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Interplay between Inflammation and Cellular Stress Triggered by Flaviviridae Viruses
Ana L C Valadão1, Renato S Aguiar1, Luciana B de Arruda2
1Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro Rio de Janeiro, Brazil.
Frontiers in Microbiology
|September 10, 2016
Summary
Flaviviruses trigger cellular stress and inflammation by replicating RNA. This review explores how these viruses evade immune detection by manipulating stress sensors and inflammatory pathways.
Area of Science:
- Virology
- Immunology
- Cellular Biology
Background:
- Flaviviridae viruses, including Dengue and Zika, are significant human pathogens.
- Viral replication occurs in the endoplasmic reticulum and Golgi complex, producing abundant viral components.
- Viral RNA is detected by cellular sensors like TLRs, RIG-I, MDA5, and PKR, initiating immune responses.
Purpose of the Study:
- To review recent findings on the interplay between inflammatory pathways and cellular stress sensors.
- To elucidate Flaviviridae strategies for evading host immune responses.
Main Methods:
- Literature review of recent scientific findings.
- Analysis of molecular mechanisms of viral replication and host-pathogen interactions.
Main Results:
- Flavivirus replication induces cellular stress responses, including oxidative stress and unfolded protein response.
- Viral RNA sensing triggers inflammatory mediators and interferons.
- Flaviviruses employ strategies to counteract cellular defense mechanisms.
Conclusions:
- Understanding the connection between inflammation and cellular stress is crucial for combating Flaviviridae infections.
- Flaviviruses actively manipulate host pathways to ensure their survival and propagation.
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