Viral MicroRNAs: Interfering the Interferon Signaling.
JAK-STAT
Viruses
immune response
interferons
post-transcriptional silencing
viral microRNA.
Journal
Current pharmaceutical design
ISSN: 1873-4286
Titre abrégé: Curr Pharm Des
Pays: United Arab Emirates
ID NLM: 9602487
Informations de publication
Date de publication:
2020
2020
Historique:
received:
11
10
2019
accepted:
22
12
2019
pubmed:
12
1
2020
medline:
4
11
2020
entrez:
12
1
2020
Statut:
ppublish
Résumé
Interferons are secreted cytokines with potent antiviral, antitumor and immunomodulatory functions. As the first line of defense against viruses, this pathway restricts virus infection and spread. On the contrary, viruses have evolved ingenious strategies to evade host immune responses including the interferon pathway. Multiple families of viruses, in particular, DNA viruses, encode microRNA (miR) that are small, non-protein coding, regulatory RNAs. Virus-derived miRNAs (v-miR) function by targeting host and virus-encoded transcripts and are critical in shaping host-pathogen interaction. The role of v-miRs in viral pathogenesis is emerging as demonstrated by their function in subverting host defense mechanisms and regulating fundamental biological processes such as cell survival, proliferation, modulation of viral life-cycle phase. In this review, we will discuss the role of v-miRs in the suppression of host genes involved in the viral nucleic acid detection, JAK-STAT pathway, and cytokine-mediated antiviral gene activation to favor viral replication and persistence. This information has yielded new insights into our understanding of how v-miRs promote viral evasion of host immunity and likely provide novel antiviral therapeutic targets.
Identifiants
pubmed: 31924149
pii: CPD-EPUB-103587
doi: 10.2174/1381612826666200109181238
pmc: PMC7476571
mid: NIHMS1607081
doi:
Substances chimiques
MicroRNAs
0
RNA, Viral
0
Interferons
9008-11-1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
446-454Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE027980
Pays : United States
Organisme : NIDCR NIH HHS
ID : R03 DE027147
Pays : United States
Organisme : NIDCR NIH HHS
ID : R21 DE026259
Pays : United States
Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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