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Journal of Clinical Microbiology, December 2006, p. 4441-4443, Vol. 44, No. 12
0095-1137/06/$08.00+0     doi:10.1128/JCM.01312-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Relationship between Preexisting Anti-Varicella-Zoster Virus (VZV) Antibody and Clinical VZV Reactivation in Hematopoietic Stem Cell Transplantation Recipients{triangledown}

Masahiro Onozawa,1* Satoshi Hashino,1 Mutsumi Takahata,1 Fumie Fujisawa,1 Takahito Kawamura,1 Masao Nakagawa,1 Kaoru Kahata,1 Takeshi Kondo,1 Shuichi Ota,1 Junji Tanaka,2 Masahiro Imamura,2 and Masahiro Asaka1

Department of Gastroenterology and Hematology, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan,1 Department of Hematology and Oncology, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan2

Received 26 June 2006/ Returned for modification 23 September 2006/ Accepted 30 September 2006

Reactivation of latent varicella-zoster virus (VZV), presenting as localized zoster or as disseminated infection, is a common and potentially serious complication in hematopoietic stem cell transplantation (HSCT) recipients. We retrospectively studied anti-VZV immunoglobulin G titers by the immune adherence hemagglutination method after HSCT and also studied VZV DNA by real-time PCR during clinical VZV reactivation using cryopreserved serum samples. No significant difference was found between anti-VZV titers in 13 patients with VZV infection (localized zoster in 11 patients and disseminated zoster in 2 patients) and in 13 subjects without VZV infection at each time point after HSCT. Preexisting anti-VZV titers of disseminated zoster cases tended to be lower than those of localized zoster cases (P = 0.10). Serum VZV DNA copy numbers at the onset of disseminated zoster cases tended to be higher than those of localized zoster cases (P = 0.09). A strong inverse correlation was found between preexisting anti-VZV titer and serum VZV DNA at onset (r = –0.90, P = 0.006). In HSCT recipients, preexisting antibody does not prevent the development of VZV reactivation but may contribute to decreased viral load at onset, resulting in a mild clinical course.

* Corresponding author. Mailing address: Department of Gastroenterology and Hematology, Hokkaido University Graduate School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo, Hokkaido 060-8638, Japan. Phone: 81-11-716-1161, ext. 5920. Fax: 81-11-706-7867. E-mail: masahiro.onozawa{at}nifty.ne.jp.

{triangledown} Published ahead of print on 11 October 2006.

Journal of Clinical Microbiology, December 2006, p. 4441-4443, Vol. 44, No. 12
0095-1137/06/$08.00+0     doi:10.1128/JCM.01312-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.





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