Cytomegalovirus infection - Pathogenesis

The decisive condition for the development of antenatal cytomegalovirus infection is viremia in the mother. The presence of the virus in the blood leads to infection of the placenta, its damage and infection of the fetus with possible consequences in the form of defects and intrauterine growth retardation, a pathological process with damage to internal organs, primarily the central nervous system. If the virus is present in the cervical canal of a pregnant woman, an ascending (transcervical) route of infection of the fetus is possible without the pathogen entering the blood. Reactivation of Cytomegalovirus in the endometrium is one of the factors of early abortions. Intranatal infection with the virus occurs when the fetus passes through the infected birth canal due to aspiration of amniotic fluid containing cytomegalovirus and/or secretions of the birth canal or through damaged skin and can also lead to the development of a clinically expressed disease. In postnatal cytomegalovirus infection, the mucous membranes of the oropharynx, respiratory system, digestive and genital tracts serve as entry points for the pathogen. After the virus has overcome the entry points and locally reproduced, short-term viremia occurs, monocytes and lymphocytes carry the virus to various organs. Despite the cellular and humoral response, cytomegalovirus induces a chronic latent infection.

Monocytes, lymphocytes, endothelial and epithelial cells serve as a reservoir of viral particles. In the future, with minor immunosuppression, "local" activation of cytomegalovirus is possible with the release of the virus from the nasopharynx or urogenital tract. In the case of deep immunological disorders with a hereditary predisposition to this pathology, there is a resumption of active replication of the virus, viremia, dissemination of the pathogen, and the development of a clinically expressed disease. Activity of viral replication, the risk of manifestation of cytomegalovirus infection, the severity of its course are largely determined by the depth of immunosuppression, primarily by the level of decrease in the number of CD4 lymphocytes in the blood. A wide range of organ lesions is associated with cytomegalovirus infection: lungs, gastrointestinal tract, adrenal glands, kidneys, brain and spinal cord, retina. In immunosuppressed patients with cytomegalovirus infection, postmortem findings include pulmonary fibroatelectasis, sometimes with cysts and encapsulated abscesses; erosive and ulcerative lesions of the esophagus, colon, and less commonly the stomach and small intestine with pronounced fibrosis of the submucosal layer; massive, often bilateral necrosis of the adrenal glands; encephaloventriculitis, necrotic lesions of the spinal cord, and retina with the development of necrotic retinitis. The specificity of the morphological picture in cytomegalovirus infection is determined by large cytomegalocytic cells, lymphohistiocytic infiltrates, and productive-infiltrative panvasculitis with cytomegalic transformation of cells in all walls of small arteries and veins with an outcome in sclerosis. Such vascular damage serves as a basis for thrombus formation, leads to chronic ischemia, against the background of which destructive changes, segmental necrosis and ulcers, pronounced fibrosis develop. Widespread fibrosis is a characteristic feature of CMV organ damage. In most patients, the pathological process associated with cytomegalovirus is generalized.

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