Abstract
In order to thrive, viruses have evolved to manipulate host cell machinery for their own benefit. One major obstacle faced by pathogens is the immunological synapse. To enable efficient replication and latency in immune cells, viruses have developed a range of strategies to manipulate cellular processes involved in immunological synapse formation to evade immune detection and control T‐cell activation.In vitro, viruses such as human immunodeficiency virus 1 and human T‐lymphotropic virus type 1 utilise structures known as virological synapses to aid transmission of viral particles from cell to cell in a process termed trans‐infection. The formation of the virological synapse provides a gateway for virus to be transferred between cells avoiding the extracellular space, preventing antibody neutralisation or recognition by complement.This review looks at how viruses are able to subvert intracellular signalling to modulate immune function to their advantage and explores the role synapse formation has in viral persistence and cell‐to‐cell transmission.
Highlights
The adaptive immune response is essential for the control of pathogen invasion and is regulated by co-ordinated communication between immune cells
Viruses such as Human Immunodeficiency Virus (HIV)-1 and HTLV-1 utilise structures known as virological synapses to aid transmission of viral particles from cell-to-cell in a process termed trans-infection
This review looks at how viruses are able to subvert intracellular signalling to modulate immune function to their advantage and explores the role synapse formation has in viral persistence and cell-cell transmission
Summary
The adaptive immune response is essential for the control of pathogen invasion and is regulated by co-ordinated communication between immune cells. T-lymphotropic viruses are able to strike a balance between subversion of intracellular signalling and trafficking to impair IS formation and T-cell activation, whilst still allowing sufficient T-cell activation to maintain viral replication Viruses such as retroviruses, herpesviruses and paramyxoviruses have developed specific mechanisms to alter TCR regulated pathways resulting in inhibition of IS formation and immune detection, whilst promoting viral replication and release of progeny virus. These two requirements have evolved into controlled modulation of components of the IS and downstream T-cell activation Viruses such as those mentioned strike this perfect balance, increasing T-cell activation at low levels to aid infection and replication whilst prevent TCR signalling and complete T-cell activation, to prevent over expression of viral proteins and apoptosis of the host cell
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