Pathogenesis
Most healthy people who are infected by HCMV after birth have no symptoms. Some develop a syndrome similar to infectious mononucleosis or glandular fever, with prolonged fever, and a mild hepatitis. A sore throat is common. After infection, the virus remains latent in the body for the rest of the person's life. Overt disease rarely occurs unless immunity is suppressed either by drugs, infection or old age. Initial HCMV infection, which often is asymptomatic, is followed by a prolonged, inapparent infection during which the virus resides in mononuclear cells without causing detectable damage or clinical illness.
Infectious CMV may be shed in the bodily fluids of any infected person, and can be found in urine, saliva, blood, tears, semen, and breast milk. The shedding of virus can occur intermittently, without any detectable signs or symptoms.
CMV infection can be demonstrated microscopically by the detection of intranuclear inclusion bodies. On H&E staining, the inclusion bodies stain dark pink and are called "owl's eye" inclusion bodies.
HCMV infection is important to certain high-risk groups. Major areas of risk of infection include pre-natal or postnatal infants and immunocompromised individuals, such as organ transplant recipients, persons with leukemia, or those infected with human immunodeficiency virus (HIV). In HIV infected persons, HCMV is considered an AIDS-defining infection, indicating that the T-cell count has dropped to low levels.
Lytically replicating viruses disrupt the cytoskeleton, causing massive cell enlargement, which is the source of the virus' name.
A study published in 2009 links infection with CMV to high blood pressure in mice, and suggests that the result of CMV infection of blood vessel endothelial cells (EC) in humans is a major cause of atherosclerosis. Researchers also found that when the cells were infected with CMV, they created renin, a protein known to contribute to high blood pressure.
CMV encodes a protein, UL16, which is involved in the immune evasion of NK cell responses. It binds to ligands ULBP1, ULBP2 and MICB of NK cell activating receptor NKG2D, which prevents their surface expression. These ligands are normally upregulated in times of cellular stress, such as in viral infection, and by preventing their upregulation, CMV can prevent its host cell from dying due to NK cells
Read more about this topic: Human Cytomegalovirus