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Mouse Anti-Hepatitis A Virus VP3 Antibody (1881)

$334.80 excl. VAT

Mouse monoclonal antibody specific for Hepatitis A virus VP3 (1881).

MOUSE ANTI-HEPATITIS A VIRUS VP3 ANTIBODY (1881)

Mouse anti Hepatitis A virus VP3 antibody recognises the capsid polypeptide VP3 antigen of hepatitis A virus. The antibody reacts with a neutralising epitope on the VP3 antigen. Mouse anti Hepatitis A virus VP3 antibody is suitable for immunoassay research and development.

 

PRODUCT DETAILS – MOUSE ANTI-HEPATITIS A VIRUS VP3 ANTIBODY (1881)

  • Mouse anti-Hepatitis A virus VP3 monoclonal IgG1 antibody (clone 1881).
  • Greater than 90% purity by SDS-PAGE and buffered in PBS, pH7.2.

 

BACKGROUND

Hepatitis A virus (HAV) is a non-enveloped, positive-sense, single stranded RNA virus that is a member of the Hepatovirus genus of the family Picornaviridae. One serotype and six genotypes, I to VI, of HAV have been defined. Genotypes I, II and III are known to infect humans and are further divided into subtypes A and B. Infection with any subtype provides an individual with lifelong immunity against all HAV subtypes affecting humans. Humans are a natural reservoir for hepatitis A virus. Transmission of HAV occurs primarily via the oral-faecal route through ingestion of HAV contaminated food and water or through direct contact with an individual infected with HAV. In developing countries, Hepatitis A virus infection commonly occurs in children and is associated with poor sanitation and low socio-economic status. In developed countries, cases of HAV infection may occur in young adults that are in high-risk groups such as care workers, people who inject drugs and individuals travelling from HAV endemic countries.

HAV is thermostable and resistant to treatment with acids, ether and disinfectants. The hepatitis A virus infects the liver and replicates in hepatocytes, causing liver inflammation. During the incubation stage of HAV infection, the infected individual may be asymptomatic, but virus particles are actively shed and can be present in the patient’s stools. A range of non-specific clinical symptoms may then develop, which include nausea, vomiting, joint pain, malaise, fatigue and fever. Additional symptoms that can occur include cough, pharyngitis, itchiness and hives. As the infection develops, the patient becomes jaundiced and, in some cases, hepatomegaly occurs. The mortality rate associated with HAV infection is low, but complications can lead to acute liver failure and death in a small percentage of cases. Although effective vaccines for the prevention of HAV infection are available there is currently no specific treatment for patients infected with HAV (WHO).

 

REFERENCES

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