The Role of Interferons in Viral Infections in Immune Compromised Patients
Herpesgroup viruses remain cause of morbidity among renal allograft recipients. Over the past several years the development of antiviral drugs such as adenine arabinoside and acyclovir have resulted in major improvements in management of herpes simplex (HSV) and varicella zoster virus (VZV) infections (1). Cytomegalovirus (CMV) and Epstein-Barr virus (EBV), however, continue to contribute to the morbidity of renal transplantation (2–6). CMV infection has several effects on the host. Between 30 and 40% of all renal allograft recipients develop clinically apparent CMV syndromes and 2–3% will have fatal infections. CMV infection following transplantation may be either primary or due to reactivation of latent virus. Primary infection occurs in 60–70% of CMV seronegative renal allograft recipients who receive grafts from CMV seropositive donors. Reactivation of CMV occurs in approximately 60% of CMV seropositive recipients. Because most adult allograft recipients in the United States are CMV seropositive, primary CMV infections are less common than reactivation infections, but may be associated with more morbidity when they are observed.
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