Risk factors for cytomegalovirus DNAemia following haploidentical stem cell transplantation and its association with host hepatitis B virus serostatus

Chen, Yao; Xu, Lei; Liu, Kai-Yan; Chen, Huan; Chen, Yuhong; Zhang, Xiao-Hui; Wang, Yu; Wang, Feng-Rong; Han, Wei; Wang, Jing‐Zhi; Yan, Chen‐Hua; Huang, Xiao‐Jun

doi:10.1016/j.jcv.2015.12.003

Cited by 22 publications

(14 citation statements)

References 57 publications

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“…Hepatitis after allo‐HSCT is receiving an increasing amount of attention, but the focus remains mainly concentrated on hepatitis B. We have also performed a series of studies on hepatitis after haplo‐HSCT with a particular focus on hepatitis B (Chen et al , , ). While HEV can also cause severe liver disease, including acute liver failure, chronic hepatitis and end‐stage liver disease in immunocompromised patients (e.g., allo‐HSCT and SOT patients; Mallet et al , ; van der Eijk et al , ; Kamar et al , ; Hoofnagle et al , ; Kamar et al , ; Versluis et al , ; Kamar et al , ), little is known about HEV infection in patients treated with haplo‐HSCT, especially those treated with the “Beijing protocol”.…”

Section: Discussionmentioning

confidence: 99%

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Hepatitis E virus infection after haploidentical haematopoietic stem cell transplantation: incidence and clinical course

Tang

Wang

et al. 2018

Br J Haematol

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Summary Hepatitis E virus (HEV) is increasingly found to cause hepatitis in allogeneic haematopoietic stem cell transplantation (HSCT) patients. However, little is known about HEV infection in patients receiving haploidentical HSCT (haplo‐HSCT). Here, we retrospectively evaluate the incidence and clinical course of HEV infection in haplo‐HSCT patients. From January 2014 to July 2017, 177 patients with unexplained elevated transaminases after receiving haplo‐HSCT at Peking University Institute of Haematology were screened for HEV using HEV serology. HEV RNA was assessed in blood samples when HEV‐IgG and/or IgM antibodies were positive. Acute HEV infection was identified in 7 patients (3·9%), 1 of whom had developed a chronic HEV infection. The median time from haplo‐HSCT to HEV infection was 17·5 (range, 6–55) months. HEV infection was confirmed by the presentation of anti‐HEV IgM + anti‐HEV IgG (rising) (n = 5) or HEV‐RNA + anti‐HEV IgM + anti‐HEV IgG (n = 2). None of the patients died of HEV infection directly: 2 patients with HEV infection died showing signs of ongoing hepatitis, and 5 patients cleared HEV with a median duration of HEV infection of 1·5 (range, 1·0–5·7) months. In conclusion, HEV infection is a rare but serious complication after haplo‐HSCT. We recommend screening of HEV in haplo‐HSCT.

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Section: Discussionmentioning

confidence: 99%

“…HBV infection after haplo-HSCT is of great concern (Mallet et al, 2016). We previously reported hepatitis B after haplo-HSCT (Chen et al, 2008(Chen et al, , 2016. However, no data are available on infection with hepatitis E virus (HEV) after haplo-HSCT.…”

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confidence: 99%

Hepatitis E virus infection after haploidentical haematopoietic stem cell transplantation: incidence and clinical course

Tang

Wang

et al. 2018

Br J Haematol

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“…In haplo-SCT with G-CSF modality, the cumulative incidence of cytomegalovirus (CMV) DNAemia varies from 63.7 to 66.1%, which remains one of the main causes of morbidity and mortality. The risk factors for CMV DNAemia include HBsAg seropositivity, acute GVHD before CMV DNAemia, and poor CMV-specific CD8 + T central memory subset recovery (93). In contrast, transplantation from HLA-mismatched family donors ( P < 0.001), acute GVHD ( P < 0.001), and donor-recipient KIR ligand mismatched ( P = 0.012) were associated with an increased risk of refractory CMV infection (31, 32).…”

Section: Recent Advances In the Beijing Protocolmentioning

confidence: 99%

Granulocyte Colony-Stimulating Factor-Primed Unmanipulated Haploidentical Blood and Marrow Transplantation

2019

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Granulocyte colony-stimulating factor (G-CSF), a growth factor for neutrophils, has been successfully used for stem cell mobilization and T cell immune tolerance induction. The establishment of G-CSF-primed unmanipulated haploidentical blood and marrow transplantation (The Beijing Protocol) has achieved outcomes for the treatment of acute leukemia, myelodysplastic syndrome, and severe aplastic anemia with haploidentical allografts comparable to those of human leukocyte antigen (HLA)-matched sibling donor transplantation. Currently, G-CSF-mobilized bone marrow and/or peripheral blood stem cell sources have been widely used in unmanipulated haploidentical transplant settings. In this review, we summarize the roles of G-CSF in inducing T cell immune tolerance. We discuss the recent advances in the Beijing Protocol, mainly focusing on strategies that have been used to improve transplant outcomes in cases of poor graft function, virus infections, and relapse. The application of G-CSF-primed allografts in other haploidentical modalities is also discussed.

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“…Direct effects are clinical manifestations due to CMV replication (e.g., pneumonitis, gastrointestinal diseases, hepatitis, marrow suppression, retinitis, and CNS diseases) whereas indirect effects based on CMV-immunodulatory activities may lead to an increase in the incidence of other opportunistic infections, an increase of the risk for acute and chronic organ rejection, and a decrease in patient survival (reviewed in [79]). The co-infection between HBV and CMV in an HSCT setting has been little investigated [80,81,82]. In the allo-HSCT setting, a study found an association between HBsAg seropositivity and increased risk of CMV DNAemia [82], while another study did not show any relation between HBsAg serostatus and the incidence of CMV reactivation [81].…”

Section: Interplay Of Risk Factors For Hbv Reactivation In Hsctmentioning

confidence: 99%

HBV Reactivation in Patients Undergoing Hematopoietic Stem Cell Transplantation: A Narrative Review

Gentile

Antonelli

2019

Viruses

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HBV reactivation (HBVr) can occur due to the ability of HBV to remain latent in the liver as covalently closed circular DNA and by the capacity of HBV to alter the immune system of the infected individuals. HBVr can occur in patients undergoing hematopoietic stem cell transplantation (HSCT) with a clinical spectrum that ranges from asymptomatic infection to fulminant hepatic failure. The risk of HBVr is determined by a complex interplay between host immunity, virus factors, and immunosuppression related to HSCT. All individuals who undergo HSCT should be screened for HBV. HSCT patients positive for HBsAg and also those HBcAb-positive/HBsAg-negative are at high risk of HBV reactivation (HBVr) due to profound and prolonged immunosuppression. Antiviral prophylaxis prevents HBVr, decreases HBVr-related morbidity and mortality in patients with chronic or previous HBV. The optimal duration of antiviral prophylaxis remains to be elucidated. The vaccination of HBV-naïve recipients and their donors against HBV prior to HSCT has an important role in the prevention of acquired HBV infection. This narrative review provides a comprehensive update on the current concepts, risk factors, molecular mechanisms, prevention, and management of HBVr in HSCT.

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Risk factors for cytomegalovirus DNAemia following haploidentical stem cell transplantation and its association with host hepatitis B virus serostatus

Cited by 22 publications

References 57 publications

Hepatitis E virus infection after haploidentical haematopoietic stem cell transplantation: incidence and clinical course

Hepatitis E virus infection after haploidentical haematopoietic stem cell transplantation: incidence and clinical course

Granulocyte Colony-Stimulating Factor-Primed Unmanipulated Haploidentical Blood and Marrow Transplantation

HBV Reactivation in Patients Undergoing Hematopoietic Stem Cell Transplantation: A Narrative Review

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