In summary, our study suggests that HBV precore protein, specifically the p22 form, impedes JAK-STAT signaling to help the virus evade the host innate immune response and, thus, causes resistance to IFN therapy.<b>IMPORTANCE</b> Chronic hepatitis B virus (HBV) infection continues to be a major global health concern, and patients who fail to mount an efficient immune response to clear the virus will develop a life-long chronic infection that can progress to chronic active hepatitis, cirrhosis, and primary hepatocellular carcinoma.
For targeted delivery, hepatocellular carcinoma (HCC)-targeting peptide (SP94, SFSIIHTPILPL) is synthesized and chemically conjugated to the exterior surface of the P22 viral capsid nanocomposites.