Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.
The toxins that some bacteria secrete to kill off rival species can also generate mutations that help toxin-resistant populations adapt to new environments.
Virus infection of the central nervous system disrupts the homeostasis of the immune-neural-synaptic axis via induction of pleiotropic genes with an unintended off-target negative impact on the neurotransmission.
The first structures of Kaposi’s sarcoma-associated herpesvirus ORF68 and Epstein–Barr virus BFLF1, conserved and essential proteins required in herpesviruses, reveal new insights into viral genome packaging.
Patients with paucigranulocytic asthma may be more susceptible to severe influenza and could potentially be source of new, more virulent, influenza virus variants.
