Cryo EM and a custom subvolume refinement approach applied to mouse polyomavirus revealed the in vivo impact of polyomavirus capsid mutations on antiviral antibody immunoevasion and neurovirulence.

A peptide derived from BK and JC polyomavirus protein VP2/3 inhibits viral infection by targeting a binding site in the pore of polyomavirus VP1 pentamers, enabling future VP1-targeted therapeutic strategies.

Loss of T cell control during persistent polyomavirus infection, in the setting of a limited antiviral antibody response, facilitates emergence of antibody-escape viruses carrying the potential for neurovirulence.

Nearly half of bladder cancers of solid organ transplant recipients harbor papillomaviruses or polyomaviruses, with many tumors showing evidence of clonal viral integration and viral oncogene effects on tumor gene expression patterns.

SIMC1 and SLF1 bind exclusively to SLF2 to form two separate complexes that direct the human SMC5/6 complex to its antiviral defense or DNA lesion repair activities.

ST recruitment of STRIPAK facilitates PP2A-mediated dephosphorylation of MAP4K4 and induces cell transformation highlighting that STRIPAK complex plays a key role in defining PP2A specificity and activity.

In a prospective, population-based cohort, high polygenic risk and infection with Fusobacterium nucleatum have a small, yet independent impact on coronary heart disease risk.

Novel cell-free biochemical experiments show that the host GTPase MxB can restrict the infection of alphaherpesviruses by disassembling the sturdy viral capsids so that they can no longer protect the viral genomes.

Biochemical and cell-based analyses reveal how a non-enveloped virus exploits the chaperone activity of an ER transmembrane protein to penetrate the ER membrane required for successful virus infection.