Acute liver failure has been associated with HHV-6 infection in both the immunocompetent (Cacheux 2005) and the immunocompromised (Hill 2014, Kuntzen 2005). A recent article demonstrated that high intrahepatic HHV-6 DNA levels were significantly associated with decreased graft survival following diagnosis of graft hepatitis, while elevated levels of CMV and EBV were not associated with decreased graft survival (Pischke 2012). HHV-6 has also been shown to directly infect the liver (Gallegos-Orozco 2010), and many believe HHV-6B may be an underappreciated cause of hepatitis in the post-transplant population (Hill 2014, Buyse 2013).
Studies have shown that HHV-6 is a cause of many hepatobilliary diseases including fulminant hepatic failure and acute decompensation of chronic liver disease in children (Chevret 2008), post-infantile giant cell hepatitis (Kuntzen 2005), acute liver failure in adults (Cacheux 2005), and hepatitis (Schenke 2010). Liver dysfunction due to HHV-6 Mononucleosis has also been well documented. An indirect role in the development of cirrhosis and hepatocellular carcinoma has also been proposed (Nakayama-Ichiyama 2011). A typical liver biopsy can be very helpful in the diagnosis of HHV-6—induced liver failure (Gallegos-Orozco 2010), and HHV-6 liver infection has been successfully treated with ganciclovir antiviral therapy (Cacheux 2005).