Abstract:
:The induction of hundreds of Interferon Stimulated Genes (ISGs) subsequent to virus infection generates an antiviral state that functions to restrict virus growth at multiple steps of their replication cycles. In the context of Human Immunodeficiency Virus-1 (HIV-1), ISGs also possess antiviral functions, but some ISGs show proapoptotic or proviral activity. One of the most studied ISGs, the RNA activated Protein Kinase (PKR), shuts down the viral protein synthesis upon activation. HIV-1 has evolved to evade its inhibition by PKR through viral and cellular mechanisms. One of the cellular mechanisms is the induction of another ISG, the Adenosine Deaminase acting on RNA 1 (ADAR1). ADAR1 promotes viral replication by acting as an RNA sensing inhibitor, by editing viral RNA and by inhibiting PKR. This review challenges the orthodox dogma of ISGs as antiviral proteins, by demonstrating that two ISGs have opposing and clashing effects on viral replication.
journal_name
Cytokine Growth Factor Revjournal_title
Cytokine & growth factor reviewsauthors
Radetskyy R,Daher A,Gatignol Adoi
10.1016/j.cytogfr.2018.03.007subject
Has Abstractpub_date
2018-04-01 00:00:00pages
48-58eissn
1359-6101issn
1879-0305pii
S1359-6101(18)30032-7journal_volume
40pub_type
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journal_title:Cytokine & growth factor reviews
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