Research for innate immune system sensor molecules in HBV infection
Description: In acute HBV infection phase, it takes time for the virus to grow and liver damage to appear, but the nucleic acid recognition for HBV-DNA and mechanism of innate immunity during that period are not well understood. In chronic HBV infection, immunologically tolerated state is established, and complete elimination of the virus is difficult because HBV covalently closed circular DNA (cccDNA) remains in the nucleus for life. Based on the above,the purpose of this study was to investigate the role of intracellular DNA sensor molecules in HBV infection, the effect on HBV-DNA replication, and the immune response. Focusing on various DNA sensor molecules, especially DDX41, we analyzed the expression in various hepatocyte cell lines, In NTCP-C4-HepG2 cells in which DDX41 was constitutively knocked down, HBV-DNA and RNA increased in an early stage compared with the control. This results suggested that DDX41 suppresses HBV proliferation in hepatocytes.
Amount: ¥3,900,000
Funding type: fellowship
Funder scheme: Grant-in-Aid for Young Scientists (B)
Start date: 2016-04-01
End date: 2020-03-31
Investigator: MASATO NAKAI
Institution: Hokkaido University
Topic: Hepatitis B Virus Studies
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Funded outputs count: 10
Funder award ID: 16K19324
OpenAlex ID: G3761440259