ONE CHAIN, REPEATED SPILLOVER, OR AN UNRELATED EARLY SIGNAL?

Abstract Background: A retrospective field investigation described substantial illness and mortality in and around Mongbwalu from January 2026, several months before Bundibugyo virus disease (BVD) was formally recognised in May. Historical BDBV evidence includes a genomic reconstruction compatible with multiple spillovers, while other orthoebolavirus outbreaks have involved survivor-associated resurgence, concurrent lineages and substantial syndromic misclassification. We evaluated whether the early Mongbwalu signal was most compatible with continuous acute transmission, a later introduction, survivor-mediated reseeding, or mixed/non-ancestral mortality. Methods: We combined a structured rapid review of 35 sources with official confirmed surveillance, a published report of an unpublished retrospective investigation, and a soft genomic timing constraint. A resample-move approximate Bayesian computation sequential Monte Carlo model simulated 20 weekly periods across Mongbwalu, Bunia, Rwampara and Nizi. Four hypotheses were compared: continuous acute transmission (H1), repeated zoonotic introduction or temporarily elevated shared exposure (H2), survivor-mediated sexual transmission from persistent virus in semen (H3), and mixed or substantially non-ancestral retrospective mortality (H4). Three independent chains of 450 particles were run for each hypothesis over seven decreasing tolerances. Model recovery, prior sensitivity, posterior-predictive checks and leave-one-component-out analyses assessed identifiability and robustness. Results: Under equal priors, H4 received 36.2%, H2 32.6%, H3 21.6% and H1 9.6%. Under the literature-neutral prior, H2 received 50.0%, H4 34.7%, H1 11.1% and H3 4.2%. H2 and H4 jointly accounted for 84.8% under the main prior and 68.7%-89.3% across all prior families, demonstrating a robust preference for a discontinuous origin history. The approximate evidence ratio was only 1.11:1 for H4 over H2, so H2's lead under the main analysis reflected both close empirical fit and direct BDBV precedent incorporated into the prior. H1 was correctly recovered in 92% of equal-prior synthetic datasets, compared with 52% for H2, 42% for H3 and 24% for H4. Removing confirmed May counts eliminated H2's clear advantage, identifying the rapid May expansion as the principal evidence for a later successful seed. Interpretation: The findings favour a discontinuous origin: the January/February Mongbwalu signal was epidemiologically meaningful, but the lineage that expanded in May most probably arose from a later successful introduction or renewed primary exposure rather than from one uninterrupted acute chain. H2 is the preferred literature-informed explanation because it best reconciles the structured early signal, March-centred sampled ancestry and rapid May growth, while direct BDBV precedent makes the mechanism credible. H4 remains a substantial alternative because the early events were not laboratory confirmed and H2 and H4 are only partly identifiable. H3 is temporally and biologically possible but lacks survivor-specific evidence, and H1 is not the leading explanation under any tested prior family.