Susceptibility of bovine respiratory and mammary epithelial cells to avian and mammalian derived clade 2.3.4.4b H5N1 highly pathogenic avian influenza viruses.

Zoonotic transmission of avian influenza viruses into mammals is relatively rare due to anatomical differences in the respiratory tract between species. Recently, clade 2.3.

ZIC1 is a context-dependent medulloblastoma driver in the rhombic lip.

Transcription factors are frequent cancer driver genes, exhibiting noted specificity based on the precise cell of origin. We demonstrate that ZIC1 exhibits loss-of-function (LOF) somatic events in group 4 (G4) medulloblastoma through recurrent point mutations, subchromosomal deletions and mono-allelic epigenetic repression (60% of G4 medulloblastoma). In contrast, highly similar SHH medulloblastoma exhibits distinct and diametrically opposed gain-of-function mutations and copy number gains (20% of SHH medulloblastoma).

Intraductal infection with H5N1 clade 2.3.4.4b influenza virus.

The ongoing outbreak of highly pathogenic avian influenza (HPAI) H5N1 of the clade 2.3.4.

kills in a polyphosphate-dependent manner.

Due to their frequent coexistence in many polymicrobial infections, including in patients with cystic fibrosis or burn/chronic wounds, many studies have investigated the mechanistic details of the interaction between the opportunistic pathogens and rapidly outcompetes under cocultivation conditions which is mediated by several of 's virulence factors. Here, we report that polyphosphate (polyP), an efficient stress defense system and virulence factor in , plays a role in the pathogen's ability to inhibit and kill in a contact-independent manner. We show that cells characterized by low polyP levels are less detrimental to growth and survival while the Gram-positive pathogen is significantly more compromised by the presence of cells that produce high levels of polyP.