الفهرس Only 14 pages are availabe for public view
 |  | from | 130 |  |  |
| | | from | 130 | | |
Abstract
Viruses are among the most common causes of opportunistic infection after transplantation and the most important. The risk for viral infection is a function of the specific virus encountered, the intensity of immune suppression used to prevent graft rejection, and other host factors governing susceptibility.
Viruses are responsible for 25% to 30% of all post-transplant infections.The 2 major etiologic pathogens are cytomegalovirus (CMV) and the human herpes viruses (HHV). Both types of virus are widely distributed in the general population, with seroprevalence rates of CMV ranging from 30 to 97 %.
In addition to CMV and HHV, BK virus(a polyomavirus) associated nephropathy (BKVN) in renal transplant recipients has been observed with increasing frequency recently and has emerged as a cause of allograft failure linked to highly potent new immunosuppressive regimens containing tacrolimus or mycophenolate mofetil (MMF).
The effects of viral infection are classified as ”direct” and ”indirect” .This classification serves to separate the effects of invasive viral infection (cellular and tissue injury) from effects mediated by inflammatory responses (e.g., cytokines) or by alterations in host immune and inflammatory responses.Syndromes such as fever and neutropenia (e.g., with CMV infection) or invasive disease resulting in pneumonia, enteritis, meningitis, or encephalitis are considered direct effects. Indirect effects of viral infections include responses to viral infections such as release of cytokines, chemokines, or growth factors. These effectors are immunomodulatory, resulting in further immune suppression and increasing the risk of other opportunistic infections.