【Animal Modeling】-Animal Model of Hepatitis Vaccine and Antiviral Therapy

  Experimental cell lines for studying human hepatitis B (HBV) or hepatitis C (HCV) virus infection have been developed, but these cell lines do not support the entire life cycle of these viruses.

  These limitations on existing cell lines have left a gap in understanding the etiology of virus invasion, replication, assembly, and hepatitis B/C virus co-infection. Currently, cell lines derived from human liver tumors show hepatitis B and C infections and disease progression similar to normal liver cells, and hepatitis vaccines and antiviral treatment models have been developed, which may be the method.

  Haizhen Zhu et al. isolated hepatocellular carcinoma cells from liver tumors in males with chronic hepatitis C, and screened cell lines that may support the entire life cycle of hepatitis B and C viruses. One of the cell lines, called HLCZ01, has been inoculated with laboratory and clinical hepatitis B and C virus strains and subsequently infected. The authors found that these infected HLCZ01 cultures produced viral proteins and completely produced hepatitis B and C virus particles similar to normal human hepatocytes, and that these viruses were natural cells, and it was reported that the culture was successfully infected. These results indicate that the HLCZ01 cell line can support the entire life cycle of these viruses. The addition of antibodies prevented the culture of HLCZ01 cells infected with hepatitis B and C viruses, indicating that this infection pattern is similar to normal liver cells. When the hepatitis B and C viruses co-infect HLCZ01, the authors observed that due to the presence of other viruses, these viruses would not prevent the infection.

  The authors found that due to the similarity between HLCZ01 infection and normal hepatocyte infection and the ability of HLCZ01 to infect various clinical hepatitis B and C isolates, HLCZ01 is very promising in the development of vaccines and antiviral therapies. Be a good candidate.