P0533
THE EFFICACY OF ZINC FINGER ANTIVIRAL PROTEIN AGAINST
HEPATITIS B VIRUS TRANSCRIPTION AND REPLICATION IN
TRANSGENIC MOUSE MODEL
E.-Q. Chen1,2, H. Tang1,2, J. Dai1,2, L. Bai1,2. 1Center of Infectious
Diseases, West China Hospital of Sichuan University, 2Division of
Infectious Diseases, State Key Laboratory of Biotherapy, Sichuan
University, Chengdu, China
E-mail: [email protected]
Background and Aims: The zinc finger antiviral protein (ZAP) is
a mammalian host restriction factor, and it could inhibit HBV RNA
synthesis in vitro experiments. However, the role of ZAP against
HBV in vivo environment is unclear. This study aimed to investigate
whether ZAP could act against HBV transcription and replication in
ZAP tansgenic mouse model.
Methods: HBV-replication-competent plasmid pHBV4.1 was
transferred to ZAP transgenic ICR mice via the tail vein, using
a hydrodynamic in vivo transfection procedure. HBV RNA and
HBVDNA replication intermediates in the liver were respectively
analyzed by Northern blotting and Southern blotting. The
expression of hepatitis B surface antigen (HBsAg) and hepatitis B
core antigen (HBcAg) in the liver tissue was detected by
immunohistochemical staining.
Results: As compared to control ICR mouse, the level of HBVRNA
in ZAP transgenic mouse liver tissue was only decreased by 8.4%;
while the level of HBVDNA replication intermediates was decreased
by 82%. In addition, the expression levels of HBsAg and HBcAg in
ZAP transgenic mouse liver were both significantly less than that
of control ICR mouse.
Conclusions: Our findings suggest that ZAP could inhibit HBV
replication in vivo in mice, which offers a new target for anti-HBV
drug development.