HBV Specific Neutra™ Antibody Products

Hepatitis B virus (HBV) is a hepatotropic DNA virus causing acute and chronic liver disease. It belongs to the Hepadnaviridae family. HBV exhibits various serotypes and genotypes, influencing disease progression and treatment response. It's a major cause of cirrhosis and hepatocellular carcinoma globally. Transmission occurs through blood, bodily fluids, and perinatal routes. Symptoms range from asymptomatic to acute hepatitis with jaundice, fatigue, and abdominal pain. Chronic infection can lead to severe liver damage. HBV remains a significant public health burden worldwide.

Structure and Genome

HBV is an enveloped virus with an icosahedral nucleocapsid. Its genome is a partially double-stranded circular DNA molecule, approximately 3.2 kilobases in length. The genome encodes four overlapping open reading frames (ORFs): S, C, P, and X. The S ORF encodes the surface antigens (HBsAg), the C ORF encodes the core antigen (HBcAg) and the e antigen (HBeAg), the P ORF encodes the polymerase, and the X ORF encodes the X protein (HBx). The viral DNA is packaged within the nucleocapsid along with the polymerase.

Fig. 1 The structure of the HBV.^{1, 4}

HBV Life Cycle

HBV infection begins with the virus attaching to hepatocytes via the sodium taurocholate cotransporting polypeptide (NTCP) receptor. Following entry, the nucleocapsid is transported to the nucleus, where the partially double-stranded DNA is converted into covalently closed circular DNA (cccDNA). The cccDNA serves as the template for viral mRNA transcription. Viral mRNAs are translated into viral proteins. The viral polymerase reverse transcribes pregenomic RNA into new DNA genomes. Nucleocapsids are assembled, encapsidating the DNA and polymerase. Enveloped virions are then released from the cell via exocytosis. The persistent cccDNA reservoir in the hepatocyte nucleus is a major obstacle to complete viral eradication.

Fig. 2 The life cycle of HBV.^{2, 4}

HBV Infection Mechanism

HBV primarily interferes with the functions of the liver by replicating in hepatocytes. HBV infection initiates an adaptive immune response, predominantly driven by cytotoxic T lymphocytes (CTLs). CTLs play a dual role, causing hepatocellular damage while also clearing the virus. They eliminate infected cells directly and release antiviral cytokines, which purge HBV from surviving hepatocytes. Though vital for viral clearance, CTL activity induces liver injury. Non-antigen-specific inflammatory cells amplify this CTL-mediated immunopathology, exacerbating the damage. Furthermore, activated platelets at the infection site facilitate CTL accumulation within the liver, intensifying the immune response and contributing to the extent of liver damage. Thus, the immune response, while essential for viral control, is also the primary driver of HBV-related liver pathology.

Anti-HBV Neutralizing Antibodies

Antibodies targeting the HBV surface antigen (anti-HBs) are essential for protective immunity. Vaccination induces anti-HBs antibodies, preventing infection. Antibodies against the core antigen (anti-HBc) indicate past or current infection. Anti-HBe antibodies may appear after the clearance of HBeAg, often signifying a less active phase of infection. Monoclonal antibodies targeting HBsAg are being developed for therapeutic use, aiming to block viral entry and spread. Passive immunization with anti-HBs immunoglobulin is used for post-exposure prophylaxis, providing immediate protection. Understanding these antibody responses is crucial for the diagnosis, prevention, and treatment of HBV infection.

Fig. 3 Multiple pathways mediated by anti-HB antibodies against HBV infection.^{3, 4}

Creative Biolabs provides high-quality anti-HBV neutralizing antibody products for a variety of applications, including FC, IF, ICC, ELISA, Neut, etc., to help advance research, diagnostics, and therapeutic development in hepatitis B studies.

REFERENCES

1. Abu, Norhidayah, Noremylia Mohd Bakhori, and Rafidah Hanim Shueb. "Lateral flow assay for hepatitis B detection: a review of current and new assays." Micromachines 14.6 (2023): 1239.
2. Diogo Dias, João, Nazim Sarica, and Christine Neuveut. "Early steps of hepatitis B life cycle: from capsid nuclear import to cccDNA formation." Viruses 13.5 (2021): 757.
3. Cai, Ying, and Wenwei Yin. "The multiple functions of B cells in chronic HBV infection." Frontiers in immunology 11 (2020): 582292.
4. Distributed under Open Access license CC BY 4.0, without modification.