Available kits: TOX-IgM/IgG, Anti-CMV IgM/IgG, RuV-IgM/IgG, HSV-I-IgM/IgG, HSV-II-IgM/IgG
Introduction
Anti-CMV IgM ELISA
The Loncare anti-CMV IgM ELISA is intended for the qualitative determination of IgM antibodies to cytomegalovirus in human serum or plasma specimens (EDTA, heparin or sodium citrate).
Human cytomegalovirus (CMV) is a member of the Herpesviridae family and is one of the seven human herpesviruses pathogenic for man. It is ubiquitous, species-specific and is spread by close human contact. The viral capsid, which has a DNA core, is icosahedral in shape and is formed of 162 capsomers. Surrounding the capsid, is one or more oval membranes containing lipids. CMV infection can be primary or secondary. Primary infection may be acquired through different transmission routes and in different periods of life (i.e., congenital and post-natal infections). Following primary infection, CMV enters a latency phase during which the virus can be found in B lymphocytes. Subsequent reactivation of viral replication (secondaryinfection) may take place concomitantly with changes in the relationship between host and virus, such as pregnancy, serious illness, immunosuppressive therapy or stress.
Congenital infection is transmitted transplacentally or at birth and can occur even if pregnant women already present antibodies to CMV (reinfection with exogenous virus), unlike rubella or toxoplasmosis. If seronegative women contract primary CMV infection during pregnancy, sequelae may be abortion, stillbirth or neonatal malformation. This is the case even if the birth of a normal, seronegative child is possible in almost 50% of maternal infections. The clinical picture of congenital CMV infection is always severe and includes psychomotor retardation, deafness, retinochoroiditis, microcephaly, hydrocephalus, cardiac disease, hepatitis, hepatosplenomegaly, thrombocytopoenia. The mortality rate is quite high. Most individuals (40-90%) acquire primary CMV infection during childhood or adulthood.
Post-natal infections are transmitted through close contact with infected biological fluids (urine, saliva, breast milk, semen, cervical secretions, faeces), infected blood products and, occasionally, organ transplants. In immunocompetent individuals, the clinical picture of post-natal CMV infection is usually mild or asymptomatic. The commonest signs include fever, malaise, and increased serum transaminase levels without jaundice.By contrast in immunocompromized patients (organ transplant recipients, patients with AIDS, lymphoproliferative diseases or cancer), symptoms may be severe because of disseminated and/or visceral infection, and include splenomegaly, pneumonia, haemolytic anemia, myocarditis and encephalitis. In these patients the disease may be fatal. The immune response to CMV involves synthesis of antibodies of the IgM class some weeks after infection by CMV and, one week later, of antibodies of the IgG class. Levels of IgM to CMV usually increase for some weeks and decrease slowly thereafter, in four to six months. Occasionally, IgM may circulate for years. Specific IgM assay is instrumental in diagnosing acute CMV infection, which remains difficult to identify on symptoms alone. However, it is not always possible to distinguish between primary and secondary infection, because reactivation may induce synthesis of IgM in immunocompromized patients. Specific IgG assay is useful in distinguishing subjects having acquired the disease from those who have not. This is particularly important in order to adopt suitable prophylaxis in susceptible individuals. |
