Viral infections, including cytomegalovirus and human herpesvirus 6, are discussed as potential triggers for cardiac-allograft dysfunction.
Do viral infections such as cytomegalovirus and human herpesvirus 6 contribute to cardiac-allograft dysfunction in transplant recipients?
This editorial discusses the emerging evidence and ongoing debate regarding the role of viral infections, including CMV and HHV-6, in triggering cardiac-allograft dysfunction and vasculopathy.
The question of a viral contribution to allograft dysfunction after solid-organ transplantation has long been debated. This debate has focused primarily on cytomegalovirus, which has been identified as a risk factor for bronchiolitis obliterans in lung-transplant recipients1 and may be associated with a variety of forms of chronic allograft dysfunction in other solid-organ transplants. There is considerable evidence, but still some controversy, concerning the role of cytomegalovirus in cardiac-allograft vasculopathy, one of the primary conditions limiting survival in cardiac-transplant recipients.2 Recent reports have raised the possibility that human herpesvirus 6 (HHV-6) infection may also be associated with allograft dysfunction.3 In . . .
Robin K. Avery (2001) conducted an editorial in Cardiac-allograft dysfunction. Viral infection (cytomegalovirus, HHV-6) was evaluated. Viral infections, including cytomegalovirus and human herpesvirus 6, are discussed as potential triggers for cardiac-allograft dysfunction.