Human HBcAg ELISA Kit

Hepatitis B virus (HBV) is an encapsulated double-stranded DNA virus from the Hepadnaviridae family with a significant diversity. To date, ten genotypes (A-J) have been identified. The HBV genome is about 3.2 kb in size and encodes four key proteins: surface antigen (HBsAg), HBV polymerase, core antigen (HBcAg), and e antigen (HBeAg). Among these, the HBcAg is the primary structural protein of the viral nucleocapsid, surrounding the partially double-stranded DNA genome within the viral particle. HBcAg plays a crucial role in viral replication and the lifecycle, making it a key target for antiviral research. In the cytoplasm, HBcAg assembles into nucleocapsids composed of 180 or 240 monomers, which encapsulate the viral pregenomic RNA (pgRNA). After the viral genome matures, the nucleocapsid migrates to the endoplasmic reticulum (ER), where it interacts with viral envelope proteins, eventually forming complete viral particles. Mature nucleocapsids can also re-enter the nucleus, where they disassemble into individual HBcAg molecules through the nuclear pore complex, releasing the viral genome into the nucleus. This recycling mechanism helps maintain the quantity of viral genomes within the nucleus and regulates sustained viral replication. Nuclear HBcAg also acts as a transcriptional repressor of the interferon (IFN)-induced antiviral protein MxA, thereby partially resisting the host's immune response. Due to its complex role in the viral lifecycle, the nucleocapsid has become a focal point in the development of new antiviral drugs targeting HBV.

Currently, around 300 million people worldwide are living with chronic hepatitis B, with 1.5 million new infections occurring annually. More than 800,000 people die each year from HBV-related complications. Sexual contact and unsafe injections remain the primary routes of transmission. As HBV infection often presents no obvious symptoms in its early stages, many patients are diagnosed only after the disease has progressed significantly. Without timely treatment, 30-40% of chronic hepatitis B patients may develop cirrhosis or hepatocellular carcinoma (HCC). Additionally, co-infection with human immunodeficiency virus (HIV) is common due to similar transmission routes. HDV (Hepatitis D virus), which relies on HBsAg for replication, typically infects humans in a co-infection or superinfection form with HBV. These co-infections often result in more severe disease outcomes and complicate treatment strategies.

Although the hepatitis B vaccine has been in use for over 40 years and can be administered during the neonatal period, approximately 15% of newborns worldwide are still not covered by vaccination. Moreover, as time passes, the efficacy of the vaccine-induced antibodies may gradually wane, and escape mutants have emerged, meaning that acute infections may still occur even after vaccination. HBV can persist in the host's liver for an extended period, and current treatment options primarily rely on lifelong antiviral therapy. The preferred drugs include nucleoside analogs such as entecavir and tenofovir, as well as pegylated interferon-alpha (PEG-IFNα), to achieve sustained viral suppression. However, issues such as low vaccine efficacy, viral rebound after discontinuing medication, and inevitable drug resistance highlight the urgent need to develop new gene therapies that can completely eliminate HBV and cure hepatitis B.

Human Hepatitis B Core Antigen ELISA Kit
Human HBc ELISA Kit
HBV Core Antigen ELISA Kit