HAV Specific Neutra™ Antibody Products

Hepatitis A virus (HAV) is a non-enveloped RNA virus belonging to the Picornaviridae family, within the Heptavirus genus. There are two types of HAV particles: quasi-enveloped virions with a lipid membrane found in blood and culture supernatants, and naked virions, which lose their membrane due to bile acids before excretion in feces. It features a genome that is roughly 7.5 kb long with a single ORF. HAV is classified into several genotypes, but only one serotype. The virus primarily causes acute liver disease. Symptoms of HAV infection include fatigue, jaundice, elevated liver enzymes, and abdominal pain. While most cases resolve without complications, HAV can cause severe illness in some individuals.

HAV Transmission Routes of HAV and Epidemiology

HAV is primarily transmitted by the fecal-oral route, often via consuming contaminated food, water, or coming into close touch with an infected individual. HAV exhibits strong resistance to extreme physical conditions, including high temperatures, acidic environments, and freezing for hours or even months. Risk factors include poor sanitation, unclean drinking water, and travel to areas with high HAV prevalence. Children, travelers, and individuals in close-contact settings are particularly vulnerable. The virus is widespread, with greater frequencies in areas with low or middle incomes. Outbreaks often occur in communities with poor hygiene or during natural disasters.

Replication Cycle of HAV

HAV enters host cells via receptor-mediated endocytosis. Once inside, the virus uncoats, releasing its RNA genome into the cytoplasm. The RNA is translated into a single polyprotein, which is processed into functional viral proteins. The viral RNA replicates in the cytoplasm, and new virions are generated in the endoplasmic reticulum. These new viral particles are transported to the cell surface and released, often through exocytosis, to infect neighboring cells.

Fig. 1 HAV replication cycle.^1,3

Pathogenesis of HAV

HAV primarily infects liver cells, causing inflammation. After ingestion, the virus reaches the circulation and replicates in the liver. HAV is responsible for approximately 40% of all cases of acute viral hepatitis. Immune responses lead to liver cell damage. Hepatocellular injury and the destruction of infected hepatocytes are driven by HAV-specific CD8+ T lymphocytes and natural killer cells, which are restricted by human leukocyte antigens. An exaggerated immune response, indicated by a significant decrease in circulating HAV RNA during acute infection, is linked to severe hepatitis. The liver's ability to regenerate usually leads to recovery, but in rare cases, severe liver failure can occur.

Fig. 2 Proposed mechanisms of liver injury mediated by HAV.^2,3

Anti-HAV Neutralizing Antibodies

Antibodies targeting HAV, including neutralizing antibodies, play a crucial role in preventing and treating infection. These antibodies bind to viral epitopes on the HAV capsid, blocking the virus from entering host cells and neutralizing its infectivity. Neutralizing antibodies can be used for passive immunization, providing immediate protection, especially for individuals exposed to the virus. Research examples include monoclonal antibodies developed for therapeutic research, which have shown promise in inhibiting HAV replication in vitro. Additionally, anti-HAV antibodies are commonly used in diagnostic tests to detect past infections or immunity.

Fig. 3 HAV specific diagnosis based on antibody detection and other methods.^1,3

Creative Biolabs possesses an experienced team of experts, combined with our advanced antibody platform, can provide a wide range of high-quality anti-HAV neutralizing antibodies tailored to meet your specific research needs.

REFERENCES

1. Gholizadeh, Omid, et al. "Hepatitis A: viral structure, classification, life cycle, clinical symptoms, diagnosis error, and vaccination." Canadian Journal of Infectious Diseases and Medical Microbiology 2023.1 (2023): 4263309.
2. Wang, Minghang, and Zongdi Feng. "Mechanisms of hepatocellular injury in hepatitis A." Viruses 13.5 (2021): 861.
3. Distributed under Open Access license CC BY 4.0, without modification.