DOCK11 and DENND2A play pivotal roles in the maintenance of hepatitis B virus in host cells.
Shinichi HashimotoTakayoshi ShirasakiTaro YamashitaSadahiro IwabuchiYutaka SuzukiYuzuru TakamuraYoshiaki UkitaShungo DeshimaruToshitugu OkayamaKazuho IkeoKazuyuki KurokiKazunori KawaguchiEishiro MizukoshiKouji MatsushimaShuichi KanekoShuichi KanekoPublished in: PloS one (2021)
Human hepatitis B virus (HBV) infection remains a serious health problem worldwide. However, the mechanism for the maintenance of HBV in a latent state within host cells remains unclear. Here, using single-cell RNA sequencing analysis, we identified four genes linked to the maintenance of HBV in a liver cell line expressing HBV RNA at a low frequency. These genes included DOCK11 and DENND2A, which encode small GTPase regulators. In primary human hepatocytes infected with HBV, knockdown of these two genes decreased the amount of both HBV DNA and covalently closed circular DNA to below the limit of detection. Our findings reveal a role for DOCK11 and DENND2A in the maintenance of HBV.
Keyphrases
- hepatitis b virus
- single cell
- liver failure
- endothelial cells
- induced apoptosis
- genome wide
- healthcare
- cell cycle arrest
- single molecule
- rna seq
- cell free
- oxidative stress
- high throughput
- transcription factor
- mental health
- genome wide identification
- cell proliferation
- induced pluripotent stem cells
- bioinformatics analysis
- gene expression
- pluripotent stem cells
- nucleic acid
- human health
- real time pcr