Pulmonary involvement during cytomegalovirus infection in immunosuppressed patients

Abstract

Although cytomegalovirus (CMV) pulmonary involvement after solid organ transplantation is infrequently seen nowadays, CMV pneumonitis is still a potential lethal complication. Introduction of the pp65 antigenemia assay enabled early and rapid diagnosis of CMV viremia in transplant patients prior to symptoms. Also, in asymptomatic patients with CMV viremia, a decreased pulmonary diffusion capacity could be demonstrated. In this review, we discuss clinical and subclinical pulmonary involvement of CMV infection in the immunocompromised host with an emphasis on transplant recipients. The clinical course, diagnosis, therapy, prophylaxis, and pathophysiology of CMV pneumonitis are discussed.

Leukotriene B4 Protects Latently Infected Mice against Murine Cytomegalovirus Reactivation following Allogeneic Transplantation

“…injection in the tail vein with a sublethal dose (500 PFU) of MCMV in a final volume of 0.1 ml of DMEM and treated with exogenous LTB 4 . Mice were treated daily, starting on the third day of infection, with a placebo or varying quantities of LTB 4 (0.5-500 ng/kg).…”

“…Mice were infected with a lethal dose of MCMV and treated by i.v. injection of LTB 4 . Animal survival was monitored daily.…”

“…The frequency and the severity of CMV infections in transplant patients are variable and depend on the nature of the transplant, the immune status of the recipient, and the duration of the immunosuppressive therapy. The CMV infection, particularly when associated with pneumonitis, is an important cause of morbidity and mortality after bone marrow transplantation (4).…”

“…In animals lacking the gene coding for the 5-lipoxygenase (5-LO), a markedly increased susceptibility to bacterial pneumonia was observed (15,16). Furthermore, it was shown that this susceptibility to infection is the consequence of the inability of lung macrophages to produce LTB 4 and to ingest and kill pathogens. Another group has shown that administration of LTB 4 to mice enhances bacterial clearance (17).…”

“…Interesting observations made in AIDS patients also support the role of LTB 4 in host defense. It was reported that neutrophils and alveolar macrophages from HIV-infected individuals produced significantly less LTB 4 than the cells of healthy subjects, and that such a defect was the cause of reduced antimicrobial activity in the phagocytes (18 -20).…”