**2. CMV infection**

CMV is a double-DNA virus of the herpesvirus family transmitted via saliva, body fluids, or tissue. There are various, species-specific strains of cytomegalovirus [7]. Seroprevalence ranges between 30 and 70% in Europe and North America. Following primary infection, CMV establishes latency in myeloid progenitor cells and can be transiently reactivated in a healthy host without causing disease, similar to polyomaviruses. However, CMV reactivates frequently and causes disease in KTRs in the setting of immunocompromised, typically in the first 2–3 months after transplantation [8, 9]. CMV viremia in the 1–6 months after transplantation is significantly more frequent in KTRs older than 65 years.

Reinfection (primary infection with a different human strain) can also occur [10]. CMV infection is the most common infectious disease following solid organ transplantation, including kidney [1, 3].

In addition to the direct effects of viral infection, CMV infection and disease have been associated with acute and chronic rejection and diminished patient and graft survival [2]. The transplanted kidney itself is only rarely affected by CMV reactivation.

The greatest recognized risk factor for CMV disease is a serological mismatch between the donor and the recipient (the recipient is CMV IgG seronegative and the donor is CMV IgG seropositive: D+/R−). Furthermore, CMV D+/R+ and CMV D−/R+ transplantations are of intermediate risk for the development of disease, and CMV D−/R− transplantation is considered as low risk (<5% incidence) [11, 12].
