH fusion and contact-transmission to ferrets. This study demonstrated the ability of viruses that already exist in nature to exchange genetic material, highlighting the potential emergence of viruses from these subtypes with increased zoonotic potential. There are nine H9 influenza A subtypes carrying different neuraminidase (NA) genes, including H9N9 viruses, while they are not common they do exist in nature as wildtypes (CDC). HighlightsO_LICo-infection of chickens with H7N9 and H9N2 led to emergence of reassortant H9N9 viruses C_LIO_LIReassortant H9N9 viruses had an increased replication rate in avian and human cells C_LIO_LIReassortant H9N9 viruses had a lower pH fusion and significantly higher receptor binding to 2,3 sialoglycans C_LIO_LIReassortant H9N9 replicated in ferrets at similar levels compared to H7N9 and transmitted via direct contact C_LIO_LIFerrets exposed to reassortant H9N9 by aerosol contact were also found to be seropositive C_LIO_LIExperimental simulation of events that may occur naturally with circulating viruses has demonstrated the risk of emergence of viruses with increased zoonotic potential. C_LI

microbiology↗