HHV-6 reactivation is a significant event in patients undergoing renal transplantation, and is associated with acute rejection, cyclosporine nephropathy, and the development of chronic allograft nephropathy (Tong 2002, Hoshino 1995, Sebekova 2005). In a recent study of kidney transplant patients, HHV-6 was detected more frequently in end-stage renal disease patients than in healthy subjects (Caiola 2012). Furthermore, early HHV-6 replication is associated with increased morbidity following kidney transplantation (Schroeder 2012). HHV-6B is the primary species implicated among kidney transplantation patients, detected particularly in the mononuclear cells of renal transplants (Helantera 2008), and HHV-6B is also frequently found in the gastrointestinal tracts of these patients (Lempinen 2012). However, it is interesting to note that one group has recently reported the predominance of HHV-6A viremia in the plasma/serum amongst their cohort of kidney transplant patients (Csoma 2011).
HHV-6 may play a secondary role in the development of kidney transplant rejection. Because HHV-6 can induce immunomodulating effects (primarily through the increased production of interleukin 1b, TNFa, interferon a, lymphocyte proliferation, and the suppression of interleukin 2 synthesis), it is thought that HHV-6 reactivation may subsequently lead to increased opportunistic infection and renal graft rejection in transplant patients (Cainelli 2002). Although HHV-6 is a common finding in biopsies from renal allograft patients—particularly those with previous CMV infection (Helantera 2008)—more studies are needed to further elucidate the role of HHV-6 reactivation in renal transplant failure.