What is the Hepatitis A Virus?
Hepatitis A virus, commonly referred to as HAV, is a highly contagious virus that leads to liver diseases.
The history of Hepatitis A virus discovery dates back to the early 20th century. In 1973, Feinstone and colleagues used immune electron microscopy to identify Hepatitis A virus in fecal samples from humans affected with non-B, non-C hepatitis. Following this discovery, Kaplan NM in 1983 cloned the entire genome of HAV, a pivotal discovery that allowed in-depth study of HAV's structure and functions.
Hepatitis A virus is a Picornavirus, making it a part of the Picornaviridae family of viruses. It has a single-stranded RNA genome that is encased in an icosahedral protein shell, known as a capsid. The virus's RNA genome replicates in the cytoplasm of liver cells, leading to the production of new viral particles. This virus doesn't have an envelope, making it resistant to common disinfectants and capable of surviving outside the body for long periods.
Symptoms of Hepatitis A Virus
The symptoms of HAV infection can range from mild to severe, and they usually appear two to six weeks after the person is exposed to the virus. Symptoms include fatigue, sudden nausea, clay-colored bowel movements, loss of appetite, low-grade fever, dark urine, joint pain, and jaundice (yellowing skin and eyes). While these symptoms can be extremely discomforting, most people recover completely with no lasting liver damage.
Proteins within the Hepatitis A Virus and Their Antigenic Potential
The proteins that form the structural and functional units of Hepatitis A virus have clear antigenic potentials. HAV has four distinct capsid proteins: VP1, VP2, VP3, and VP4. The VP1 protein is exposed on the surface of the virion and has areas that can act as antigenic sites, evoking a strong immune response. The immune response to these antigens effectively represents the body's main line of defense against this virus.
The structure of the antigens, especially of the VP1 capsid protein, is pivotal to the body's production of antibodies. VP1 is a large, protruding spike on the virus surface, making it a primary target for antibodies. Its structure allows antibodies to recognize and bind to it, triggering an immune response that can neutralize the virus and prevent it from establishing an infection.
Hepatitis A Virus Antigen-related Signaling Pathways
The immune response to HAV antigens involves crucial signaling pathways. The binding of antibodies to the antigen triggers intracellular signaling, which leads to the activation of immune cells like B cells and interferon-producing cells to hinder viral replication. Furthermore, this binding stimulates the complement system, a group of proteins that enhance the ability of antibodies and phagocytic cells to clear pathogens from an organism. Finally, the cytotoxic T cells, after recognizing the viral antigen, proliferate and cause the death of virus-infected cells.
