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7-DMA inhibits Zika virus replication in hepatocyte-like cells of stem cell origin


Zika virus (ZIKV) infection has been a major healthcare concern due to its recent outbreaks in South and Central America, Asia, Africa and the Pacific Islands. Although the ZIKV infection often presents with mild or no symptoms, it can trigger more serious conditions such as Guillain-Barré syndrome. It also poses risk for pregnant women because of the close link between Zika infection and microcephaly in newborns.

ZIKV is a single-stranded RNA virus of the Flaviviridae family transmitted by mosquito species Aedes aegypti and Aedes albopictus. Given its resemblance to other hepatocyte-infecting flaviviruses, a recent study explored ZIKV infection of human hepatocyte-like cell lines and effectiveness of antiviral drugs.

In vitro experiments were performed on hepatocyte-like cells of tumoral (Huh7) and stem cell origin (hPSC-HLCs) with ZIKV strains of African (ZIKV MR766) and Asian (ZIKV PRVABC59) lineage. The study demonstrated that both cell lines support complete ZIKV life cycle.

Three viral RNA polymerase inhibitors were tested for antiviral activity on ZIKV-infected hepatocyte-like cells. Polymerase inhibitors 7-deaza-2’-C-methyladenosine (7-DMA) and 2’-C-methylcytidine (2’CMC) from Carbosynth were used with favipiravir, an experimental broad-spectrum antiviral drug for RNA virus infections.

7-DMA inhibited viral replication of the African and the Asian ZIKV strain in both cell lines in a dose-dependent manner. However, ZIKV replication was inhibited but not completely blocked even at the highest 7-DMA concentration tested. Antivirals 2’CMC and favipiravir inhibited ZIKV replication only in Huh7 cells but were ineffective in hPSC-HLC cell line.


For more details, read the original paper published in Plos One: Tricot et al., 2018.


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