Cytomegalovirus-induced immunopathology and its clinical consequences

Abstract

Human cytomegalovirus (CMV) is a ubiquitous DNA virus that causes severe disease in patients with immature or impaired immune systems. During active infection, CMV modulates host immunity, and CMV-infected patients often develop signs of immune dysfunction, such as immunosuppression and autoimmune phenomena. Furthermore, active viral infection has been observed in several autoimmune diseases, and case reports have linked primary CMV infection and the onset of autoimmune disorders. In addition, CMV infection promotes allograft rejection and graft-versus-host disease in solid organ and bone marrow transplant recipients, respectively, further implicating CMV in the genesis and maintenance of immunopathological phenomena. The mechanisms by which CMV could induce inhibition of host defense, inflammation, and autoimmunity are discussed, as is the treatment of virus-induced immunopathology with antivirals.

Human cytomegalovirus detection by real-time PCR and pp65-antigen test in hematopoietic stem cell transplant recipients: a challenge in low and middle-income countries

“…Nevertheless, primary infection or reactivation of latent CMV in the immunocompromised patients can cause life-threatening diseases with higher mortality rates. [1][2][3][4] Usually, CMV reactivation occurs within the first 3 months after transplantation. The use of steroids for prophylaxis and treatment of graft-versus-host disease (GvHD), which impair the recovery of CD4 z and CD8 z T cells including those specific for CMV, can expose the patients to the risk of CMV disease for a longer period.…”

Cytomegalovirus infection in a patient with systemic lupus erythematosus and acute myocardial infarction – cause or causal relationship?

“…The mechanism by which this occurs is unclear, but it is hypothesized to induce antibodies to U1 snRNP. CMV antibodies cross-react with Sn/RNP autoantigens in SLE patients and can induce anti-La autoantibodies accounting for flares in CMV-infected patients [9]. SLE has been established as contributing to accelerated atherosclerosis via ongoing inflammation.…”

Assessment of Cox2 and CMV in patients with chronic HCV infection

“…Rafael et al, 42 indicated that CMV infection interacted with HCV and raised the effect on the liver enzymes and cause hepatitis. Considering the fact that HCMV viruses contribute an immunomodulatory effect resulting in developed of immunosuppression 43,44 and dysregulation of cytokine which could fast HCV pathogenesis of patients in critical condition. 39 CMV infection promotes HCV pathogenesis by prohibition the normal mechanisms responsible for HCV elimination, thus playing vital role in HCV existence and pathogenicity.…”