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J Clin Virol. 2014 Oct;61(2):289-92. doi: 10.1016/j.jcv.2014.07.001. Epub 2014 Jul 12.

Human herpesvirus 6 can be detected in cerebrospinal fluid without associated symptoms after allogeneic hematopoietic cell transplantation.

Author information

1
Division of Allergy and Infectious Diseases, University of Washington, Seattle, WA, United States; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, United States. Electronic address: joshuaah@uw.edu.
2
Division of Allergy and Infectious Diseases, University of Washington, Seattle, WA, United States; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, United States.
3
Department of Laboratory Medicine, University of Washington, Seattle, WA, United States.
4
Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, United States; Department of Laboratory Medicine, University of Washington, Seattle, WA, United States.
5
Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, United States; Seattle Children's Research Institute, Seattle, WA, United States.

Abstract

BACKGROUND:

Human herpesvirus 6 (HHV-6) is an opportunistic pathogen after hematopoietic cell transplantation (HCT) that is associated with central nervous system (CNS) dysfunction.

OBJECTIVES:

The aim of this study was to determine the frequency and significance of HHV-6 DNA detection in cerebrospinal fluid (CSF) after HCT.

STUDY DESIGN:

We identified patients with HHV-6 DNA in CSF using quantitative PCR. Patients with neurologic symptoms and HHV-6 DNA in CSF without identification of an alternative etiology were categorized as having HHV-6 CNS dysfunction.

RESULTS:

Among 3902 allogeneic HCT recipients from 1998 to 2012, 51 of 124 tested patients had HHV-6 DNA in CSF; 37 met criteria for HHV-6 CNS dysfunction and 14 (27%) did not. Patients with an alternative diagnosis had longer time to HHV-6 detection and lower viral load in CSF. Six patients without HHV-6 CNS dysfunction were not treated and had no morbidity attributable to HHV-6. Kaplan-Meier analysis demonstrated poor overall survival among all patients. Variables associated with higher all-cause mortality in a multivariable Cox model included alternative diagnosis (adjusted hazard ratio [aHR], 8.4; 95% CI, 1.7-40.9; P = 0.009) and higher peak plasma viral load (log(10) scale) (aHR, 1.4; 95% CI, 1.1-1.9; P = 0.01).

CONCLUSION:

We identified a number of allogeneic HCT recipients with HHV-6 DNA in CSF who did not meet criteria for HHV-6 CNS dysfunction. All patients had poor survival. Whether CSF HHV-6 DNA detection in patients without associated CNS dysfunction independently contributes to mortality and warrants treatment is unclear; management of these patients warrants further investigation.

KEYWORDS:

CNS; Encephalitis; Herpesvirus; Neurologic; Transplant; hhv-6

PMID:
25066883
PMCID:
PMC4165730
DOI:
10.1016/j.jcv.2014.07.001
[Indexed for MEDLINE]
Free PMC Article

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