HUMAN Parvovirus B19 infection has been identified as a direct disruptor of haematopoietic stem cell function, offering new insight into the mechanisms behind pancytopenia and bone marrow failure in vulnerable patient populations.
Understanding Parvovirus B19 Beyond Red Cells
Parvovirus B19 infection is a recognised cause of aplastic anaemia and pancytopenia, particularly in patients with compromised immunity such as those undergoing haematopoietic stem cell transplantation. Until now, disease mechanisms have largely focused on the virus’s known preference for erythroid progenitor cells. However, this restricted tropism has not fully explained the development of multilineage cytopenias observed in clinical practice. Using advanced single cell approaches, including PrimeFlow RNA assay and single cell full length transcriptome sequencing, investigators demonstrated that Parvovirus B19 can infect haematopoietic stem cells directly and initiate viral transcription within these cells.
Impact on Haematopoietic Stem Cell Function
Infected haematopoietic stem cells showed increased apoptosis alongside impaired self-renewal and reduced capacity for multilineage differentiation. These functional defects provide a direct mechanistic link between Parvovirus B19 infection and pancytopenia. The data suggest that stem cell injury is not merely a downstream consequence of erythroid suppression but a primary driver of bone marrow dysfunction. This finding redefines Parvovirus B19 as a previously unrecognised stem cell tropic virus within the haematopoietic niche.
JAK2 STAT5 Signalling and Therapeutic Implications
Further analysis revealed activation of the JAK2 STAT5 signalling pathway in infected haematopoietic stem cells, a process that appeared to support viral persistence. Pharmacological inhibition of this pathway using baricitinib markedly reduced viral load in vitro and partially restored haematopoietic differentiation capacity. These results indicate that targeting host signalling pathways may represent a viable therapeutic strategy for virus induced bone marrow failure. By implicating JAK2 STAT5 signalling in Parvovirus B19 persistence, the study opens new avenues for intervention in transplant settings and other haematological diseases where cytopenias remain difficult to manage.
Reference
Pei X-Y et al. Parvovirus B19 targets hematopoietic stem cells to disrupt multilineage differentiation and drive pancytopenia. Cell Death & Differentiation. 2026; https://doi.org/10.1038/s41418-026-01671-3.
