Abstract
The Flaviviridae family comprises several human pathogens, including Dengue, Zika, Yellow Fever, West Nile, Japanese Encephalitis viruses, and Hepatitis C Virus. Those are enveloped, single-stranded positive sense RNA viruses, which replicate mostly in intracellular compartments associated to endoplasmic reticulum (ER) and Golgi complex. Virus replication results in abundant viral RNAs and proteins, which are recognized by cellular mechanisms evolved to prevent virus infection, resulting in inflammation and stress responses. Virus RNA molecules are sensed by Toll-like receptors (TLRs), RIG-I-like receptors (RIG-I and MDA5) and RNA-dependent protein kinases (PKR), inducing the production of inflammatory mediators and interferons. Simultaneously, the synthesis of virus RNA and proteins are distinguished in different compartments such as mitochondria, ER and cytoplasmic granules, triggering intracellular stress pathways, including oxidative stress, unfolded protein response pathway, and stress granules assembly. Here, we review the new findings that connect the inflammatory pathways to cellular stress sensors and the strategies of Flaviviridae members to counteract these cellular mechanisms and escape immune response.
Highlights
FLAVIVIRUS REPLICATIONThe Flaviviridae family includes several important human pathogens such as Dengue Virus (DENV), Zika Virus (ZIKV), Yellow Fever Virus (YFV), West Nile Virus (WNV), Japanese Encephalitis Virus (JEV), St
Reviewed by: Takashi Irie, Hiroshima University, Japan Sandra Laurence Lopez-Verges, Instituto Conmemorativo Gorgas de Estudios de la Salud, Panama
This polyprotein is targeted to the endoplasmic reticulum (ER), where it is processed by virus and Stress and Inflammation Induced by Flaviviruses host’s encoded proteases to form the structural proteins and non-structural proteins (NS), which participate in replication, polyprotein processing and virion assembly
Summary
The Flaviviridae family includes several important human pathogens such as Dengue Virus (DENV), Zika Virus (ZIKV), Yellow Fever Virus (YFV), West Nile Virus (WNV), Japanese Encephalitis Virus (JEV), St. The first interaction of Flavivirus with its host cell occurs via several putative receptors (Mukhopadhyay et al, 2005) They play an important role in capturing and concentrating infectious virions, leading to a cascade of events that culminates in the virus and cell membranes fusion. Stress responses triggered by virus infection may occur at multiple levels and include the ER associated stress, mitochondria stress (oxidative stress) and cytoplasmic stress [stress granules (SGs)] (Buchan and Parker, 2009; Montero and Trujillo-Alonso, 2011; Valiente-Echeverría et al, 2012; Zhang and Wang, 2012; Reshi et al, 2014; Gullberg et al, 2015) All these responses may be triggered by host cell sensing of incoming virus macromolecules, including genome RNA, double-stranded RNA intermediates, and proteins. This review will focus on the cellular stress responses triggered by flavivirus and HCV replication, addressing the connection between those responses with virus sensing and inflammation, and discussing the virus strategies to counteract these pathways
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