Short communication Lack of antibodies against the antigen domain 2 epitope of cytomegalovirus (CMV) glycoprotein B is associated with CMV disease after renal transplantation in recipients having the same glycoprotein H serotypes as their donors K. Ishibashi 1,2 , T. Tokumoto 3 , H. Shirakawa 3 , K. Hashimoto 4 , K. Ikuta 1 , N. Kushida 2 , T. Yanagida 2 , K. Shishido 2 , K. Aikawa 2 , H. Toma 3 , N. Inoue 5 , O. Yamaguchi 2 , K. Tanabe 3 , T. Suzutani 1 Departments of 1 Microbiology, 2 Urology, Fukushima Medical University, Fukushima, Japan, 3 Department of Urology, Tokyo Women’s Medical University, Tokyo, Japan, 4 Department of Pediatrics, Fukushima Medical University, Fukushima, Japan, 5 Department of Virology I, National Institute of Infectious Diseases, Tokyo, Japan K. Ishibashi T.Tokumoto, H. Shirakawa, K. Hashimoto, K. Ikuta, N. Kushida,T.Yanagida, K. Shishido, K. Aikawa, H.Toma, N. Inoue, O.Yamaguchi, K.Tanabe,T. Suzutani. Lack of antibodies against the antigen domain 2 epitope of cytomegalovirus (CMV) glycoprotein B is associated with CMVdisease after renal transplantation in recipients having the same glycoprotein H serotypes as their donors. Transpl Infect Dis 2011: 13: 318^323. All rights reserved Abstract: Cytomegalovirus (CMV) reinfection of seropositive individuals has been associated with adverse outcomes in organ transplantation and is a frequent cause of congenital infection. Previously we demonstrated that mismatching of CMVglycoprotein H (gH) serotypes was associated with CMVdisease after renal transplantation. Because the antigen domain 2 (AD2) epitope of glycoprotein B (gB) is conserved among CMV isolates and is one of the known targets of neutralizing antibodies, in this study we investigated whether antibodies against the epitope contribute to protection from CMVreinfection in renal transplantation, irrespective of gH serological matching. For this purpose, the gB and gH serology and clinical outcomes were analyzed retrospectively for 77 transplant recipients in the donor positive/recipient positive setting, who were managed by preemptive strategy.We found that there was a good negative correlation between the numbers of antigenemia-positive cells and the levels of antibodies against gB AD2 in the CMV-gH antibody matched group, but not in the CMV-gH antibody mismatched group. None of the recipients with antibodies against both gB AD2 and strain-speci¢c epitopes of gH have experienced CMVdisease during 6 month after transplantation, while 28% of those who lacked either/both antibody response needed preemptive therapy. Because the outcome was statistically signi¢cant, antibodies against gB AD2 can be a useful indicator to predict emergence of CMVdisease for preemptive therapy, in addition to antibodies against the mismatched gH types.                                                                                                                       Cytomegalovirus (CMV) infection is an important compli- cation of solid organ transplantation. CMVcauses serious CMVdisease in the immunosuppressed state that presents as fever, leukopenia, pneumonia, retinitis, hepatitis, myo- carditis, encephalitis, nephritis, enteritis, and pancreatitis (1).Therefore, antiviral drugs are given as a prophylactic or preemptive therapeutic strategy for the prevention of CMV after organ transplantation, especially for the CMV sero- negative recipients (R  ). It is well known that combina- tions of serostatus of donors and recipients are the important indicator for CMVdisease in transplantation. It is well known that some of the glycoproteins encoded by CMV induce strong antibody response, as do other viral components. Among the glycoproteins, glycoprotein H r 2010 John Wiley & Sons A/S Transplant Infectious Disease . ISSN 1398-2273 Key words: cytomegalovirus; glycoprotein H; glycoprotein B; renal transplantation; CMV disease; reinfection Correspondence to: Kei Ishibashi, MD, PhD, Department of Urology, Fukushima Medical University, 1 Hikarigaoka, Fukushima 960-1295, Japan Tel: 1 81 24 547 1316 Fax: 1 81 24 548 3393 E-mail: keikun@fmu.ac.jp Received 19 April 2010, revised 20 May, 9 June 2010, accepted for publication 21 June 2010 DOI: 10.1111/j.1399-3062.2010.00563.x Transpl Infect Dis 2011: 13: 318–323 318