Abstract
To successfully infect, replicate, and persist in the host, viruses have evolved numerous strategies to take control of multiple cellular processes, including those that target transmembrane (TM) signal transduction mediated by immune receptors. Despite tremendous advancement in recent years, the exact molecular mechanisms underlying these critical points in viral pathogenesis remain unknown. In this Opinion, based on a novel model of immune signaling, the Signaling Chain HOmoOLigomerization (SCHOOL) model, I suggest specific mechanisms used by different viruses such as human immunodeficiency virus (HIV), cytomegalovirus (CMV), severe acute respiratory syndrome coronavirus (SARS-CoV), herpesvirus saimiri (HVS), human herpesvirus 6 (HHV-6), etc., to modulate the host immune response mediated by members of the family of multichain immune recognition receptors (MIRRs). I also demonstrate how the SCHOOL model, together with the lessons learned from viral pathogenesis, can be used practically for rational drug design and the development of new therapies for immune disorders.
Highlights
To successfully infect, replicate, and persist in the host, viruses have evolved numerous strategies to take control of multiple cellular processes, including those that target transmembrane (TM) signal transduction mediated by immune receptors
Predicted and molecularly explained by the Signaling Chain HOmoOLigomerization (SCHOOL) model [7,10,11,12,13], manipulation of multichain immune recognition receptors (MIRRs) signaling is performed by numerous unrelated viruses throughout their life cycle
The ability viruses have developed over centuries of evolution [13,14] to modulate T cell receptor (TCR) signaling plays a crucial role in viral pathogenesis
Summary
Despite tremendous advancement in recent years, the exact molecular mechanisms underlying these critical points in viral pathogenesis remain unknown In this Opinion, based on a novel model of immune signaling, the Signaling Chain HOmoOLigomerization (SCHOOL) model, I suggest specific mechanisms used by different viruses such as human immunodeficiency virus (HIV), cytomegalovirus (CMV), severe acute respiratory syndrome coronavirus (SARS-CoV), herpesvirus saimiri (HVS), human herpesvirus 6 (HHV6), etc., to modulate the host immune response mediated by members of the family of multichain immune recognition receptors (MIRRs). Predicted and molecularly explained by the SCHOOL model [7,10,11,12,13], manipulation of MIRR signaling is performed by numerous unrelated viruses throughout their life cycle In this context, the ability viruses have developed over centuries of evolution [13,14] to modulate T cell receptor (TCR) signaling plays a crucial role in viral pathogenesis.
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