The ability of Vaccinia virus to induce actin polymerisation depends on the relative binding position of adaptors within the signalling network activating the Arp2/3 complex.

Novel virus-host systems yield insights into how Lepidopterans (moths and butterflies) combat RNA virus infection and reveal that poxvirus A51R proteins can suppress the host's immune system and stabilize microtubules in host cells.

Active selfish genetic elements in infected cells aid virus adaptation by catalyzing the transfer of host genes to virus genomes.

An adaptive process of genetic homogenization in poxviruses facilitates the propagation of single nucleotide variation within gene copies and might favor the persistence of large gene copy arrays.

A new experimental system of horizontal gene transfer demonstrates that host retrotransposons facilitate the transfer of host genes into poxviruses.

As long suspected, poxviruses capture host genes through a reverse-transcription process now shown to be mediated by retrotransposons.

Evolutionary innovation and turnover in the IFIT1 antiviral gene family has led to diverse repertoires of antiviral specificity across mammals.

HIV-1 Vpr antagonises innate immune sensing of viral and non-viral stimuli by preventing activated IRF3 and NF-κB nuclear transport.

Intersectin counterparts in yeast recruit WASP and WIP to endocytic sites to establish a robust multivalent SH3 domain-PRM interaction network which gives actin assembly onset a switch-like behavior in vivo.

Experiments in mice have shown than an enzyme that repairs broken DNA inside the nucleus also has a central role in the innate immune system because it is able to detect foreign DNA outside the nucleus.