Conference Abstracts - 2025 Summit on Hematologic Cancers
Vol. 5, Issue Supplement 1, 2025 · S1-2
Parvovirus B19-Induced Myelodysplastic Syndrome Progressing to Acute Myeloid Leukemia
Malvika Gupta, MD,Christopher Graham, MD
Submission received: 2025-07-13 / Accepted: 2025-07-28 / Published: 2025-09-16
Introduction
Acute myelogenous leukemia (AML) is associated with poor prognosis and typically presents with either pancytopenia or leukocytosis, and a hypercellular marrow with immature myeloid precursors. Parvovirus B19, a ubiquitous single-stranded DNA virus with a tropism for hematopoietic cells, can cause aplastic anemia in immunocompromised patients or those with hemolytic anemias. However, it does not commonly cause leukemogenesis. We present a rare case of Parvovirus B19-induced bone marrow failure which progressed to AML.
Case Discussion
A 44-year-old Asian female presented with pancytopenia (White Blood Cells 0.75 k/μL, Absolute Neutrophil Count 0.25 k/μL, Hemoglobin 7.3 g/dL, Platelets 9 k/μL). Initial bone marrow biopsy revealed 40–50% cellularity with numerous erythroid precursors with nuclear viral inclusions (Figure 1A), immunostaining positive for Parvovirus B19 (Figure 1B), with polymerase chain reaction showing 25,154,010 copies/mL of viral DNA. Cytogenetics were normal, with no increased blasts. She was treated with monthly IVIG for four months, after which, her viral load dropped to <100 copies/mL. Despite this, pancytopenia persisted.
A repeat bone marrow biopsy at three months revealed hypocellularity, atypical megakaryocytes with dysplasia, and 3% blasts consistent with myelodysplastic syndrome (MDS) (Figure 1C). Karyotyping was normal. Next-generation sequencing (NGS) revealed mutations in RUNX1, BCOR, PHF6, and ASXL1. She began Eltrombopag for transfusion-dependent thrombocytopenia. Two months later, she developed 1% peripheral blasts (absolute blast 0.02 k/μL, progressing to 0.20 k/μL in four weeks). A bone marrow biopsy was hypercellular (80%) with 40–50% CD34+ blasts (Figure 1D). NGS confirmed prior mutations; FISH showed trisomy 8 and 8q22.
She underwent induction chemotherapy with cytarabine and idarubicin (7+3), followed by consolidative allogeneic stem cell transplant from an HLA-matched donor. She remains in remission after 14 months.
Figure 1: Bone marrow core biopsy obtained showed numerous erythroid precursors with prominent nuclear inclusions (lantern cells, arrows; hematoxylin and eosin stain; 25X). B) A parvovirus B19 immunohistochemical stain taken from the same area of core biopsy demonstrates numerous infected precursors (25X). C) Bone marrow aspirate smears obtained September 2016 demonstrated atypical megakaryocytes, including micromegakaryocytes (Wright-Giemsa stain; 25X). D) Peripheral blood smear from January 2017 showed approximately 20% circulating blasts (inset). CD34 immunohistochemical stain obtained on concurrent bone marrow biopsy demonstrated 40-50% marrow blasts (inset Wright-Giemsa stain, 50X; CD34 immunohistochemical stain, 10X).
Discussion
This case highlights clonal evolution risk and leukemic transformation following Parvovirus B19 infection. Clonal evolution is a known risk in patients with bone marrow failure syndromes, including patients with Fanconi's anemia and aplastic anemia. Due to the selective stress, pro-proliferative mutations allow an immune escape phenomenon. In viral-mediated bone marrow failure, pro-proliferative mutations may confer survival advantages. Additionally, Parvovirus B19 is known to downregulate IL-10, which is responsible for the suppression of blast proliferation. An exact mechanism of action for this phenomenon is yet to be elucidated. Vigilant surveillance for clonal hematopoiesis is warranted in patients recovering from Parvovirus B19-induced marrow failure.