Abstract
Human T-Cell Lymphotropic Virus Types 1 and 2 (HTLV-1/2) are delta retroviruses. HTLV-1 may lead to complications including adult T-cell leukemia-lymphoma (ATLL) and HTLV-1-associated myelopathy (HAM). Immunosuppression may result in progression from an asymptomatic carrier state to ATLL. Data on the safety of stem cell transplantation (SCT) in patients with HTLV-1/2 infection are lacking. The Center for International Blood and Marrow Transplant Research (CIBMTR) research database was queried for patients who tested positive for HTLV infection in the pre-transplantation workup and underwent either autologous SCT (AutoSCT) or allogeneic SCT (AlloSCT). Patients were excluded if they underwent SCT for ATLL. The primary outcome was overall survival at three and four years post-SCT. In those who underwent AutoSCT, 54 patients were HTLV-positive and 9,836 were HTLV-negative. In those who underwent AlloSCT, 105 patients were HTLV-positive and 18,077 were HTLV-negative. No difference in overall survival was noted in HTLV-positive patients vs HTLV-negative patients at three years following AutoSCT (76% vs 77%; p=0.916). Inferior overall survival (32% vs 46%; p=0.017) and non-relapse mortality (35% vs 27%; p=0.030) were observed in HTLV-positive patients at four years following AlloSCT. Future work should examine the mechanism by which HTLV-1/2 impact survival in AlloSCT recipients.
Keywords: Human T-Cell Lymphotropic Virus Type 1, Stem Cell Transplantation
Introduction
Human T-Cell Lymphotropic Virus Type 1 (HTLV-1) is a delta retrovirus endemic to Japan and the Caribbean islands;1 its complications include adult T-cell leukemia-lymphoma (ATLL) and HTLV-1-associated myelopathy (HAM).2 HTLV-2 is endemic among people who inject drugs in the United States and Europe, American Indian populations, and Brazil.3 HTLV-2 infrequently causes HAM. Historically, it was difficult to distinguish HTLV-1 infection from HTLV-2 infection.4 Less than 5% of patients with HTLV-1 will go on to develop ATLL; the time from latency to disease progression is typically greater than ten years.5 Immunosuppression may be a risk factor for HTLV-1 reactivation and development of ATLL, a finding demonstrated in case series of renal transplant recipients.6,7,8 There are limited data on HTLV-1/2 patient outcomes after bone marrow transplantation.9
Methods
The Center for International Blood and Marrow Transplant Research (CIBMTR) collects data from over 500 transplant centers worldwide; participating centers report all consecutive transplants. Computerized error checks, physician review of submitted data and on-site audits of participating centers ensure data quality. Observational studies conducted by the CIBMTR are performed in compliance with all applicable federal regulations pertaining to the protection of human research participants.
The CIBMTR was queried for data on all adult patients 18 years or older who tested positive in the pre-transplantation period for HTLV-1 or 2 antibodies based on CIBMTR Form 2000, Question 64 “HTLV-1 antibody”. Patients listed as “Reactive” on this question were compared with those marked “Non-reactive”. Of note, CIBMTR instructions are to include positive HTLV-2 serologies as being reactive for HTLV-1. Further break down of HTLV-1 vs 2 testing is not collected by CIBMTR. Data provided by CIBMTR included summary tables of demographic characteristics and unadjusted survival comparisons between HTLV-positive and negative groups. All included patients underwent either AutoSCT or AlloSCT. Patients who were transplanted for ATLL were excluded from the study. We examined these two groups for baseline demographic and transplant-related characteristics. The outcomes of interest were overall survival (OS) and non-relapse mortality (NRM) at 1-year, 2-years, and 3-years post-transplantation. Outcomes at 4-years post-transplantation were also included for AlloSCT.
Statistical Analysis
HTLV-positive and negative group demographic and treatment-related variables were compared in summary tables for evidence of possible confounders using a chi-square test or Fisher’s exact test, as appropriate. The Kaplan–Meier and log-rank test were used to estimate and compare OS. The cumulative Incidence Function and Fine and Gray’s test was used to estimate and compare NRM rates. Data for patients who were alive or lost to follow-up were censored for OS at the time they were last known to be alive. No adjustment for differences in patient-, disease- or treatment-related variables was performed due to limitations in the available data. Summary table analyses were conducted using SAS v9.4 with p<0.05 considered statistically significant.
Results
Data were obtained for those who underwent AutoSCT or AlloSCT between 2008–2017. Among AutoSCT patients, fifty-four tested positive for HTLV-1/2 and 9,836 tested negative, and 989 had an unknown HTLV status (Table 1a). The median age in the HTLV-positive group was 56 (range 31–74), compared to 59 (range 18–82) in the HTLV-negative group. The majority of patients who tested positive or negative underwent AutoSCT for a plasma cell disorder (54% and 62% respectively) and Non-Hodgkin lymphoma (NHL) (33% and 26% respectively). In those who underwent AutoSCT, women were more prevalent in the HTLV-positive group compared to men (57% vs 42%; p=0.02). There was no significant difference by HTLV status in the numbers of patients who underwent AutoSCT for the three major indications (Hodgkin lymphoma (HL), NHL, and plasma cell disorders). There was no significant difference in OS between the HTLV-negative and HTLV-positive groups at three years post-AutoSCT (77% vs 76%; p=0.916). The most common cause of death in both groups was relapse of primary disease (Table 2a).
Table 1a. Characteristics of patients who underwent AutoSCT by HTLV serostatus reported to CIBMTR 2008–2017.
| Characteristic | HTLV Negative (n, %) | HTLV Positive (n,%) | P-Value | ||
|---|---|---|---|---|---|
| No. of patients | 9836 | 54 | |||
| Patient age - no. (%) | 0.1108^ | ||||
| Median (min-max) | 59 (18–82) | 56 (31–74) | |||
| 18 – 30 | 532 (5) | 0 (0) | |||
| 31 – 40 | 624 (6) | 4 (7) | |||
| 41 – 50 | 1478 (15) | 11 (20) | |||
| 51 – 60 | 3215 (33) | 24 (44) | |||
| 61 – 70 | 3402 (35) | 13 (24) | |||
| 71+ | 585 (6) | 2 (4) | |||
| Sex - no. (%) | 0.025* | ||||
| Male | 5676 (58) | 23 (43) | |||
| Female | 4160 (42) | 31 (57) | |||
| Race - no. (%) | |||||
| Caucasian | 6888 (70) | 25 (46) | 0.0001* | ||
| African-American | 2176 (22) | 25 (46) | <0.0001* | ||
| Asian | 341 (3) | 3 (6) | 0.4367^ | ||
| Pacific islander | 18 (0) | 0 (0) | >0.9999^ | ||
| Native American | 81 (1) | 0 (0) | >0.9999^ | ||
| More than one race | 51 (1) | 1 (2) | 0.2483 | ||
| Missing | 281 (3) | 0 (0) | |||
| HCT-CI - no. (%) | 0.4390 | ||||
| 0 | 3111 (32) | 18 (33) | |||
| 1 | 1385 (14) | 5 (9) | |||
| 2 | 1553 (16) | 6 (11) | |||
| 3+ | 3709 (38) | 25 (46) | |||
| Missing | 78 (1) | 0 (0) | |||
| Disease - no. (%) | 0.0882 | ||||
| Non-Hodgkin lymphoma | 2532 (26) | 18 (33) | |||
| Hodgkin lymphoma | 736 (7) | 2 (4) | |||
| Plasma cell disorder/multiple myeloma | 6146 (62) | 29 (54) | |||
| Other | 390 (4) | 5 (0) | |||
| CMV Status – no. (%) | 0.001639* | ||||
| Negative | 3735 (38) | 9 (17) | |||
| Positive | 5968 (61) | 45 (83) | |||
| Not Reported | 133 (1) | 0 (0) | |||
|
| |||||
| HTLV Negative (N = 9836) | HTLV Positive (N = 54) | ||||
| Outcomes | N | % (95% CI) | N | % (95% CI) | P Value |
|
| |||||
| Overall Survival | 9835 | 54 | 0.916 | ||
| 1-year | 90 (90–91)% | 89 (79–96)% | |||
| 2-year | 83 (83–84)% | 81 (69–90)% | |||
| 3-year | 77 (77–78)% | 76 (62–87)% | |||
All p-values calculated using a Chi-Square test except when designated with (^), then Fisher’s Exact Test performed
Significant at alpha level = 0.05
HCT-CI: Hematopoietic Cell Transplantation -Comorbidity Index
Table 2a:
Cause of Death by HTLV Status following AutoSCT
| Cause of Death by HTLV Status | ||||
|---|---|---|---|---|
| HTLV Status | ||||
| Negative | Positive | Total | ||
|
Occurrences (n)
Percent (%) Chi-Square P-Valuê |
Primary disease | 2388 | 13 | 2401 |
| 71.54 | 81.25 | |||
| 0.5796^ | ||||
| Graft failure | 4 | 0 | 4 | |
| 0.12 | 0 | |||
| >0.9999^ | ||||
| Infection | 152 | 0 | 152 | |
| 4.55 | 0 | |||
| >0.9999^ | ||||
| Acute Respiratory Distress Syndrome/Pneumonitis |
45 | 0 | 45 | |
| 1.35 | 0 | |||
| >0.9999^ | ||||
| Organ failure/toxicity | 181 | 0 | 181 | |
| 5.42 | 0 | |||
| >0.9999^ | ||||
| Secondary malignancy | 136 | 0 | 136 | |
| 4.07 | 0 | |||
| >0.9999^ | ||||
| Other cause | 269 | 2 | 271 | |
| 8.06 | 12.5 | |||
| 0.3566^ | ||||
| Not Reported | 130 | 1 | 131 | |
| 3.89 | 6.25 | |||
| Total | 3338 | 16 | 3354 | |
In the AlloSCT group, 126 patients tested positive for HTLV-1/2 and 18,077 tested negative, and 2824 patients had an unknown HTLV status (Table 1b). Twenty-one patients underwent AlloSCT for ATLL and were excluded from the analysis. The median age in the HTLV-positive and negative groups were 56 (18–74) and 55 (18–88) respectively. There were 27 donors that were HTLV-positive in the HTLV-positive group, and none in the HTLV-negative group. There was a higher rate of prior CMV infection in the HTLV-positive group compared to the HTLV-negative group. Selection of graft-versus-host disease prophylaxis and donor type were not significantly different between groups. The most common indications for AlloSCT were acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) in both groups. NHL/other leukemia was disproportionately represented in the HTLV-positive group (19% vs 11%; P=0.004), even after excluding cases categorized as ATLL. Inferior OS (32% vs 46%; p=0.017; Figure 1a) and NRM (37% vs 25%; p=0.030; Figure 1b) were noted in the HTLV-positive group compared to the HTLV-negative group at 4 years post-AlloSCT in this unadjusted analysis. There was no predominant cause of death (ie GVHD or infection) to explain the increased NRM in the HTLV-positive group (Table 2b).
Table 1b: Characteristics of patients who underwent AlloSCT by HTLV serostatus reported to CIBMTR 2008–2017.
| Characteristic | HTLV Negative | HTLV Positive | Chi Square P-Value | ||||
|---|---|---|---|---|---|---|---|
| No. of patients | 18077 | 105 | |||||
| Patient age - no. (%) | 0.4711 | ||||||
| Median (min-max) | 55 (18–88) | 56 (18–74) | |||||
| 18 – 30 | 2402 (13) | 13 (12) | |||||
| 31 – 40 | 1898 (10) | 7 (7) | |||||
| 41 – 50 | 2931 (16) | 20 (19) | |||||
| 51 – 60 | 4948 (27) | 29 (28) | |||||
| 61 – 70 | 5101 (28) | 28 (27) | |||||
| 71+ | 797 (4) | 8 (8) | |||||
| Sex - no. (%) | 0.4101 | ||||||
| Male | 10532 (58) | 57 (54) | |||||
| Female | 7545 (42) | 48 (46) | |||||
| Race - no. (%) | |||||||
| Caucasian | 14903 (82) | 91 (87) | 0.2563 | ||||
| African-American | 1497 (8) | 9 (9) | 0.9143 | ||||
| Asian | 827 (5) | 2 (2) | 0.2434^ | ||||
| Pacific islander | 69 (0) | 1 (1) | 0.3338^ | ||||
| Native American | 104 (1) | 0 (0) | >0.9999^ | ||||
| More than one race | 114 (1) | 0 (0) | >0.9999^ | ||||
| Missing | 563 (3) | 2 (2) | |||||
| HCT-CI - no. (%) | 0.3857 | ||||||
| 0 | 4881 (27) | 30 (29) | |||||
| 1 | 2571 (14) | 13 (12) | |||||
| 2 | 2532 (14) | 13 (12) | |||||
| 3+ | 8000 (44) | 48 (46) | |||||
| Missing | 93 (1) | 1 (1) | |||||
| Disease - no. (%) | |||||||
| AML | 7068 (39) | 31 (30) | 0.0449* | ||||
| ALL | 2020 (11) | 12 (11) | 0.9343 | ||||
| CML | 643 (4) | 3 (3) | >0.9999^ | ||||
| MDS | 5149 (28) | 33 (31) | 0.5051 | ||||
| Non-Hodgkin lymphoma/other leukemia | 1895 (11) | 20 (19) | 0.0044* | ||||
| Severe aplastic anemia | 634 (4) | 2 (2) | 0.5903 | ||||
| Other | 668 (4) | 4 (4) | 0.7965 | ||||
| Conditioning regimen intensity - no. (%) | 0.4374 | ||||||
| MAC | 9265 (51) | 48 (46) | |||||
| RIC | 5525 (31) | 34 (32) | |||||
| NMA | 2779 (15) | 20 (19) | |||||
| Missing | 508 (3) | 3 (3) | |||||
| GVHD prophylaxis - no. (%) | 0.1422 | ||||||
| Post-CY | 1756 (10) | 4 (4) | |||||
| TAC or CSA + MMF ± other(s) (except post-CY) | 5013 (28) | 30 (29) | |||||
| TAC or CSA + MTX ± other(s) (except MMF, post-CY) | 8243 (46) | 50 (48) | |||||
| Other(s) | 2861 (16) | 16 (15) | |||||
| Missing | 204 (1) | 5 (5) | |||||
| Donor type - no. (%) | 0.8492 | ||||||
| Related | 4906 (27) | 30 (29) | |||||
| Other related | 1934 (11) | 8 (8) | |||||
| Unrelated (8/8) | 8683 (48) | 52 (50) | |||||
| Multi-donor | 52 (0) | 0 (0) | |||||
| Cord blood | 2502 (14) | 15 (14) | |||||
| Graft type in merge - no. (%) | 0.4154 | ||||||
| Bone marrow | 2731 (15) | 11 (10) | |||||
| Peripheral blood | 12844 (71) | 79 (75) | |||||
| Umbilical cord blood | 2502 (14) | 15 (14) | |||||
| Recipient CMV Status - no. (%) | 0.002478* | ||||||
| Negative | 6448 (36) | 22 (21) | |||||
| Positive | 11510 (64) | 82 (78) | |||||
| Not Reported | 119 (1) | 1 (1) | |||||
| Donor HTLV - no. (%) | >0.9999^ | ||||||
| Negative | 7644 (42) | 45 (43) | |||||
| Positive | 27 (0) | 0 (0) | |||||
| Not Reported | 10406 (58) | 60 (57) | |||||
| HTLV Negative (N = 18077) | HTLV Positive (N = 105) | ||||||
| Outcome | N | % (95% CI) | N | % (95% CI) | P Value | ||
|
| |||||||
| Overall Survival | 18069 | 105 | 0.017 | ||||
| 1-year | 65 (64–65)% | 61 (51–70)% | |||||
| 2-year | 55 (54–56)% | 45 (36–55)% | |||||
| 3-year | 50 (49–51)% | 38 (29–47)% | |||||
| 4-year | 46 (46–47)% | 32 (23–42)% | |||||
|
| |||||||
| HTLV Negative (N = 17166) | HTLV Positive (N = 101) | ||||||
| Outcome | N | % (95% CI) | N | % (95% CI) | P Value | ||
|
| |||||||
| Non-relapse mortality | 16802 | 99 | 0.030 | ||||
| 1-year | 18 (18–19)% | 24 (16–33)% | |||||
| 2-year | 22 (21–22)% | 34 (25–43)% | |||||
| 3-year | 24 (23–24)% | 35 (26–44)% | |||||
| 4-year | 25 (24–26)% | 37 (28–47)% | |||||
All p-values calculated using a Chi-Square test except when designated with (^), then Fisher’s Exact Test performed
Significant at alpha level = 0.05
AML: Acute myeloid leukemia; ALL: Acute lymphoblastic leukemia; CML: Chronic myeloid leukemia; MDS: myelodysplastic syndrome; MAC: myeloablative conditioning; RIC: Reduced intensity conditioning; NMA: Non-myeloablative; CY: cyclophosphamide; TAC: tacrolimus; CSA: cyclosporine A; MMF: mycophenolate mofetil; MTX: methotrexate
Figure 1a:
Kaplan-Meier overall survival curves for allogeneic stem cell transplantation by HTLV status
Figure 1b:
Kaplan-Meier non-relapse mortality curves for allogeneic stem cell transplantation by HTLV status
Table 2b:
Cause of Death by HTLV Status following AlloSCT
| Cause of Death by HTLV Status | ||||
|---|---|---|---|---|
| HTLV Status | ||||
| Negative | Positive | Total | ||
|
Occurrences (n)
Percent (%) Chi-Square P-Value ^ |
Primary disease | 4313 | 24 | 4337 |
| 43.59 | 32.88 | |||
| 0.08531 | ||||
| Graft failure | 120 | 1 | 121 | |
| 1.21 | 1.37 | |||
| 0.5913^ | ||||
| GVHD | 1322 | 12 | 1334 | |
| 13.36 | 16.44 | |||
| 0.5504 | ||||
| Infection | 1516 | 15 | 1531 | |
| 15.32 | 20.55 | |||
| 0.2841 | ||||
| Acute Respiratory Distress Syndrome/Pneumonitis |
361 | 2 | 363 | |
| 3.65 | 2.74 | |||
| >0.9999^ | ||||
| Organ failure/toxicity | 1080 | 8 | 1088 | |
| 10.9 | 10.96 | |||
| >0.9999^ | ||||
| Secondary malignancy | 195 | 2 | 197 | |
| 1.97 | 2.74 | |||
| 0.6565^ | ||||
| Other cause | 766 | 3 | 769 | |
| 7.74 | 4.11 | 0.348 | ||
| Not Reported | 222 | 6 | 228 | |
| 2.24 | 8.22 | |||
| Total | 9895 | 73 | 9968 | |
Fisher’s Exact Test
Results generated with RStudio 1.2.5019 “Elderflower”
Discussion
These data support earlier findings that AutoSCT may be safe in patients who are asymptomatic carriers of HTLV-1/2.10 Patients with HTLV infection however showed inferior OS and NRM following AlloSCT in this unadjusted analysis.
Patient deaths due to GVHD and infection were more common in the HTLV-positive group, although there was no single statistically-significant reason for increased NRM. HTLV infection is thought to be immune-altering irrespective of its transformation into fulminant ATLL. For example, HTLV-1 infection is a significant risk factor for disseminated strongyloidiasis.11 Mogamulizumab, a treatment for ATLL, predisposes to severe GVHD,12 but we are aware of no direct effects of HTLV on GVHD. Prior CMV infection was more common in patients who were HTLV-positive who underwent either AutoSCT or AlloSCT. The higher prevalence is expected, as we know that both HTLV and CMV can be transmitted from mother to child via breast milk and they tend to coexist.13 While there was no difference in OS by HTLV status in those who underwent AutoSCT, it is possible that HTLV may interact with CMV in the post-AlloSCT setting and may contribute to inferior NRM in HTLV-positive patients.
Most people in the United States with HTLV-1 are immigrants from the Carribean.1,14,15 Unexpectedly, Caucasians made up the majority (82%) of the HTLV-positive cohort who underwent AlloSCT. This may include a high proportion of patients with HTLV-2. Alternatively, HTLV-positive African American patients may be less likely to be offered or make it to AlloSCT.
There were statistically significant differences between the HTLV-positive and negative groups for certain characteristics. In those who underwent AlloSCT, there were significantly more patients with NHL in the HTLV-positive group, even after excluding ATLL cases. This may be because ATLL can be difficult to distinguish from other T-cell lymphomas and may go unrecognized.16 It is unclear if the higher prevalence of NHL in the HTLV-positive group influenced the survival comparison. There were also differences in gender in those who underwent AutoSCT. A higher incidence of HTLV infection in females is well-known, and has been attributed to the virus’s propensity for male-to-female sexual transmission.17 This difference by sex was not seen in the AlloSCT group.
There are limitations to this study. Because progression from an asymptomatic carrier state to ATLL/HAM often occurs after decades, the 3-year follow up collected by CIBMTR may be inadequate to capture these events. The CIBMTR grouping of patients with HTLV-1 and 2 into a single category may obscure important differences between these infections. Adjustment for confounding or propensity score matching to account for potential differences between HTLV-positive and HTLV-negative patients could not be performed due to limitations in the available data. Survival outcomes by underlying disease were not available. Although we included data on donor HTLV status, we are unable to make associations with outcomes due to the lack of patient-level data. However, it is worth noting that cases of donor-derived ATLL have occurred and this should be considered during donor selection.9 Lastly, the number of cases of HTLV-1/2 infection that underwent transplant were too small to provide meaningful survival estimates for individual diseases. Post-transplant survival is strongly influenced by the disease being treated. More data are needed to better answer this question.
In conclusion, these data support the relative safety of AutoSCT as a treatment option for patients who test positive for HTLV-1/2. For AlloSCT, physicians should consider the possibility of inferior NRM in the HTLV-positive population. These results from the CIBMTR dataset represent a diverse patient population and are broadly applicable across health systems.
Footnotes
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Disclosure of Conflicts of Interest
Dr. John Mark Sloan consults for Abbvie and Stemline Pharmaceuticals. Dr. Areej El-Jawahri is a Scholar in Clinical Research for the Leukemia and Lymphoma Society. Dr. Janice Weinberg consults for Janssen Pharmaceuticals. Dr. Murali Janakiram gets research funding from Takeda, Fate, and Nektar. The remainder of the authors have no disclosures or conflicts of interest.
References
- 1.Gessain A, Cassar O. Epidemiological Aspects and World Distribution of HTLV-1 Infection. Frontiers in Microbiology 2012;3. doi: 10.3389/fmicb.2012.00388 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Mahieux R, Gessain A. HTLV-1 and associated adult T-cell leukemia/lymphoma. Reviews in clinical and experimental hematology 2003;7(4):336–361. [PubMed] [Google Scholar]
- 3.Murphy EL, Cassar O, Gessain A. Estimating the number of HTLV-2 infected persons in the world. Retrovirology 2015;12(S1). doi: 10.1186/1742-4690-12-S1-O5 [DOI] [Google Scholar]
- 4.Stramer SL, Foster GA, Dodd RY. Effectiveness of human T-lymphotropic virus (HTLV) recipient tracing (lookback) and the current HTLV-I and -II confirmatory algorithm, 1999 to 2004. Transfusion 2006;46(5). doi: 10.1111/j.1537-2995.2006.00788.x [DOI] [PubMed] [Google Scholar]
- 5.Dittus C, Sloan JM. Adult T-cell Leukemia/Lymphoma: A Problem Abroad and at Home. Hematology/oncology clinics of North America 2017;31(2):255–272. doi: 10.1016/j.hoc.2016.11.005 [DOI] [PubMed] [Google Scholar]
- 6.Jenks PJ, Barrett WY, Raftery MJ, et al. Development of human T-cell lymphotropic virus type I-associated adult T-cell leukemia/lymphoma during immunosuppressive treatment following renal transplantation. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 1995;21(4):992–993. doi: 10.1093/clinids/21.4.992 [DOI] [PubMed] [Google Scholar]
- 7.Williams NP, Buchner LM, Shah DJ, Williams W. Adult T-Cell Leukemia/Lymphoma in a Renal Transplant Recipient: An Opportunistic Occurrence. American Journal of Nephrology 1994;14(3):226–229. doi: 10.1159/000168722 [DOI] [PubMed] [Google Scholar]
- 8.Tsurumi H, Tani K, Tsuruta T, et al. Adult T-cell leukemia developing during immunosuppressive treatment in a renal transplant recipient. American journal of hematology 1992;41(4):292–294. doi: 10.1002/ajh.2830410414 [DOI] [PubMed] [Google Scholar]
- 9.Tamaki H, Matsuoka M. Donor-derived T-cell leukemia after bone marrow transplantation. The New England journal of medicine 2006;354(16):1758–1759. doi: 10.1056/NEJMc053295 [DOI] [PubMed] [Google Scholar]
- 10.Gupta VK, White PS, Brauneis D, et al. Safety of autologous stem cell transplantation in patients with known Human T-cell Lymphotropic Viruses Type 1 and 2 infection: A case series of four patients. American Journal of Hematology 2019;94(12):E317–E319. doi: 10.1002/ajh.25631 [DOI] [PubMed] [Google Scholar]
- 11.Gotuzzo E, Terashima A, Alvarez H, et al. Strongyloides stercoralis hyperinfection associated with human T cell lymphotropic virus type-1 infection in Peru. The American journal of tropical medicine and hygiene 1999;60(1):146–149. doi: 10.4269/ajtmh.1999.60.146 [DOI] [PubMed] [Google Scholar]
- 12.Sugio T, Kato K, Aoki T, et al. Mogamulizumab Treatment Prior to Allogeneic Hematopoietic Stem Cell Transplantation Induces Severe Acute Graft-versus-Host Disease. Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation 2016;22(9):1608–1614. doi: 10.1016/j.bbmt.2016.05.017 [DOI] [PubMed] [Google Scholar]
- 13.Prendergast AJ, Goga AE, Waitt C, et al. Transmission of CMV, HTLV-1, and HIV through breastmilk. The Lancet Child & adolescent health 2019;3(4). doi: 10.1016/S2352-4642(19)30024-0 [DOI] [PubMed] [Google Scholar]
- 14.Bhatnagar B, Zhao Q, Fisher JL, et al. Poor Treatment Outcomes of Young (<60 Years) African American Patients (Pts) Diagnosed with Acute Myeloid Leukemia (AML) (Alliance). Blood 2020;136(Supplement 1):5–7. doi: 10.1182/blood-2020-140999 [DOI] [Google Scholar]
- 15.Shah UA, Shah N, Qiao B, et al. Epidemiology and survival trend of adult T‐cell leukemia/lymphoma in the United States. Cancer 2020;126(3). doi: 10.1002/cncr.32556 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Khanlari M, Ramos JC, Sanchez SP, et al. Adult T-cell leukemia/lymphoma can be indistinguishable from other more common T-cell lymphomas. The University of Miami experience with a large cohort of cases. Modern Pathology 2018;31(7). doi: 10.1038/s41379-018-0037-3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Eshima N, Iwata O, Iwata S, et al. Age and gender specific prevalence of HTLV-1. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology 2009;45(2):135–138. doi: 10.1016/j.jcv.2009.03.012 [DOI] [PubMed] [Google Scholar]