Viral escape mechanisms – escapology taught by viruses

Abstract

Viruses have 'studied' immunology over millions of years of coevolution with their hosts. During this ongoing education they have developed countless mechanisms to escape from the host's immune system. To illustrate the most common strategies of viral immune escape we have focused on two murine models of persistent infection, lymphocytic choriomeningitis virus (LCMV) and murine cytomegalovirus (MCMV). LCMV is a fast replicating small RNA virus with a genome prone to mutations. Therefore, LCMV escapes from the immune system mainly by two strategies: 'speed' and 'shape change'. At the opposite extreme, MCMV is a large, complex DNA virus with a more rigid genome and thus the strategies used by LCMV are no option. However, MCMV has the coding capacity for additional genes which interfere specifically with the immune response of the host. These escape strategies have been described as 'camouflage' and 'sabotage'. Using these simple concepts we describe the spectrum of viral escapology, giving credit not only to the researchers who uncovered this fascinating area of immunology but also to the viruses themselves, who still have a few lessons to teach.

Viral mutation rates: modelling the roles of within-host viral dynamics and the trade-off between replication fidelity and speed

“…High mutation rates in viruses are not likely to be an adaptation to produce advantageous mutations; that is, they are probably not maintained in a Red Queen scenario. An exception to this principle may occur in viruses causing persistent infections, such as HIV, in which immune escape mutants occur frequently over long periods [41]. Nevertheless, the model presented here generally supports the hit-andrun view of viruses, according to which they transmit to other hosts without having to escape immunity through mutation [18,19].…”

Quantitative Proteomics of Spodoptera frugiperda Cells during Growth and Baculovirus Infection

“…Interestingly, we observed expression changes in two proteins that together are counterintuitive with an activation of UPR, namely decreased levels of the chaperone ERp57, a central UPR effector also involved in Ca 2+ homeostasis, and the polypeptide transporter SRP57. These findings suggest that, through unknown mechanisms, BVs are able to take advantage of ER stress while avoiding negative effects associated with UPR, probably in different ways than already described for other viruses [45], [46]. Failure to induce HSC70 expression at HCD infection can mean less ER capacity for viral protein processing and thus less BV progeny.…”

T cell epitope redundancy: cross-conservation of the TCR face between pathogens and self and its implications for vaccines and autoimmunity

“…Other means of immune escape by pathogens have been well described [29]. For example, Gram-negative bacteria can escape innate immunity through structural modifications of their PAMPs, thus escaping recognition by phagocytes [30].…”