Cytomegalovirus infection is a sexually transmitted disease caused by cytomegalovirus (cmv). Cytomegalovirus is a DNA virus. The characteristic lesions are enlarged infected cells with eosinophilic and basophilic inclusions in the nucleus and cytoplasm, respectively.CMV infection is distributed worldwide and humans are the only host of CMV. The rate of infection varies by country and economic status. There is a close relationship between CMV infection and immune function in adults. What causes cytomegalovirus infection? CMV infection can cause a decrease in the immune function of the body, especially cellular immune function. CMV infection has a significant effect on thymus development and the function of splenocytes, mononuclear phagocytes, NK cells and CTL cells. 1. Effects on thymus and spleen In neonatal guinea pigs with acute CMV infection in the laboratory, thymus development was suppressed and the number of T cells decreased. In adult rats infected with CMV, CMV was detected in 88% of the thymus. CMV infection affected splenic function, the proliferation of splenic lymphocytes in response to conA stimulation decreased, and IL-2 production by splenocytes decreased significantly. 2, the effect on immune cells The immunosuppression caused by CMV infection is related to the replication of the virus in cells. CMV can replicate in mononuclear phagocytes, T cells, B cells and some as yet unidentified monocytes, among which mononuclear phagocytes are most susceptible to CMV infection. lymphocytes have important regulatory and effector functions in the immune response. CMV infection can cause multiple CMV infection can cause a variety of impaired immune functions in lymphocytes. CMV infection mostly manifests as acute mononucleosis. Peripheral blood lymphocytes have a diminished proliferative response to mitogens, CMV antigens, and HSV antigens, inducing a decrease in interferon levels, a decrease in the CD4/CD8 ratio from 1.7±0.7 to 0.2+0.2, and a decrease in T-cell activity. This change can last for quite a long time, and 10 months after the disease, the ratio of T-cell subsets has not completely returned to normal in most patients. The immunosuppressive effect of CMV infection is mainly due to the abnormal function of large monocytes and CD8 cells infected by the virus. Mononuclear phagocytes play a pivotal role in anti-CMV immunity, not only directly engulfing and killing the virus, but more importantly, processing and presenting antigens, secreting cytokines, and regulating and amplifying the immune response. After CMV infection, the function of mononuclear phagocytes is affected, and CMV infection of macrophages causes a decrease in their phagocytic function, a decrease in intracellular oxygen radical production, and changes in the expression of FC receptors and complement receptors, as well as a decrease in their antigen-presentation function, a decrease in IL-1 production, and a decrease in the response to IL-1 and IL-2. The decrease in IL-1 production can cause an imbalance in the TH/TS cell ratio. NK cells have an antagonistic effect on the spread of CMV. nK cells are actively involved in the whole process of anti-CMV infection, but the presence of high NK activity is not necessarily a protective response, but evidence of active infection. nK cells do not prevent the emergence of primary CMV infection, but once infection is present, nK cells can emerge early in CMV infection and have a role in limiting the spread and confining the infection. nK cells, CTL cells, and CTL cells are the most important elements of the anti-CMV response. cells and CTL cells are important effector cells against CMV. They can lyse infected cells early in CMV replication, before the production of infectious virosomes, and abort the spread of virus between cells. In mouse models, the antiviral effect is mediated by NK cells when the virus has acted for 3-5 days, and NK cell activity can be enhanced by IFN. 6-21 days, killing activity of CTL cells is present in spleen and peripheral blood. the level of NK cell and CTL cell activity determines the susceptibility of the organism to CMV infection and the ease of recovery from infection. However, NK cell and CTL cell activities are also severely affected by CMV infection. In addition, specific cellular immunity has a role in preventing the re-emergence of CMV infection. The T-cell response of 20 renal transplant recipients with CMV infection was examined and 14 had a cytotoxic response to CMV, whereas 6 who did not have a cytotoxic response had severe clinical consequences. Therefore, the presence of specific T cells has a role in preventing the re-emergence of CMV infection. 3, antibodies have a role in reducing the virulence of CMV infection The body can develop a variety of antibodies after infection by CMV. Breast milk, cervical secretions, saliva despite the appearance of specific antibodies, including neutralizing antibodies. However, CMV can still be detected, indicating that antibodies do not prevent the spread of the virus. Antibodies passively acquired by the fetus from the mother do not block infection transmitted intrauterine, through the birth canal or through breast milk. It was demonstrated that 0.2 ml of high potency anti-CMV globulin injected intraperitoneally or intravenously into mice before lethal CMV attack completely protected the animals from death. 1 month after a second attack with CMV and others, the animals all still survived, indicating that antibodies have the effect of reducing the virulence of CMV. After the initial infection, CMV will exist indefinitely in the host cells into a latent state. A variety of tissues and organs may be involved, and necropsy suggests that the lungs, liver, pancreas, salivary glands, central nervous system and intestine may also be sites of viral latency. The severity of congenital infection is related to the lack of ability to produce precipitating antibodies and the T-cell response to CMV. After CMV infection in children and adults, activated T lymphocytes with a suppressive cytotoxic phenotype appear in the peripheral blood, and if the host’s T cell function is impaired, the latent virus may resurface and cause a variety of syndromes. The chronic stimulation that occurs after tissue transplantation provides the conditions for CMV activation and induces disease. Certain strong immunosuppressive agents that target T cells, such as anti-thymocyte globulin, are associated with a high incidence of clinical CMV syndromes. In addition, CMV can function as a cofactor to activate latently infected HIV.