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Human herpesvirus‐6 infections in kidney, liver, lung, and heart transplantation: review
Author(s) -
Lautenschlager Irmeli,
Razonable Raymund R.
Publication year - 2012
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.2012.01443.x
Subject(s) - medicine , cidofovir , foscarnet , immunology , valganciclovir , encephalitis , transplantation , ganciclovir , organ transplantation , disease , human herpesvirus 6 , retinitis , virology , human cytomegalovirus , viral disease , herpesviridae , virus
Summary Human herpesvirus‐6 (HHV‐6), which comprises of HHV‐6A and HHV‐6B, is a common infection after solid organ transplantation. The rate of HHV‐6 reactivation is high, although clinical disease is not common. Only 1% of transplant recipients will develop clinical illness associated with HHV‐6 infection, and most are ascribable to HHV‐6B. Fever, myelosuppression, and end‐organ disease, including hepatitis and encephalitis, have been reported. HHV‐6 has also been associated with various indirect effects, including a higher rate of CMV disease, acute and chronic graft rejection, and opportunistic infection such as invasive fungal disease. All‐cause mortality is increased in solid organ transplant recipients with HHV‐6 infection. HHV‐6 is somewhat unique among human viruses because of its ability to integrate into the host chromosome. The clinical significance of chromosomally integrated HHV‐6 is not yet defined, although a higher rate of bacterial infection and allograft rejection has been suggested. The diagnosis of HHV‐6 is now commonly made using nucleic acid testing for HHV‐6 DNA in clinical samples, but this can be difficult to interpret owing to the common nature of asymptomatic viral reactivation. Treatment of HHV‐6 is indicated in established end‐organ disease such as encephalitis. Foscarnet, ganciclovir, and cidofovir have been used for treatment.

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