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Blood, 1 February 2002, Vol. 99, No. 3, pp. 1085-1088
BRIEF REPORT
Development of drug-resistant herpes simplex virus infection
after haploidentical hematopoietic progenitor cell transplantation
Amelia A. Langston,
Istvan Redei,
Angela M. Caliendo,
Jyoti Somani,
Don Hutcherson,
Sagar Lonial,
Silvana Bucur,
Judy Cherry,
Andrew Allen, and
Edmund K. Waller
From the Emory University School of Medicine, Winship
Cancer Institute, Department of Hematology-Oncology, Bone Marrow and
Stem Cell Transplant Center, and Departments of Pathology and
Infectious Diseases, Emory University, Atlanta, Georgia.
An unusually high incidence of acyclovir- and foscarnet-resistant
herpes simplex virus (HSV) infection was noted after
lymphocyte-depleted blood hematopoietic progenitor cell (HPC)
transplantation from HLA-haploidentical family donors. Fourteen adults
with hematologic malignancies underwent blood HPC transplantation from
haploidentical family donors. Pheresis products were stringently
depleted of T and B cells by immunomagnetic adsorption, and patients
received no immunosuppression after transplantation. HSV
reactivation occurred in all 7 evaluable HSV-1- or HSV-2-seropositive
patients, at a median of 40 days after transplantation. Susceptibility
testing of clinically resistant viral isolates demonstrated acyclovir resistance in all 5 cases tested. Second-line therapy produced only
partial responses, and in vitro evidence of foscarnet resistance developed rapidly in all 3 patients treated with foscarnet. Healing of
lesions coincided with T-cell recovery. The prolonged immunodeficiency associated with stringent lymphocyte depletion of the graft appears to
strongly predispose to emergence of drug-resistant HSV. Furthermore, immune reconstitution is necessary for eradication of infection.
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