Abstract

Zika virus (ZIKV) still constitutes a public health concern, however, no vaccines or therapies are currently approved for treatment. A fundamental process involved in ZIKV infection is autophagy, a cellular catabolic pathway delivering cytoplasmic cargo to the lysosome for degradation—considered as a primordial form of innate immunity against invading microorganisms. ZIKV is thought to inhibit the Akt-mTOR signaling pathway, which causes aberrant activation of autophagy promoting viral replication and propagation. It is therefore appealing to study the role of autophagic molecular effectors during viral infection to identify potential targets for anti-ZIKV therapeutic intervention.

Highlights

  • Zika virus (ZIKV) is an arthropod-borne virus, member of the Flaviviridae family, first isolated in 1947 from a febrile rhesus macaque monkey in the Zika Forest (Uganda)

  • Inhibition of autophagy by the depletion of essential autophagy autophagy-related proteins (Atgs) proteins, namely Atg5 and Atg7, is not associated to an alteration of West Nile virus (WNV) replication in infected cells suggesting that a functional autophagy pathway is not required for WNV infectious particle production [10,45,46]. Taken together these findings indicate that the involvement of autophagy in WNV infection remains controversial, and further investigations are required to unravel the role of this pathway in WNV pathogenesis

  • There is the necessity to unravel ZIKV biology and the mechanisms involved in virus–host cell attention

Read more

Summary

Introduction

Zika virus (ZIKV) is an arthropod-borne virus (arbovirus), member of the Flaviviridae family, first isolated in 1947 from a febrile rhesus macaque monkey in the Zika Forest (Uganda). Symptomatic ZIKV infections have always been limited to small clusters of patients and to sporadic cases causing localized outbreaks throughout Africa, Asia, and Oceania This emerging arbovirus infection reached a global scale of diffusion since its arrival in the Americas in 2015, devastating in the northeastern territories of Brazil. ZIKV, a 50 nm enveloped and icosahedral particle with an 11 kb positive-strand RNA genome, is typically transmitted by bites from infected Aedes genus mosquitoes, in addition to mother-to-child. Sci. 2019, ZIKV, a 50 20, nm1048 enveloped and icosahedral particle with an 11 kb positive‐strand RNA genome, is typically transmitted by bites from infected Aedes genus mosquitoes, in addition to mother‐to‐child transmission, blood transfusion, sexual contact, and organ transplantation [2]. Previous findings strongly suggest that a greater insight and description of the effectors participating in these cellular processes might be required for highlighting potential molecules to be used as possible therapeutic targets, and to design compounds able to modulate the activity of autophagy in ZIKV-infected cells [8,10]

Autophagy
Regulation of Autophagic Flux
Flavivirus Infection and Autophagy
Deregulation of endosomes autophagy during
ZIKV Infection and Autophagy
Therapy Development and Approaches to Counteract ZIKV Infection
Conclusions
1.References
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.