What is it about?
This paper reveals how rabies virus is able infect and replicate in cells that have been placed in an antiviral state by the host immune system. This is a critical process in the spread of a virus through an infected animal, and so is essential to disease, providing important potential targets for the development of vaccines or antivirals.
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Why is it important?
The findings show that rabies virus targets a cellular immune protein called STAT1, and that this enables the virus to progressively turn off the antiviral system established in host cells. In this way the virus can overwhelm established defences and spread through the host. By preventing this targeting, we can prevent viral deactivation of the antiviral state as a method to combat infection.
Perspectives
This work provided the first evidence that viral targeting of an activated ('phosphorylated') form of the host immune protein STAT1 is a mechanism to turn off the antiviral state in cells already protected by an immune response. This identified a new mechanism in infection and disease, enhancing understanding of how viruses function and their relationship to the host, as well as supporting the importance of this process for potential vaccine/therapeutic approaches.
Gregory Moseley
Monash University
Read the Original
This page is a summary of: Deactivation of the antiviral state by rabies virus through targeting and accumulation of persistently phosphorylated STAT1, PLoS Pathogens, May 2022, PLOS,
DOI: 10.1371/journal.ppat.1010533.
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