HHV-6 is a DNA virus part of the beta-herpesvirus family and
can be divided into HHV-6 A and B.
Primary infection is mild and occurs usually in childhood; therefore the
majority of healthy adults have serologic evidence of prior infection. HHV-6 can re-activate in the
immunocompromised transplant recipient leading to asymptomatic viral
replication or less commonly active infection.
The highest prevalence by pcr has been shown to occur in bone marrow
transplant recipients (28% to 75%) but viral replication has also been shown to
occur in liver (28% to 32%) and renal transplant recipients (23% to 36%). Although asymptomatic viremia is common,
clinically active infection carries a high mortality and may be susceptible to
specific antiviral treatments.
How does HHV-6
infection present?
HHV-6 infection commonly presents with high fever often
associated with leukopenia, and encephalitis between 2-4 weeks post
transplantation. Other clinical
manifestations include pneumonitis, hepatitis, colitis and bone marrow
suppression. Rash typical of a leukocytoclastic
vasculitis can also be seen.
Encephalitis may be associated with seizure activity and
hyponatremia. Encephalitis is more
commonly seen in BMT patients but has been described in solid organ transplant
patients as well. HHV-6 infections
commonly co-exist with other viral infections including CMV.
HHV-6 reactivation has also been associated with drug
induced hypersensitivity syndromes, malignancies, multiple sclerosis, fulminant
hepatitis and mycocarditis though causality has not been demonstrated.
What are the
associated laboratory and imaging findings?
CBC: Bone marrow suppression, leucopenia, thrombocytopenia
Chemistry: Transaminitis, hyponatremia
CSF: High lymphocyte
cell count with elevated protein. HHV-6
can be detected in CSF by pcr.
MRI of brain:
Symmetric non-enhancing white matter lesions. MRI may be normal in patients infected with
HHV-6.
How can you
diagnose active infection?
Serologic testing:
Sensitivity varies and most tests cross react with HHV-7. A fourfold increase in titers or
seroconversion is considered diagnostic.
Virus culture from affected tissue or blood can be done but
are difficult to perform.
Viral detection:
Virus may be present in PMBC’s of patients with latent infection leading
to a “false” positive pcr. Therefore
HHV-6 should be identified in affected tissue or acellular plasma or
serum.
What are the
treatment options?
No therapy has been clearly documented to treat HHV-6
although several agents with in-vitro activity have been tried. Ganciclovir is effective against HHV-6B but
may not be active against HHV-6A (minority of infections). Foscarnet has activity against both A and B
however; its use is complicated by nephrotoxicity. In severe cases both agents can be tried and
whenever possible a reduction in immunosuppression should be considered.
References:
By
Dr. Vinay Nair
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