Human cytomegalovirus (CMV, herpesvirus 5) is a member of the herpesvirus family. CMV, similarly to other herpes viruses, shares a characteristic ability to remain dormant within the body for (...)
Human cytomegalovirus (CMV, herpesvirus 5) is a member of the herpesvirus family. CMV, similarly to other herpes viruses, shares a characteristic ability to remain dormant within the body for life. After initial infection, which may cause few symptoms, CMV becomes latent, residing in cells without causing detectable damage or clinical illness. CMV is widespread in human populations, and around a half of adult humans in developed countries are CMV carriers.
CMV infects most humans without harm. However infection with CMV causes serious, life-threatening disease in two circumstances: (1) in immunosuppressed adults and (2) in congenital infections of developing fetuses. In immunocompromised patients (organ transplant recipients, patients with lymphoid cancers, and HIV-infected patients) CMV is a major cause of disease and death. The common manifestations of disease in those patients are pneumonia, retinitis, and gastrointestinal diseases.
Congenital CMV (CCMV) infection is mostly (86% of all cases) asymptomatic. Symptoms, if they develop, include jaundice, pneumonia, a rash, an enlarged liver and spleen, low birth weight, seizures, small head. Mortality of children under symptomatic CCMV is around 20%. Around a half of symptomatic infants and around 12% of asymptomatic ones later develop physical or mental problems. These can include hearing loss, visual impairment or blindness, learning difficulties, epilepsy. Around 1% of children in developed countries are born with congenital CMV syndrome and around 0,2% of all children in these countries develop long-term consequences.
Primary infection poses the greatest risk for the fetus. A recurrent or reactivated infection is much less likely to result in serious fetal injury. The risk of serious fetal injury is greatest when maternal infection develops in the first trimester or early in the second trimester.
IgM antibodies are usually detected after 2-3 weeks following primary infection and generally persist during a few weeks. Level of specific IgM decrease in 4-6 months. CMV specific IgG antibodies appear 1-2 weeks later IgM; the level of IgG begins to rise and reaches a maximum 3 months after the infection. IgG antibodies remains within the body throughout life.
Detection of CMV-specific IgM cannot be regarded as absolute proof of primary CMV infection for several reasons. Firstly, about 25% of patients with primary CMV infection still have detectable IgM 4 months after the infection, with IgM sometimes persisting for over a year. Secondly, IgM antibody may reappear during reactivation of a latent infection or reinfection. False-positive IgM results may also occur due to non-specific IgM reactivity and false-negative onces due to the lack of CMV-specific IgM are also possible. Taking into account the special importance to properly diagnose primary CMV infection in pregnant women, the serological testing of suspected primary CMV infection in this category of patients should include the measurement of not only the level of IgM, but also the avidity of IgG.