CMV is a lytic virus, which produces the CPE in vitro and in vivo. The pathogenesis of CMV infection is similar to that of other herpesviruses in many ways.
The virus infects the epithelial cells of the salivary glands, caus-ing a persistent infection and shedding of viruses in the salivary secretion. Activation and multiplication of the virus in the kid-ney and secretory glands facilitate secretion of CMV in urine and other body secretions including serum and milk.
CMV infection is acquired by coming in contact with blood, tissue, and most body secretions containing viruses. On enter-ing the human host, CMV primarily affects epithelial cells and causes infection of those cells. Subsequently, CMV infection progresses to establish persistent and latent infection in T cells, macrophages, and other cells and in different organs, such as the kidney and heart.
In the infected cells, CMV infection produces characteristic enlarged cells with viral inclusion bodies. This histopathologi-cal change, most commonly referred to as owl’s eye, is considered diagnostic of the CMV infections. These histological findings, however, may be minimal or absent in infected organs.
Immunity to CMV involves both humoral immunity and CMI. CMI is more important and essential (a) for resolution of infec-tion and (b) also for controlling progression of CMV infection. The production of cytotoxic T cells against CMV is very crucial in CMI response to control the infection.
CMV-specific CD4 and CD8 lymphocytes play an impor-tant role in protection after primary infection or reactivation of latent disease. Studies have shown that patients who do not develop CMV-specific CD4 or CD8 cells are at higher risk for developing CMV pneumonitis. Suppression of CMI, which is caused by therapy with corticosteroid or infection with HIV, induces reactivation of the latent viral infection. Recent studies have also shown that many viral gene products appear to modulate host inflammatory response and are responsible for symptoms of the disease.
The humoral immunity is characterized by development of CMV IgM antibodies during 4–7 weeks of infection. These neutralizing antibodies are directed mostly against an envelope glycoprotein gB. More than 50% of neutralizing antibodies in convalescent serum are found to be produced against glyco-protein gB. Antibodies are also produced against other viral proteins, such as pp153, pp28, and pp65. The antibodies have some role in control of severe disease, but do not prevent trans-placental infection, which can occur even in pregnant mothers who are CMV seropositive.