Dissecting the role of the HA1-226 leucine residue in the fitness and airborne transmission of an A(H9N2) avian influenza virus.

Unlabelled: A better understanding of viral factors that contribute to influenza A virus (IAV) airborne transmission is crucial for pandemic preparedness. A limited capacity for airborne transmission was recently observed in a human A(H9N2) virus isolate (A/Anhui-Lujiang/39/2018, AL/39) that possesses a leucine (L) residue at position HA1-226 (H3 numbering), indicative of human-like receptor binding potential. To evaluate the roles of the residue at this position in virus fitness and airborne transmission, a wild-type AL/39 (AL/39-wt) and a mutant virus (AL/39-HA1-L226Q) with a single substitution at position HA1-226 from leucine to glutamine (Q), a consensus residue in avian influenza viruses, were rescued and assessed in the ferret model.

Transmission of a human isolate of clade 2.3.4.4b A(H5N1) virus in ferrets.

Since 2020, there has been unprecedented global spread of highly pathogenic avian influenza A(H5N1) in wild bird populations with spillover into a variety of mammalian species and sporadically humans. In March 2024, clade 2.3.

Low asparagine wheat: Europe's first field trial of genome edited wheat amid rapidly changing regulations on acrylamide in food and genome editing of crops.

We review the undertaking of a field trial of low asparagine wheat lines in which the asparagine synthetase gene, , has been knocked out using CRISPR/Cas9. The field trial was undertaken in 2021-2022 and represented the first field release of genome edited wheat in Europe. The year of the field trial and the period since have seen rapid changes in the regulations covering both the field release and commercialisation of genome edited crops in the UK.

Calreticulin and JAK2V617F driver mutations induce distinct mitotic defects in myeloproliferative neoplasms.

Myeloproliferative neoplasms (MPNs) encompass a diverse group of hematologic disorders driven by mutations in JAK2, CALR, or MPL. The prevailing working model explaining how these driver mutations induce different disease phenotypes is based on the decisive influence of the cellular microenvironment and the acquisition of additional mutations. Here, we report increased levels of chromatin segregation errors in hematopoietic cells stably expressing CALRdel52 or JAK2V617F mutations.