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Evolutionary dynamics of paroxysmal nocturnal hemoglobinuria
Nathaniel Mon Père1,2, Tom Lenaerts1,2,3, Jorge M Pacheco4,5,6
1Interuniversity Institute of Bioinformatics in Brussels, ULB-VUB, Brussels, Belgium.
Plos Computational Biology
|June 19, 2018
Summary
Paroxysmal nocturnal hemoglobinuria (PNH) clonal expansion is likely due to neutral drift, not immune selection. This model explains disease incidence and age at diagnosis, suggesting only one PNH clone originates in hematopoietic stem cells.
Area of Science:
- Hematology
- Genetics
- Computational Biology
Background:
- Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal blood disorder with hemolysis and thrombosis risk.
- PNH arises from PIG-A gene mutations in hematopoietic stem cells (HSCs), leading to deficient cell surface proteins.
- The mechanism of PNH clonal expansion in HSCs remains debated, with immune selection and neutral drift as leading hypotheses.
Purpose of the Study:
- To investigate the neutral drift model for PNH clonal expansion.
- To explore the occurrence and evolution of multiple PNH clones within the HSC pool.
- To compare model predictions with clinical observations of PNH incidence and patient age.
Main Methods:
- Numerical evolution of a Markov chain to model HSC pool dynamics.
- Probabilistic analysis of PIG-A mutated clone expansion under neutral drift.
- Investigation of multiple independent clone emergence and stability.
Main Results:
- Model predictions align with PNH incidence and average age at diagnosis.
- Observed relative stability of PNH clone size across multiple cases.
- Calculated low probability of patients harboring a second independent HSC clone.
Conclusions:
- Neutral drift is a plausible mechanism for PNH clonal expansion.
- The model supports the origin of a single dominant PNH clone in HSCs for most clinical cases.
- Observed dual PNH clones in patients may indicate non-HSC origins for one clone.
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