Hepatitis A Virus P2C Recombinant
Hepatitis A Virus P2C-P3A Recombinant
Hepatitis A Virus P2C-P3B Recombinant
Hepatitis A Virus P3C Recombinant
Hepatitis A Virus VP1-P2A (669-782 a.a.) Recombinant
Hepatitis A Virus VP1-P2A (722-830 a.a.) Recombinant
Hepatitis A Virus VP3 Recombinant
The E.coli derived a recombinant protein contains the VP3 immunodominant regions, having 245 amino acids. HAV VP3 protein is fused to a 6xHis--tag at C-terminus & purified by proprietary chromatographic techniques.
Hepatitis A Virus VP4-VP2 Recombinant
Hepatitis A Virus Cellular Receptor 1 Human Recombinant
Hepatitis A Virus Cellular Receptor 1 Human Recombinant, HEK
Hepatitis A is an acute infectious disease of the liver caused by the hepatitis A virus (HAV), a small, non-enveloped RNA virus classified in the genus Hepatovirus within the family Picornaviridae . Unlike hepatitis B and C, hepatitis A does not cause chronic liver disease but can lead to debilitating symptoms and, in rare cases, fulminant hepatitis (acute liver failure), which can be fatal .
Key Biological Properties: HAV is a small, spherical virus with a diameter of 27-32 nm, containing a single-stranded, positive-sense RNA genome of approximately 7.5 kb . The virus has icosahedral symmetry and lacks an envelope .
Expression Patterns and Tissue Distribution: HAV primarily targets hepatocytes in the liver. The virus attaches to liver cells through an immunoglobulin-like cellular receptor and enters the cell via receptor-mediated endocytosis . Once inside, the viral genome is released into the host’s cytoplasm, leading to hepatocyte damage .
Primary Biological Functions: HAV causes liver inflammation, affecting the liver’s ability to process nutrients, filter blood, and fight infections . The virus is primarily transmitted through the fecal-oral route, often via contaminated food or water .
Role in Immune Responses and Pathogen Recognition: The immune response to HAV involves the activation of lymphocytes, which engulf the viral antigen and release inflammatory mediators. This stimulates B and T cells to attack the viral antigen, leading to the production of specific antibodies against HAV .
Mechanisms with Other Molecules and Cells: HAV interacts with hepatocytes by binding to specific receptors on the cell surface, leading to endocytosis and release of the viral genome into the host cell . The virus then hijacks the host’s cellular machinery to replicate and produce viral proteins .
Binding Partners and Downstream Signaling Cascades: The viral RNA is translated into a single polyprotein, which is cleaved into functional viral proteins by the viral protease . These proteins are involved in viral replication and assembly, leading to the production of new virions .
Regulatory Mechanisms Controlling Expression and Activity: The expression of HAV proteins is regulated by the internal ribosomal entry site (IRES) in the 5’ untranslated region (UTR) of the viral RNA . This allows for cap-independent translation of viral proteins .
Transcriptional Regulation and Post-Translational Modifications: The viral polyprotein undergoes post-translational modifications, including cleavage by the viral protease to produce mature viral proteins . These proteins are essential for viral replication and assembly .
Biomedical Research: HAV is used in research to study viral pathogenesis, immune responses, and the development of antiviral drugs . Animal models, such as nonhuman primates and mice, are instrumental in understanding HAV infection and testing potential therapies .
Diagnostic Tools: Diagnostic tests for HAV include serological assays to detect anti-HAV antibodies and molecular techniques to identify viral RNA . These tools are crucial for diagnosing acute HAV infection and monitoring outbreaks .
Therapeutic Strategies: Vaccination is the most effective strategy for preventing HAV infection . Inactivated HAV vaccines are widely used and provide long-term immunity . Research is ongoing to develop antiviral drugs targeting HAV replication and protein synthesis .
Role Throughout the Life Cycle: HAV infection typically occurs in childhood in regions with poor sanitation, leading to asymptomatic or mild illness . In developed countries, infection often occurs in adolescents and adults, causing more severe symptoms . The virus induces lifelong immunity, preventing reinfection .
From Development to Aging and Disease: HAV does not cause chronic infection, but acute infection can lead to significant morbidity, especially in older adults and individuals with underlying health conditions . Vaccination programs have significantly reduced the incidence of HAV infection in many regions .