Clinical Features of Infection

Infection of the normal host is rarely associated with disease. Most children and adults do not appear to suffer any disease. An infectious mononucleosis-like syndrome, characterized by fever, malaise, myalgia, liver dysfunction and heterophil antibody-negative lymphocytosis, may follow several weeks after exposure in a small proportion of individuals and may last for several weeks. This disease occurs and was first noticed in transfusion recipients and denoted post-perfusion syndrome. It transpires in the face of an aggressive humoral response but a decrease in CD4+ T cells. Cell-mediated immunity appears to be depressed by CMV infection. Chronic diseases that have been associated with long-term CMV infection include atherosclerosis and restenosis that follows coronary angioplasty, but the role of any ubiquitous virus such as CMV in such diseases remains conjectural.

Congenital CMV disease typically follows a subclinical primary infection of an expectant mother. Disease is much less likely to follow reactivated maternal infection, although virus transmission occurs. Perinatal infection can result in a similar disease pattern, but at a much lower frequency. While 0.5-1% of infants are infected in utero, fewer than 10% suffer disease. Cytomegalic inclusion disease is the worst manifestation of congenital CMV, representing an extremely broad spectrum of different syndromes, including petechia, hepatosplenomegaly, jaundice, microencephaly and other serious neurological damage. A majority of symptomatic infants suffer subclinical disease with slowly developing hearing loss and mental retardation. Cytomegalic inclusion disease is the most significant disease caused by CMV, and seems to be a manifestation of widespread viral growth before the immune system has had a chance to develop. Congenitally infected neonates may present with rashes, hepatitis, pneumonitis and gastroenteritis, in addition to long-term neurological damage affecting hearing and IQ. The risk of a similar generalized disease in premature, low birth weight infants who are transfused with CMV-contaminated blood products has led to the use of screened products in this population.

CMV poses a great risk to the immunocompromised host. Primary infection results from transfer of CMV-positive transplants or blood and reactivated infection results when latent virus reactivates due to immunosuppression. In solid organ transplant settings, the transplanted organ is likely to be a target of viral disease and a CMV seronegative individual who receives a seropositive organ is at greatest risk. In bone marrow allografting, the serological status of the recipient seems to be the primary determinant of disease, with seropositive recipients being more likely to suffer the consequences of disease. Disease is often targeted to the transplanted solid organ, and may include pneumonitis, hepatitis, gastroenteritis and other organ-specific diseases. Although prophylaxis for CMV with antiviral drugs and antibodies prevents serious disease in many solid organ transplant settings, CMV remains a serious consequence in other settings. Interstitial pneumonia remains a prominent disease in both bone marrow allograft and heart-lung recipients, despite efforts to control CMV infection with antivirals. In many of the situations where CMV is a major problem, viral immunity is either severely depressed or nonexistent. Adoptive transfer of autologous cytotoxic T cell lines into bone marrow allograft recipients can prevent disease. The humoral response is often intact, and even elevated, in immunocompromised hosts, but to little avail. The experience with immunocompromised hosts reinforces the importance of the cellular immune response in preventing virus reactivation and systemic dissemination in normal hosts.

CMV is one of the most common opportunistic infections in individuals with T cell deficiency and patients with AIDS, where the likelihood of CMV disease correlates with a decrease in CD4+ helper T cell function. Prior to the advent of highly active antiretroviral therapy to control human immunodeficiency virus (HIV) infection, CMV was one of the most common AIDS-defining pathogens. Retinitis, with progressive blindness, and gastroenteritis were the two most common diseases. It remains to be seen what will happen in individuals as HIV resistance to these therapies develops.

Serological diagnosis is widely used to assess past infection, and detection of viral antigen in leukocytes, bronchial lavage, semen or infected tissue is used to assess the level of active infection. The presence of high levels of viral DNA in peripheral blood cells or plasma has also been used to detect active infection. There are no reliable serological assays to assess recent infections, although all classes of antibodies rise during primary infection. Histopathology and virus isolation are used to detect CMV in tissues of bodily fluids, but the presence of virus does not always indicate an ongoing disease process.

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