Drawing on disorder: How viruses use histone mimicry to their advantage

Tarakhovsky, Alexander; Prinjha, Rab K.

Virus-induced changes to the mammalian immune system that benefit the host are also common. The mouse norovirus can replace the function of commensal gut bacteria in the establishment of intestinal architecture and subsequent establishment of the innate immune system (Kernbauer et al., 2014) . Mouse γ-herpesvirus protects mice from the bacterial pathogens that cause bubonic plague (Yersinia pestis) and the foodborne disease listeriosis (Listeria monocytogenes) via prolonged production of IFN-γ and macrophage activation (Barton et al., 2007) . Human cytomegalovirus, a nearly ubiquitous latent herpesvirus, provides enhanced immune response to influenza, especially in young adults, with evidence for heightened immune activation (Furman et al., 2015) . This appears not to be an isolated case because other herpesviruses may also increase the immune response to other pathogens (Sandalova et al., 2010) . In humans, the Flavivirus GB virus C, also known as hepatitis G virus, is asymptomatic and could thus be considered a commensal virus, but under some conditions it behaves as a mutualist. For example, HIV-positive patients who are infected with GBV0C show slower disease progression, a process that involves down-regulation of cell receptors for HIV entry, normalization of IFN and other cytokine levels, and decreased HIV replication (Bhattarai and Stapleton, 2012) . The beneficial effect of viruses on the host are indicative of the existence of virus-encoded molecules that can drive the establishment of complex nondevelopmentally predetermined phenotypes in animal or human cells.