Open AccessDOCK11 and DENND2A play pivotal roles in the maintenance of hepatitis B virus in host cells
Author(s) -
Shinichi Hashimoto,
Takayoshi Shirasaki,
Taro Yamashita,
Sadahiro Iwabuchi,
Yutaka Suzuki,
Yuzuru Takamura,
Yoshiaki Ukita,
Shungo Deshimaru,
Toshitugu Okayama,
Kazuho Ikeo,
Kazuyuki Kuroki,
Kazunori Kawaguchi,
Eishiro Mizukoshi,
Kouji Matsushima,
Masao Honda
Publication year - 2021
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0246313
Subject(s) - hepatitis b virus , gene knockdown , virology , biology , gene , cccdna , virus , rna , dna virus , hepatitis b , rna interference , dna , genome , genetics , hbsag
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.