Varicella zoster Virus Antibodies, IgG, Serum

Varicella-zoster virus (VZV), a double stranded DNA virus, is a ubiquitous aα-herpesvirus whose only known reservoir is man. Primary infection causes a diffuse cutaneous rash accompanied by viraemia. After primary infection, VZV establishes latency in sensory ganglia and can cause herpes zoster upon reactivation. Primary VZV infection begins with respiratory mucosal inoculation and the characteristic chickenpox rash develops after an incubation period of 10 to 21 days. In temperate climates, almost all children usually acquire varicella during the first 5 to 10 years of life. Second episodes of varicella infection are rare. Herpes zoster occurs only in individuals who have had primary VZV infection with most cases occurring at an age of more than 45 years old. Herpes zoster is common in patients treated with immunosuppressive drugs for malignant diseases, or to prevent rejection of bone marrow or organ transplants and in individuals with HIV infection. In childhood, risk factors for herpes zoster include varicella acquired during the first year of life and VZV infection in utero as a result of maternal varicella during gestation.

Primary VZV infection elicits IgG, IgM, and IgA antibodies that have neutralising effects on the virus. However, the role of humoral immunity in controlling primary VZV infection appears to be limited. Antibody production is usually detectable within 3 days after the onset of symptoms in healthy subjects. IgG antibodies to many viral proteins persist for years after primary VZV infection as part of the long-term immune response to VZV and may help to protect against re-infection by neutralising any infectious virus at mucosal sites of inoculation. The presence of VZV IgG antibodies indicates recent or past infection.

1 ml Serum Stability: 14 Days at 2-8 °C

Negative <50miu>