Value of donor and recipient anti-CMV IgG titer in predicting CMV reactivation after allogeneic hematopoietic stem cell transplantation

Value of donor and recipient anti-CMV IgG titer in predicting CMV reactivation after allogeneic hematopoietic stem cell transplantation | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 8 December 2025 V1 Latest version Share on Value of donor and recipient anti-CMV IgG titer in predicting CMV reactivation after allogeneic hematopoietic stem cell transplantation Authors : Siwar Frigui 0009-0003-5675-7969 [email protected] , Salma Daly , Samia Rekaia , Yosra Chebbi , Hedia Bellali , Monia Ben Khaled , Monia Ouederni , and Wafa Achour Authors Info & Affiliations https://doi.org/10.22541/au.176518995.57222205/v1 247 views 107 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Despite advances in diagnosis and treatment, cytomegalovirus (CMV) reactivation remains a serious complication following allogeneic Hematopoietic Stem Cell Transplantation (allo-HSCT). Our objectives were to explore the impact of pre-transplant anti-CMV IgG titers in both donor and recipient on the occurrence of post-transplant CMV reactivation and to determine a threshold titer that would allow for better stratification of the post-transplant reactivation risk. We conducted a case-control study involving pediatric allo-HSCT recipients. We included 24 cases and 48 randomly selected controls. In univariate analysis, D-/R+ pre-transplant CMV serostatus (p=0.013), recipient anti-CMV IgG titer (p=0.012) and anti-CMV IgG titer R/D ratio (p=0.049) were associated with CMV reactivation. Donor anti-CMV IgG titer was a protective factor (p=0.046). Multivariate analysis showed that D-/R+ pre-transplant CMV serologic status (adjusted OR=6.874; 95% CI (1.37 – 34.4); p=0.019) and recipient anti-CMV IgG titer (adjusted OR=1.005; 95% CI (1.00 – 1.01); p=0.033) were independent risk factors. ROC curve analysis showed that optimal cut-off value to predict CMV reactivation was 113.75 AU/ml for the recipient anti-CMV IgG titer (Se=72.2%; Sp= 64.9%; AUC=0.701; p=0.016) and 1 for the anti-CMV IgG titer R/D ratio (Se=77.8%; Sp=78.4%; AUC=0.814; p113.75 AU/mL (50% versus 16%; p= 0.002) and in those with anti-CMV IgG titer R/D ratio >1 (64% versus 15%; p<0.001). In summary, we have shown that both pre-transplant anti-CMV IgG titer in recipient and anti-CMV IgG titer R/D ratio were associated with the risk of CMV reactivation following allo-HSCT. Furthermore, a high pre-transplant anti-CMV IgG titer in the donor would be a protective factor. These findings would be useful for better risk stratification of CMV reactivation and adaptation of surveillance strategies. INTRODUCTION Cytomegalovirus (CMV) reactivation remains one of the main complications of allogeneic Hematopoietic Stem Cell Transplantation (allo-HSCT). Although the preemptive strategy has proven effective in reducing the prevalence of CMV disease after allo-HSCT and its associated mortality, the frequency of CMV reactivation remains high, particularly in countries with high prevalence and where no prophylactic treatment with letermovir is administered [1,2]. Optimal control of risk factors would be the best way to control this infection in such conditions. Anti-CMV D-/R+ serostatus is the main factor determining this complication [3]. Some recent studies suggest that not only qualitative serological status is a risk factor for CMV reactivation, but also the anti-CMV IgG titer [4,5]. This quantitative parameter has been investigated in recipients, but to our knowledge not in donors. Our objectives were to explore the impact of pre-transplant anti-CMV IgG titers in both donor and recipient on the occurrence of post-transplant CMV reactivation and to determine a threshold titer that would allow for better stratification of the post-transplant reactivation risk. Study design A case-control study was performed over a 5-year period (from January 1 st , 2018 to December 31 st , 2022), involving allo-HSCT recipients from the Immunohematology and Pediatric Transplant Department at the National Bone Marrow Transplant Centre, Tunis. In the Pediatrics Department, a 5-bed transplant unit is dedicated to allo-HSCT for children under the age of 16, with an average of 30 allografts per year. The National Bone Marrow Transplant Centre is the only structure where allo-HSCT is performed in Tunisia. Case definition A case was defined as an allo-HSCT recipient who presented at least one episode of CMV reactivation within the first 100 days post-transplant confirmed by quantitative PCR on plasma. This test was performed weekly in all allograft recipients up to 100 days post-transplant, as part of our preemptive strategy. A CMV reactivation was defined by a viral load ≥ 150 IU/ml on plasma [6]. No prophylactic anti-CMV treatment was administered. Preemptive treatment with ganciclovir or foscarnet was started if the plasmatic viral load was ≥ 150 IU/ml, for at least 14 days and until a negative PCR in all cases. Patients transplanted for a primary immunodeficiency (PID) were not included (their pre-transplant serologies were not interpretable). Patients who received more than one allo-HSCT during the study period were also not included. Definition and selection of controls For every case, two controls were selected randomly out of the pool of patients with allo-HSCT who did not have CMV reactivation up to 100 days post-transplant. They received the allograft in the same period as cases did and they had at least a 100-day follow-up after allo-HSCT. As well as cases, patients transplanted for PID and those who received more than one allo-HSCT during the study period were not included. Patients who presented CMV disease without viremia (negative CMV PCR on plasma) were excluded from the group of controls. CMV serology for the measurement of anti-CMV IgG CMV serologies were performed in both donor and recipient prior to transplantation. Determination of anti-CMV IgG titer was performed by electrochemiluminescence (ECLIA) (Cobas e601, Roche®). The limits of quantification for this technique ranged from 1 to 500 AU/ml. Levels above the upper limit of quantification were expressed as > 500 AU/ml. For statistical analysis, an anti-CMV IgG level > 500 AU/mL was considered equal to 500 AU/mL. For each donor/recipient pair, the ratio of the anti-CMV IgG titer in the recipient to that in the donor (anti-CMV IgG titer R/D ratio) was calculated. When calculating this ratio, values > 500 AU/ml were excluded. CMV Viral Load Detection and quantification of the CMV genome were carried out by automated real-time PCR, COBAS® Ampliprep / COBAS® TaqMan®, with a detection threshold of 60 cp/mL and a quantification range from 150 to 10 7 cp/ml (1 cp = 0.91 IU). Data collection The following data was retrospectively collected from medical records: age and sex of both recipient and donor, HLA compatibility between recipient and donor, underlying pathology, pre-transplant CMV serologic status of both recipient and donor, including anti-CMV IgG titer, type of pre-transplant conditioning, Graft versus Host Disease (GvHD) prophylaxis, occurrence of rejection (primary or secondary) and acute GvHD. Statistical analysis Data are presented as percentages for qualitative variables or as mean ± standard deviation for quantitative variables. The comparison of clinical features between cases and controls was performed using the Chi-square test or Fisher’s exact test (when applicable) for categorical variables or the student t test for independent samples for continuous variables. Crude Odds ratios (OR) were calculated using the Mantel-Haenszel method to identify potential risk factors for CMV reactivation. Multivariate analysis was performed using stepwise logistic regression. Variables were introduced into the model if they had a p value less than 0.20 in the univariate analysis. A p value <0.05 was considered statistically significant. ROC curves were plotted to determine cut-offs predictive of CMV reactivation for recipient anti-CMV IgG titer and anti-CMV IgG R/D ratio. Ethical issues The study was approved by the Ethics Committee of the National Bone Marrow Transplant Center of Tunis (Ref. number: CNGMOEC-1124). Patient confidentiality was respected throughout the study, thanks to anonymous data collection. The retrospective nature of the study had no influence on the quality of care. RESULTS During the study period, 130 patients received an allo-HSCT in the Pediatrics Department at our center. We identified 24 cases of CMV reactivation (Fig. 1). The median time until the CMV reactivation was 35 days post-transplant (IQR, 12 to 54 days). Table I summarizes demographic and clinical data from our patients and shows univariate comparisons between cases and controls for each studied variable. In univariate analysis, factors associated with CMV reactivation were D-/R+ pre-transplant CMV serostatus (p=0.013), recipient anti-CMV IgG titer (p=0.012), anti-CMV IgG titer R/D ratio (p=0.049), HLA haploidentical related donor (p=0.0001), GvHD prophylaxis with combination of cyclosporin A, cyclophosphamide and mycophenolate mofetil (p=0.0001), acute GvHD (p=0.001) and corticosteroids (p=0.0001). Donor anti-CMV IgG titer was a protective factor (p=0.046) (Table I). Multivariate analysis showed that male donor gender (adjusted OR=4.919; 95% CI (1.103 – 21.942); p=0.037), D-/R+ pre-transplant CMV serologic status (adjusted OR=6.874; 95% CI (1.372 – 34.444); p=0.019), recipient anti-CMV IgG titer (adjusted OR=1.005; 95% CI (1.000 – 1.010); p=0.033), HLA haploidentical related donor (adjusted OR=5.472; 95% CI (1.334 – 22.453); p=0.018) and acute GvHD (OR=7.116; 95% CI (1.770 – 28.604) ; p=0.006) were independent risk factors for CMV reactivation after allo-HSCT (Table II). We calculated, from ROC curve analysis (Fig. 2), sensitivity and specificity for the optimal cut-off value for the recipient anti-CMV IgG titer and the anti-CMV IgG titer R/D ratio to predict CMV reactivation after allo-HSCT. The optimal cut-off value for the recipient anti-CMV IgG titer was 113.75 AU/ml, with a sensitivity of 72.2% and a specificity of 64.9% (Table III). The optimal cut-off value for the anti-CMV IgG titer R/D ratio was 1, with a sensitivity of 77.8% and a specificity of 78.4% (Table III). The prevalence of CMV reactivation was higher in patients with pre-transplant anti-CMV IgG titer anti-CMV IgG titer R/D ratio >1 (64% versus 15%; p<0.001). DISCUSSION CMV reactivation remains the most frequent viral infection after allo-HSCT. Before the advent of letermovir (a molecule not yet available in Tunisia and in many other countries), preemptive treatment was the method of choice for CMV disease prevention in the majority of HSCT centers around the world, including our center [2,7]. This approach has gained in effectiveness with the introduction of PCR, which has proved reliable for CMV detection [8]. Weekly monitoring between D7 and D100 post-transplant is currently recommended using quantitative PCR (on whole blood or plasma) [7]. All patients included in our study, both cases and controls, had weekly PCR monitoring on plasma until D100 post-transplant or beyond. Pre-transplant CMV serologic status remains the most important determinant of CMV reactivation after allo-HSCT in the era of preemptive therapy [9]. In our study, a D-/R+ status was an independent risk factor for CMV reactivation. It’s known in the literature that CMV reactivation was more frequent in recipients with previous contact with CMV (R+) prior to transplantation, especially if the donor was seronegative (D-) [3,10]. On the other hand, a donor with previous contact with CMV (D+) seemed to protect the recipient. Indeed, the graft from the seropositive donor (D+) provides mature T lymphocytes specific to the virus, thus enabling the host’s immunity to be restored [11,12]. The prognosis of patients who underwent HSCT depends significantly on the CMV serostatus of their donors. If the donors are CMV-positive, immune recovery in recipients after transplantation is faster, with a higher number of CD4+CD25 high T lymphocytes specific to CMV being recorded, compared with transplants from seronegative donors [13]. In our study, we were able to demonstrate that not only qualitative anti-CMV serostatus is a risk factor, but also that anti-CMV IgG titer is associated with CMV reactivation: the higher the IgG anti-CMV titer in the recipient, the higher the risk of reactivation, and conversely, the higher the IgG anti-CMV titer in the donor, the lower the risk. Similar results regarding recipient anti-CMV IgG titer have been reported in some recent studies [4,5]. The recipient IgG anti-CMV titer could reflect the subclinical activity of the latent viral reservoir [14]. Thus, a high IgG titer represents a higher latent CMV viral load in the recipient’s body. In immunocompetent hosts, attempts at reactivation are suppressed by the adaptive immune response. Following allo-HSCT, the process of immune reconstitution compromises this ability, particularly in patients with high pre-transplant anti-CMV IgG titers [15]. Furthermore, anti-CMV IgG titer increases with each episode of CMV reactivation due to a more effective immune response compared to primary infection [16]. Since a history of CMV reactivation is a risk factor for post-transplant reactivation, a high anti-CMV IgG titer in the recipient could be a biological marker of previous CMV reactivations, associated with a higher risk of post-transplant reactivation of CMV. In univariate analysis, a high pre-transplant anti-CMV IgG titer in the donor was a protective factor against CMV reactivation. Although immune control of CMV infection is primarily cellular, some studies suggest that humoral immunity contributes to the control of viremia during CMV reactivation [17,18]. Hypotheses that may explain the protective activity of anti-CMV antibodies include early neutralization of the virus in its extracellular phase and improved phagocytosis of CMV-infected cells for more effective opsonization [18]. In fact, intravenous injections of human immunoglobulins containing high titers of anti-CMV neutralizing antibodies can be used as an adjuvant treatment for CMV reactivation after HSCT [19]. Based on ROC curves analysis, threshold values were identified for both the recipient pre-transplant anti-CMV IgG titer (113.75) and the anti-CMV IgG titer R/D ratio (1), with good sensitivity and specificity values. A comparable threshold of recipient anti-CMV IgG titer of around 100 AU/mL was reported by Arcuri et al, with a significantly higher CMV reactivation incidence in recipients with titers above the threshold [5]. CMV diseases were observed exclusively in the group of patients with a pre-transplant anti-CMV IgG titer above the threshold [4]. Since CMV reactivation depends on the anti-CMV IgG titer in both recipient and donor, the sensitivity and specificity values were better for the ratio threshold value than for the recipient anti-CMV IgG titer. In our study, the ratio cut-off was 1, which means that the lower the recipient’s titer compared to the donor’s, the lower the risk of reactivation. These results would be useful for better risk stratification of CMV reactivation and adaptation of surveillance strategies. Even in the era of letermovir prophylaxis, it’s always useful to identify a group of high-risk patients who should benefit from closer monitoring and, if necessary, earlier therapeutic intervention, especially after discontinuation of prophylaxis [14]. Our study has some limitations to mention. The exact value of IgG anti-CMV titers >500 was not determined (no routine dilution performed), so we could not explore the performance of higher cut-offs and their potential relationship with the risk of CMV reactivation. Another potential limitation is that we reported serological results in AU/ml (other manufacturers may use different units of measurement). This compromises comparability between different studies. Indeed, there is currently no common standard for comparison. Furthermore, the retrospective nature of this study resulted in missing data and the small sample size reduces the performance of statistical analyses. Additional studies, particularly prospective multicenter studies, would be necessary to refine our findings. We recommend diluting sera with an anti-CMV IgG titer above the upper limit of quantification. CONCLUSION CMV serology remains the only test available prior to transplantation to assess the risk of CMV occurrence post-transplantation. So far, the determination of CMV serostatus in transplant recipients has been used as a qualitative parameter. In this study, we have shown that both pre-transplant anti-CMV IgG titer in recipient and anti-CMV IgG titer R/D ratio were associated with the risk of CMV reactivation following allo-HSCT. Furthermore, a high pre-transplant anti-CMV IgG titer in the donor would be a protective factor. More studies are needed to explore how these findings can be incorporated into the CMV reactivation risk algorithm. CONFLICT OF INTEREST None. REFERENCES 1. Marty FM, Ljungman P, Chemaly RF, Maertens J, Dadwal SS, Duarte RF, et al. Letermovir Prophylaxis for Cytomegalovirus in Hematopoietic-Cell Transplantation. N Engl J Med. 2017 Dec 21;377(25):2433–44. 2. Boeckh M, Ljungman P. How we treat cytomegalovirus in hematopoietic cell transplant recipients. Blood. 2009 Jun 4;113(23):5711–9. 3. Dziedzic M, Sadowska-Krawczenko I, Styczynski J. Risk Factors for Cytomegalovirus Infection After Allogeneic Hematopoietic Cell Transplantation in Malignancies: Proposal for Classification. Anticancer Res. 2017 Dec;37(12):6551–6. 4. Kawamura S, Nakasone H, Takeshita J, Kimura S ichi, Nakamura Y, Kawamura M, et al. Prediction of Cytomegalovirus Reactivation by Recipient Cytomegalovirus-IgG Titer before Allogeneic Hematopoietic Stem Cell Transplantation. 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George B, Pati N, Gilroy N, Ratnamohan M, Huang G, Kerridge I, et al. Pre-transplant cytomegalovirus (CMV) serostatus remains the most important determinant of CMV reactivation after allogeneic hematopoietic stem cell transplantation in the era of surveillance and preemptive therapy. Transpl Infect Dis Off J Transplant Soc. 2010 Aug 1;12(4):322–9. 10. Zhou W, Longmate J, Lacey SF, Palmer JM, Gallez-Hawkins G, Thao L, et al. Impact of donor CMV status on viral infection and reconstitution of multifunction CMV-specific T cells in CMV-positive transplant recipients. Blood. 2009 Jun 18;113(25):6465–76. 11. Grob JP, Grundy JE, Prentice HG, Griffiths PD, Hoffbrand AV, Hughes MD, et al. Immune donors can protect marrow-transplant recipients from severe cytomegalovirus infections. Lancet Lond Engl. 1987 Apr 4;1(8536):774–6. 12. Ljungman P, Brand R, Einsele H, Frassoni F, Niederwieser D, Cordonnier C. Donor CMV serologic status and outcome of CMV-seropositive recipients after unrelated donor stem cell transplantation: an EBMT megafile analysis. Blood. 2003 Dec 15;102(13):4255–60. 13. Jaskula E, Dlubek D, Tarnowska A, Lange J, Mordak-Domagala M, Suchnicki K, et al. Anti-CMV-IgG positivity of donors is beneficial for alloHSCT recipients with respect to the better short-term immunological recovery and high level of CD4+CD25high lymphocytes. Viruses. 2015 Mar 23;7(3):1391–408. 14. Eberhardt KA, Jung V, Knops E, Heger E, Wirtz M, Steger G, et al. CMV-IgG pre-allogeneic hematopoietic stem cell transplantation and the risk for CMV reactivation and mortality. Bone Marrow Transplant. 2023 Jun;58(6):639–46. 15. Griffiths P, Reeves M. Pathogenesis of human cytomegalovirus in the immunocompromised host. Nat Rev Microbiol. 2021 Dec;19(12):759–73. 16. Linde GA, Hammarström L, Persson MA, Smith CI, Sundqvist VA, Wahren B. Virus-specific antibody activity of different subclasses of immunoglobulins G and A in cytomegalovirus infections. Infect Immun. 1983 Oct;42(1):237–44. 17. Goldstein G, Rutenberg TF, Mendelovich SL, Hutt D, Oikawa MT, Toren A, et al. The role of immunoglobulin prophylaxis for prevention of cytomegalovirus infection in pediatric hematopoietic stem cell transplantation recipients. Pediatr Blood Cancer. 2017 Jul;64(7). 18. Pouteil-Noble C, Touraine JL, Gibert R, Aymard M. [Clinical use of immunoglobulin titers of anti-cytomegalovirus antibodies]. Rev Fr Transfus Immunohematol. 1984 Jun;27(3):365–74. 19. Zhang P, Yang D, Tian J, Feng S, Jiang E, Han M. A clinical study of lyophilized intravenous human immunoglobulin containing high-titer cytomegalovirus-neutralizing antibody for the treatment of cytomegalovirus viremia after allogeneic hematopoietic stem cell transplantation. Ann Palliat Med. 2021 May;10(5):5533–40. Figure 1. Flow chart of patient recruitment Figure 2. ROC curves for recipient anti-CMV IgG titer and anti-CMV IgG titer R/D ratio TABLE I. Univariate analysis of potential risk factors for CMV reactivation in HSCT recipients Variable Cases (n=24) Controls (n=48) Crude Odd-Ratio (95% CI) p value Demographics Recipient gender Male Female 15 (63%) 9 (37%) 25 (52%) 23 (48%) 1.53 (0.56 – 4.18) 0.402 Donor gender Male Female 16 (67%) 8 (33%) 23 (48%) 25 (52%) 2.17 (0.78 – 6.03) 0.132 Gender mismatch Yes No 15 (63%) 9 (37%) 26 (54%) 22 (46%) 1.41 (0.52 – 3.84) 0.501 Recipient age (years) 4.36 ± 3.99 5.80 ± 3.84 NA 0.144 Donor age (years) 24.21 ± 14.49 18.33 ± 16.79 NA 0.148 Pre-transplant CMV serology CMV serologic status D+/R+ D+/R- D-/R+ D-/R- 16 (70%) 0 7 (30%) 0 39 (81%) 2 (4%) 5 (10%) 2 (4%) NA 0.118 CMV serologic status D-/R+ Others 8 (35%) 15 (65%) 5 (10%) 43 (90%) 4.59 (1.30 – 16.21) 0.013 Recipient anti-CMV IgG titer (AU/ml) 203.34 ± 139.12 115.94 ± 131.20 NA 0.012 Donor anti-CMV IgG titer (AU/ml) 162.35 ± 175.29 255.47 ± 186.76 NA 0.046 Anti-CMV IgG titer R/D ratio 238.61 ± 479.52 6.71 ± 18.38 NA 0.049 Underlying pathology Acute leukemia Aplastic anemia Hemoglobinopathy 17 (71%) 3 (12%) 4 (17%) 23 (48%) 15 (31%) 10 (21%) NA 0.142 Acute leukemia Others 17 (71%) 7 (29%) 23 (48%) 25 (52%) 2.64 (0.93 – 7.52) 0.065 HLA compatibility HLA haploidentical related donor HLA genoidentical related donor 13 (54%) 11 (46%) 7 (15%) 41 (85%) 6.92 (2.23 – 21.53) 0.0001 Pre-transplant conditioning Myeloablative Not myeloablative 24 (100%) 0 43 (90%) 5 (10%) 1.56 (1.30 – 1.86) 0.101 GvHD prophylaxis CSA+MMF+CYC Others 13 (54%) 11 (46%) 7 (15%) 41 (85%) 6.92 (2.23 – 21.53) 0.0001 Antilymphocyte serum Yes No 6 (25%) 18 (75%) 16 (33%) 32 (67%) 0.67 (0.22 – 2.01) 0.469 Acute GvHD Yes No 16 (67%) 8 (33%) 12 (25%) 36 (75%) 6.00 (2.06 – 17.51) 0.001 Corticosteroids Yes No 14 (58%) 10 (42%) 6 (12%) 42 (88%) 9.80 (3.01 – 31.86) 0.0001 Primary rejection Yes No 1 (4%) 23 (96%) 1 (2%) 47 (98%) 2.04 (0.12 – 34.16) 0.612 Secondary rejection Yes No 0 24 (100%) 1 (2%) 47 (98%) 0.66 (0.56 – 0.78) 0.476 CMV: Cytomegalovirus; CSA: Cyclosporin A; CYC: Cyclophosphamide D: Donor; GvHD: Graft versus Host Disease; MMF: Mycophenolate Mofetil; NA: Not applicable; R: Recipient. TABLE II. Multivariate analysis of potential risk factors for CMV reactivation in HSCT recipients Donor gender Male Female 16 (67%) 8 (33%) 23 (48%) 25 (52%) 4.919 (1.103 – 21.942) 0.037 Pre-transplant CMV serology CMV serologic status D-/R+ Others 8 (35%) 15 (65%) 5 (10%) 43 (90%) 6.874 (1.372 – 34.444) 0.019 Recipient anti-CMV IgG titer 203.34 ± 139.12 115.94 ± 131.20 1.005 (1.000 – 1.010) 0.033 HLA compatibility HLA haploidentical related donor HLA genoidentical related donor 13 (54%) 11 (46%) 7 (15%) 41 (85%) 5.472 (1.334 – 22.453) 0.018 Acute GvHD Yes No 16 (67%) 8 (33%) 12 (25%) 36 (75%) 7.116 (1.770 – 28.604) 0.006 CMV: Cytomegalovirus; D: Donor; GvHD: Graft versus Host Disease; R: Recipient. TABLE III. Area under the ROC curves and Cut-off values of recipient anti-CMV IgG titer and anti-CMV IgG R/D ratio Area under the ROC curve 0.701 0.814 95% Confidence Interval (0.562 – 0.841) (0.700 – 0.928) p value 0.016 0.0001 Cut-off value 113.75 1 Sensitivity 72.2% 77.8% Specificity 64.9% 78.4% Information & Authors Information Version history V1 Version 1 08 December 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords epidemiology human cytomegalovirus immune responses immunoglobulin infection transplantation virus classification Authors Affiliations Siwar Frigui 0009-0003-5675-7969 [email protected] Centre National de Greffe de la Moelle Osseuse View all articles by this author Salma Daly Centre National de Greffe de la Moelle Osseuse View all articles by this author Samia Rekaia Centre National de Greffe de la Moelle Osseuse View all articles by this author Yosra Chebbi Centre National de Greffe de la Moelle Osseuse View all articles by this author Hedia Bellali Universite de Tunis El Manar Faculte de Medecine de Tunis View all articles by this author Monia Ben Khaled Centre National de Greffe de la Moelle Osseuse View all articles by this author Monia Ouederni Centre National de Greffe de la Moelle Osseuse View all articles by this author Wafa Achour Centre National de Greffe de la Moelle Osseuse View all articles by this author Metrics & Citations Metrics Article Usage 247 views 107 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Siwar Frigui, Salma Daly, Samia Rekaia, et al. Value of donor and recipient anti-CMV IgG titer in predicting CMV reactivation after allogeneic hematopoietic stem cell transplantation. Authorea . 08 December 2025. DOI: https://doi.org/10.22541/au.176518995.57222205/v1 If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu . 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