HHV‐6 in liver transplantation: A literature review

Abstract

Human herpesvirus 6 (HHV-6A and HHV-6B) can cause primary infection or reactivate from latency in liver transplant recipients, which can result in a variety of clinical syndromes, including fever, hepatitis, encephalitis and higher rates of graft dysfunction as well as indirect effects including increased risks of mortality, CMV disease, hepatitis C progression and greater fibrosis scores. Although HHV-6 infection is currently diagnosed by quantifying viral DNA in plasma or blood, biopsy to demonstrate

Evaluation of liver failure in a pediatric transplant recipient of a liver allograft with inherited chromosomally integrated HHV‐6B

“…It is also possible that the late acute cellular rejection might have stimulated a local HHV‐6 reactivation. Additionally, steroid therapy can exacerbate active HHV‐6 infection, rendering antiviral therapy less effective and extended antiviral treatment may have contributed to the patient's deterioration. HHV‐6 mRNA assays are available at a small number of specialized commercial laboratories in the United States and in Europe, and immunohistochemistry analysis of liver biopsies for late proteins can assist physicians in determining whether HHV‐6 specific antiviral therapy might be useful.…”

“…Human herpesvirus 6 (HHV‐6), which encompasses two distinct species HHV‐6A and HHV‐6B, is a ubiquitous virus with a seroprevalence greater than 90% in adults. It establishes lifelong latency in a wide range of cell types, including lymphocytes and hepatocytes, and can reactivate in both immunocompromised and immunocompetent patients, leading to various clinical disorders . HHV‐6B accounts for most HHV‐6 reactivations, which usually result from immunosuppressive regimens in the transplant setting.…”

“…It establishes lifelong latency in a wide range of cell types, including lymphocytes and hepatocytes, and can reactivate in both immunocompromised and immunocompetent patients, leading to various clinical disorders . HHV‐6B accounts for most HHV‐6 reactivations, which usually result from immunosuppressive regimens in the transplant setting. Clinically significant HHV‐6 infections are treated with ganciclovir, cidofovir, or foscarnet along with a reduction in immunosuppression, which often results in a favorable outcome if administered in a timely manner …”

“…HHV‐6B accounts for most HHV‐6 reactivations, which usually result from immunosuppressive regimens in the transplant setting. Clinically significant HHV‐6 infections are treated with ganciclovir, cidofovir, or foscarnet along with a reduction in immunosuppression, which often results in a favorable outcome if administered in a timely manner …”

“…Clinically significant HHV-6 infections are treated with ganciclovir, cidofovir, or foscarnet along with a reduction in immunosuppression, which often results in a favorable outcome if administered in a timely manner. 2 In addition to this conventional herpesvirus latency, about 1% of the human population harbors inherited chromosomally integrated HHV-6 genome (iciHHV-6), present in all somatic and germ cells and vertically transmitted in a Mendelian manner. 1,3 Consequently, viral loads in biological samples from these individuals are persistently high and may be mistaken as severe viral reactivation, leading to unnecessary, prolonged, and potentially harmful treatments, due to toxicity of conventional HHV-6 antivirals.…”