397
END Organ Disease in the Context of Human Herpes VIRUS 6 Viremia in Pediatric Allogeneic Hematopoietic STEM CELL Transplant Patients: A Case Series

Track: Poster Abstracts
Saturday, March 1, 2014, 6:45 PM-7:45 PM
Longhorn Hall E (Exhibit Level 1) (Gaylord Texan)
Lena Winestone, MD , Pediatrics, Stanford University, Palo Alto, CA
Rajni Agarwal, MD , Pediatric Stem Cell Transplantation, Stanford University, Palo Alto, CA
Jose Montoya, MD , Stanford University, Palo Alto, CA
Kenneth I Weinberg, MD , Pediatric Stem Cell Transplantation, Stanford University, Palo Alto, CA
Matthew H. Porteus, MD , Pediatric Stem Cell Transplantation, Stanford University, Palo Alto, CA
Benjamin Pinsky, MD, Ph.D , Stanford University, Palo Alto, CA
Elizabeth Soda, MD , Stanford University, Palo Alto, CA
Jesse Waggoner, MD , Stanford University, Palo Alto, CA
John Tamaresis, Ph.D , Pediatrics, Stanford University, Palo Alto, CA
Sandhya Kharbanda, MD , Pediatric Stem Cell Transplantation, Stanford University, Palo Alto, CA
INTRODUCTION. HHV6 (Human Herpes Virus 6) reactivation occurs in approximately one-half of patients following allogeneic hematopoietic stem cell transplant (HSCT). The target tissues of HHV6 and the extent to which HHV6 causes disease in those with viremia is not resolved.

METHODS. Biopsies or body fluid sampling are routinely performed at our center to determine the cause of otherwise unexplained end-organ disease. We describe 14 pediatric HSCT patients who were found with HHV6 PCR end-organ tissue positivity on these studies. Of these 14 patients, 13 had received myeloablative conditioning, 12 had received an unrelated donor graft, 10 had underlying malignant disease, 9 patients had acute GVHD, and  3 were diagnosed with chronic GVHD.

RESULTS. Robust statistical partitioning identified two distinct subgroups within this population based on the highest HHV6 viral load in blood. In 10 of the 14 patients, a peak blood viral load (>28,000 copies/mL) occurred developed while the other 4 patients had peak blood viral loads <2000 copies/ml. All patients received antiviral treatment to treat their viremia. At the time of biopsy and/or fluid sampling, only 1 patient out of 14 had a blood viral load >28,000 copies/mL and the remainder had very low (<1500 copies/ml) or undetectable HHV6 virus in the blood despite having detectable virus in their tissues. In total, 8/14 patients biopsied patients who had tissue/body fluid viral positivity did not have concurrent detectable virus in blood, in 5/14, the blood viral load was <1500 copies/ml, while only in one patient who had encephalitis there was a high copy number of 344,488 copies/ml detected in blood at the time of detection of the virus in the cerebrospinal fluid (CSF).

HHV6 was found in CSF (3 patients), BAL fluid (3 patients), GI tract (5 patients), bone marrow (5 patients), pericardial fluid (3 patients), liver (1 patient), and gallbladder (2 patients). Statistical analysis showed no difference between the two subgroups with respect to age, gender, stem cell graft, stem cell donor, HLA compatibility between the donor and the recipient, acute/chronic graft-versus-host disease, or survival. Of note, 4 out of 14 patients had co-existent CMV viremia. There was a decreasing linear trend (Cochran-Armitage P=0.015) in the association (Fisher’s exact P=0.041) between CMV viremia and HHV6 viral load group: 3 patients with CMV viremia were in the low HHV 6 viral load group versus 1 patient in the high group. Five of the fourteen patients died (one of whom relapsed), suggesting a high non-relapse mortality rate (28%) in this population.

CONCLUSION. End-organ disease/dysfunction with HHV6 positivity can persist despite a decrease in peripheral viral load after antiviral treatment. Further studies will elucidate whether prolonged or intensive antiviral treatment is warranted in such cases.

Disclosures:
Nothing To Disclose
See more of: Poster Session 2: Allogeneic Transplants
See more of: Poster Abstracts
<< Previous Presentation | Next Presentation