Abstract
On 4 September 2025, the Ministry of Public Health, Hygiene and Social Welfare officially declared the 16th Ebola disease outbreak in the Democratic Republic of the Congo (DRC). This outbreak ended on 1 December 2025 and occurred in Bulape Health Zone, Kasaï Province, an area with limited access to appropriate healthcare facilities and resources. Here, we describe the probable index patient and molecular investigations of samples obtained from six suspected patients from the initial outbreak phase. We identified Orthoebolavirus zairense (EBOV) in five samples from different patients. In addition, we performed whole-genome sequencing and generated four complete EBOV genomes. These genomes form a well-supported phylogenetic cluster with genomes from the 1976 Yambuku/Mayinga outbreak. This study suggests a likely new zoonotic spillover event from an as-yet unidentified natural reservoir. While the close relationship to 1976 EBOV Yambuku/Mayinga genomes is striking, this poses additional challenges on the comprehension of the animal reservoir species.
Subject terms: Viral infection, Virology, Epidemiology
The study reports the emergence of a new Ebola variant in a remote area of Kasai Province, DR Congo. The findings highlight the need for rapid detection and sequencing to better identify variants and quickly respond to outbreaks.
Introduction
Ebola disease is an emerging zoonotic viral disease that poses a major public health threat in sub-Saharan Africa1. Since first identified in 1976, in independent and simultaneous outbreaks in South Sudan and the Democratic Republic of the Congo (DRC)2,3, more than 30 Ebola disease outbreaks have been reported, the largest being the 2013–2016 West Africa Ebola Virus Disease (EVD) epidemic which led to more than 28,600 infections and 11,325 deaths4. The DRC has experienced more EVD outbreaks than any other country, with 17 Ebola outbreaks reported as of 22 June 20265.
On 4 September 2025, the DRC Ministry of Public Health, Hygiene and Social Welfare officially declared an EVD outbreak in Bulape Health Zone, Kasaï Province. Bulape is one of 18 health zones in the province and has an estimated population of 350,300 over an area of 6533 km2. This outbreak ended on 1 December 2025, and occurred approximately 40 km from the location of the 2007 and 2008 EVD outbreaks in Mweka and Luebo Health Zone, Kasaï Province (Fig. 1A)4. In this study, we seek to reconstruct the early events of the Bulape EVD outbreak to determine whether it resulted from a new zoonotic spillover event or represented a resurgence linked to previous outbreaks in the region, such as those involving EVD survivors from the 2007 Luebo outbreak or the 2008–2009 Mweka outbreak in Kasaï. To address this, we discussed with the first line healthcare workers and consulted medical records at the General Referral Hospital of Bulape (“Hospital of Bulape” hereinafter) between 25 and 30 September 2025. Furthermore, we performed whole genome sequencing (WGS) on initial EBOV PCR-positive samples collected in Bulape, followed by phylogenetic analysis of the resulting complete EBOV genomes.
Fig. 1. Geographic distribution and phylogenetic analyses of Ebola virus (EBOV) genomes.
A Map showing the geographic locations of Ebola disease outbreaks in the Democratic Republic of the Congo (DRC) and neighboring countries since 1976. The circle areas are scaled by the number of reported cases. The color scale refers to the year of outbreaks. B A maximum likelihood phylogenetic tree showing the evolutionary relationship of the 2025 Ebola virus disease outbreak to previous outbreaks in the DRC and neighboring countries. Not all outbreaks represented on the map have genomes available for phylogenetic analysis. The tree is drawn with an arbitrary root, and the branch scale is the number of substitutions per genome site. A scale bar of 0.004 substitutions per genome site corresponds to roughly 76 substitutions.
Healthcare workers and review of medical records at the Hospital of Bulape revealed that the presumptive index patient was a 20–29-year-old woman, who was 32–36 weeks pregnant (Case 1) and resided in Bulape Health Zone. She reported consuming wild game (rodent) a few days before developing fever, headache and abdominal pain. In mid-August 2025, after a week of symptoms, she was admitted for 2 days to Bulape health center Poste III with persistent fever, headache and vaginal bleeding, but was transferred to the Hospital of Bulape. The initial diagnosis was malaria, and she was treated with intravenous quinine, ceftriaxone and metronidazole, and tocolytics. One day after admission, she delivered a stillborn fetus weighing 1.700 kg. On Day 2 post-admission, she developed hematemesis, bloody diarrhea and anemia, for which she received blood transfusions. Unfortunately, the patient died on Day 4 post admission and was buried in the community, without adherence to safe and dignified burial practices. No sample was collected from this probable index patient prior to burial.
During the study period, we identified 11 EVD cases, including six probable cases (2-7) and five confirmed EVD cases (8–12). Transmission chain was focused on the presumptive index patient (Case 1) and involved household and healthcare-associated transmissions. Within the household, we identified the index patient’s child (Case 2), aged 2–5 years old, as probable case. In the healthcare setting, multiple exposures were reported from the maternity ward: a laboratory technician (Case 3) and a trainee laboratory technician (Case 8), both collected blood samples from Case 1 and were infected, as well as two midwives, including Case 9 -who sustained a needle-stick injury during blood collection- and Case 10 who cared for Case 1. In addition, the index patient’s maternal aunt (Case 4) and three co-patients (Cases 5–7) were probably infected following exposure to Case 1. Finally, a likely secondary transmission event involved the trainee laboratory technician (Case 8), who had collected blood samples from two children (Cases 11 and 12) admitted to the pediatric ward (Fig. 2). Medical record reviews of confirmed EVD patients -included in this study- showed that persistent fever, abdominal pain, diarrhea, and vomiting were common among patients identified in early September 2025 (Extended Data Table 1).
Fig. 2. Transmission chain of EVD cases reported between mid-August and 03 September 2025 in Bulape, DRC.
DSO date of symptom onset, DD date of death, DRC Democratic Republic of the Congo, EVD Ebola virus disease.
On 3 September 2025, the first samples from suspected EVD cases were received at the Institut National de Recherche Biomédicale (INRB), the national reference laboratory for emerging and re-emerging pathogens. There were six samples from different patients: one oral swab obtained immediately after the death of a midwife (Case 9) and five plasma samples from two other exposed healthcare workers (Case 8 and 10), and three children hospitalized at the pediatric ward, Hospital of Bulape (no case numbers since epidemiological links not fully resolved). These samples were tested for Orthoebolavirus zairense (EBOV) using molecular diagnostic assays, including the GeneXpert Ebola assay (only for the swab sample), the automated BioFire FilmArray System (Global Fever Panel), and real-time PCR with Altona RealStar Filovirus Screen RT-PCR kit 1.0 (Altona Diagnostics GmbH, Hamburg, Germany).
Results
Laboratory analysis
Five of the six were positive for EBOV, including the oral swab. Of the plasma samples, three were positive for EBOV by both the BioFire platform and the Altona RealStar Filovirus Screen RT-PCR assay. One plasma sample (Case 10) yielded discordant results, testing positive with BioFire but negative with Altona RealStar Filovirus Screen RT-PCR assay, likely due to very low viral load. Except for one (Case 10), all samples demonstrated concordant test results (Extended Data Table 1).
Whole genome sequencing
Using EBOV-specific primer pools, designed for the variants of the 2018–2020 EVD outbreak in eastern DRC, we performed multiplex tiling PCR and whole genome sequencing as detailed in the Methods section. Four full-length EBOV genomes with >98% coverage were generated (Extended Data Table 2). Notably, one sample that was obtained from the midwife (Case 10) who had been discharged from the Ebola treatment center on 16 September 2025 did not produce a full-length EBOV genome (2098 reads mapping EBOV with 50% genome coverage). Multiple sequence alignment of the four full-length EBOV genomes with 17 representative genomes from previous outbreaks (Extended Data Table 3) was performed using MAFFT6. Phylogenetic trees were constructed using IQ-TREE v3.0.17.
Phylogenetic analysis
Phylogenetic investigation showed that the Bulape EBOV variants are most closely related to the 1976 EBOV Yambuku-Mayinga variants (GenBank accession KR063671) (Fig. 1B), confirming that the current EVD outbreak is not a resurgence of the 2007-2009 EVD outbreaks but is likely the result of a novel zoonotic spillover. Whilst the new variant shares a most recent common ancestor with the 1976 EVD outbreak, the divergence of the branch leading the 2025 EVD outbreak is considerably shorter than expected given the amount of time that has elapsed. This phenomenon has been noticed for previous outbreaks8,9, but it is not clear if this is a consequence of differences in the nature and composition of the reservoir between circulating EBOV diversity. Further, this variant might be linked to an unrecorded outbreak in the past with a persistently infected survivor triggering a resurgent outbreak years later10,11.
Discussion
To validate mutations shared by all four genomes obtained using amplicon-based sequencing approach, we sequenced one sample (Case 9) using the Twist Comprehensive Viral Research panel (Twist Bioscience, San Francisco, USA), a probe-based enrichment sequencing approach. The resulting consensus genome was identical to that obtained with the amplicon-based sequencing approach, showing 100% nucleotide identity. A deep analysis showed that the genome 25FHV168/Case 11 (Pathoplexus accession PP_003RXEP.2) exhibits six T-to-C changes relative to the other genomes (Extended Data Fig. 1) and the 1976 Yambuku genome in a tight cluster within a 101-nucleotide stretch starting at site 2812. Such a clustered pattern is consistent with “Adenosine Deaminase Acting on RNA” (ADAR)-mediated editing, as previously described12. Limited genomic data from within the outbreak precludes a detailed phylogenetic investigation but by assuming that the molecular evolutionary rate is similar to previous human outbreaks (for example 1.9 × 10−3 substitutions/site/year13 for which we would expect about one mutation to arise every 10 days), the observed diversity is compatible to the known epidemiological history.
Three of the five confirmed EVD cases from this study -one laboratory staff (Case 3) and two midwives (Cases 9 and 10) from the Hospital of Bulape- had direct contact with the presumptive index patient. Combined with information from healthcare workers and review of medical records, findings suggest that the Bulape EVD outbreak was primarily driven by human-to-human transmission with healthcare-associated transmission playing an important role in the early phase of the outbreak. A total of 64 EVD cases (53 confirmed and 11 probable), including 45 deaths (34 confirmed and 11 probable), were reported at the end of the 2025 EVD outbreak, resulting in a case-fatality rate of 64% among confirmed cases.
Our findings highlight the critical need for heightened awareness among local health authorities to promptly identify and report suspected EVD cases, coupled with rapid molecular confirmation to enable timely implementation of control measures during the early stages of an EVD outbreak. Strengthening infection prevention and control measures, particularly safe injection and blood collection practices, is essential to prevent all healthcare-associated transmissions of EBOV. Despite the remoteness and limited accessibility of the Bulape health zone, we successfully established an EVD diagnostic laboratory on site.
Taken together, our findings demonstrate the utility of rapid genomic investigation during outbreak response. The timely generation of high-quality and complete EBOV genomes provided evidence for the use of rVSV-ZEBOV candidate vaccine for the ring vaccination strategy14, as recommended by the World Health Organization. As of 1 December 2025 (end of the 2025 EVD outbreak), more than 30,000 individuals were vaccinated across Bulape health zone. While preliminary phylogenetic analyses can already guide ecological investigations, we strongly recommend integrating expanded genomic epidemiology into the outbreak response to monitor transmission chains in real time and to more accurately reconstruct the initial events of EBOV spread. However, conclusions regarding viral origin should be considered preliminary given the limited number of genomes analyzed. Additional sequencing of cases, together with ecological investigations in potential reservoir hosts, will be crucial to determine whether the Bulape variant represents a long-term persistence in nature or the result of persistence from an undetected human EBOV infection of the past. The recurrence of EVD in the same geographic area suggests high genetic diversity of EBOV in a localized natural reservoir or ecological niche that supports repeated spillover events. These findings underscore the need for targeted surveillance, reservoir studies, and strengthened preparedness in this high-risk region.
Methods
Ethics committee approval
Specimens were collected as part of the DRC Ministry of Public Health, Hygiene and Social Welfare response, and were therefore exempt from informed consent. However, permission to use anonymous data for publication was granted by the Ethics Committee of the Kinshasa School of Public Health (ESP-UNIKIN, Number ESP/CE/15/2026).
Methods
Six specimens, including five plasma and one buccal swab, were collected from six patients at the General Referral Hospital of Bulape and sent to INRB, Kinshasa for EVD confirmation. At INRB, we used the point-of-care GeneXpert Ebola assay, the automated BioFire FilmArray System (Global Fever Panel), and real-time PCR with Altona RealStar Filovirus Screen RT-PCR kit 1.0 (Altona Diagnostics GmbH, Hamburg, Germany).
GeneXpert Ebola assay for the detection of EBOV
The buccal swab was tested for the presence of EBOV RNA using the GeneXpert Ebola Assay (Cepheid, Sunnyvale, CA, USA) as performed by Kinganda-Lusamaki et al.15. The buccal swab was transferred to the 2.5 mL Xpert® Ebola Sample Reagent (SR) bottle, which contained 4.5 M guanidinium thiocyanate, and was incubated for 20 min at room temperature as recommended by the manufacturer. A volume of 1 ml of the SR buffer was transferred to the Xpert® Ebola Assay cartridge, where all steps of sample preparation, reverse transcription and multiplex fluorescent real-time PCR occurred. The cartridge was loaded into the GeneXpert® module, where processing, detection, and fluorescent readout were performed automatically for 1h30 min. Primers and probes in the Xpert® Ebola Assay detected two conserved regions within the glycoprotein (GP) and the nucleoprotein (NP) of the EBOV genome. The amplified target sequences were detected with TaqMan probes, each labeled with distinct proprietary fluorophores designed to operate with different detection channels of the GeneXpert system16.
Direct molecular testing using the BioFire FilmArray system
The BioFire FilmArray System, an automated platform developed by BioFire Defense, uses an automated system to extract nucleic acid from whole blood samples and perform multiplex RT-PCR. Following the manufacturer’s instructions, we used the Biofire Global Fever Panel, which detects 19 pathogens, including EBOV.
Viral RNA extraction and real-time qPCR amplification
Briefly, viral RNA was extracted from 140 µL of inactivated blood using the QIAamp viral RNA Mini kit (QIAGEN), according to the manufacturer’s instructions. Real-time PCR was performed in duplicate using the RealStar® Filovirus Screen RT-PCR Kit 1.0 (Altona Diagnostics GmbH, Hamburg, Germany), following the manufacturer’s protocol. Additional negative and positive controls were included to ensure the absence of carryover contamination and efficiency of the assay.
Multiplex PCR tiling and whole-genome sequencing (WGS)
All PCR-positive samples for EBOV were selected for WGS. Reverse transcription was performed with LunaScript RT SuperMix kit (New England Biolabs). Multiplex PCR was performed on the resulting cDNA using Q5 Hot Start High-Fidelity 2X master mix (New England Biolabs) and EBOV-specific primer pools designed for EBOV Mangina variant (GenBank accession MK007337.1). Sequencing library was prepared in triplicate, barcoded and multiplexed using the Rapid Sequencing DNA V14 barcoding kit (SQK-RBK114.96; Oxford Nanopore Technologies (ONT), Oxford, UK), following the manufacturer’s instructions. Library was sequenced on an ONT GridION with a R10.4.1 chemistry flowcell for 24 h.
Bioinformatics analysis
Base-calling used the Dorado basecaller with the ‘dna_r10.4.1_e8.2_400bps_hac@v5.0.0’ model. Viral consensus sequences were generated using the amplicon-nf v0.4.6dev (https://github.com/artic-network/amplicon-nf/tree/0.4.6dev) Nextflow pipeline to filter reads, align reads to reference, trim primers from aligned reads, call variants, construct consensus sequences, and perform quality control on the sequencing run.
Phylogenetic inference
We used a dataset consisting of 17 representative genomes from previous outbreaks (Extended Data Table 3), along with new EBOV sequences from Bulape, Kasaï. Global multiple sequence alignment was performed using MAFFT6. After masking out the six putative ADAR mutations in genome 25FHV168 (from Case 11) to avoid the distortion of the phylogenetic and temporal signal, the remaining 16 mutations within the 2025 EBOV genomes are listed in Extended Data Table 4. Two of the inferred mutations are phylogenetically incompatible with each other and may represent a homoplasy or reversion, or a sequencing error. A maximum likelihood tree was reconstructed using IQ-TREE v3.0.1 under the general time-reversible (GTR) nucleotide substitution model with gamma (G) distributed rate variation among sites7.
Reporting summary
Further information on research design is available in the Nature Portfolio Reporting Summary linked to this article.
Supplementary information
Acknowledgements
The authors are grateful to all staff involved in the early phase of EVD outbreak investigation in Bulape, Kasaï in the DRC. We thank the Ministry of Public Health, Hygiene and Social Welfare of the DRC. The authors gratefully acknowledge the support of the US Centers for Disease Control and Prevention (CDC), Atlanta. We also thank Culmen International LLC for their support to the Pathogen Genomics Laboratory, INRB, through funding from the US CDC, Atlanta. The authors acknowledge the support from the Belgian Directorate-General for Development Cooperation and Humanitarian Aid (DGD; grant number 914010). Routine lab activities were supported by ongoing initiatives such as Africa CDC Pathogen Genomics Initiative (Africa PGI) (grants BMGF-INV-018278, INV-033857, Saving Lives and Livelihoods program, and NU2HGH000077); and Agence Française de Développement through the AFROSCREEN project (grant agreement CZZ3209, coordinated by ANRS-MIE Maladies infectieuses émergentes in partnership with Institut de Recherche pour le Développement [IRD] and Pasteur Institute). We thank Tessa de Block from the Institute of Tropical Medicine, Antwerp, for logistical support. AAA is supported by a DGD sandwich PhD scholarship. JCMC is supported by a doctoral grant from University of Bern, Switzerland. JQ, NLom, AoT, SW, PMa & AR acknowledge the support of the Wellcome Trust through the ARTIC Network (awards 206298/Z/17/Z & 313694/Z/24/Z). We acknowledge support from the European Union (DECIPHER project under the Horizon Europe research and innovation program, and the grant agreement N° 101137242). Views and opinions expressed are those of the authors and do not necessarily reflect those of the EU or the granting authority EU Horizon Europe research and innovation program. The EU or the granting authority cannot be held responsible for them.
Author contributions
Conceptualization and study design: J.J.M.T., T.W.B., and P.M.K. Clinical investigation and sample collection: S.B.L., A.N.T., J.P.M.B., and L.T. Laboratory work: A.A.A., P.A.B., S.K., and F.C.K. Validation of PCR results: E.K.L., S.A.M., J.J.M., T.W.B., and P.M.K. Bioinformatics analysis: G.L.N., J.C.M.C., E.K.L., P.P.T., J.Q., N. Loman, and S.W. Writing—first draft: A.A.A. and T.W.B. Phylogenetic analysis: A.R. Writing—review and editing: E.K.L., C.N., D.J., M.M., R.K., I.B., E.L.L., N.R.K.S., A.A., J.N., J.O.O., O.N.T., M.K., P. Mukadi, D.M.B., O.T.M., P.A., S.M., J.Q., N. Loman, A.o.T., D.M., E.D., L.E.H., A.W.R., S.W., K.K.A., M.P., S.A.M., L.L., J.K., N. Low, M.W.C, P. Maes, K.V., J.J.M.T., K.K., A.R., T.W.B., P.M.K. All authors contributed to the writing, revisions, and approval of the final version of the manuscript.
Peer review
Peer review information
Nature Communications thanks the anonymous reviewers for their contribution to the peer review of this work. A peer review file is available.
Data availability
The full-length genome sequences from this work are available in the Pathoplexus SeqSet https://doi.org/10.62599/PP_SS_3268.1. These sequences have also been deposited in the NCBI GenBank repository under the following accession numbers: PZ867529, PZ867530, PZ867531, and PZ867532.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
These authors contributed equally: Adrienne Amuri-Aziza, Gradi Luakanda-Ndelemo.
These authors jointly supervised this work: Tony Wawina-Bokalanga, Placide Mbala-Kingebeni.
Contributor Information
Tony Wawina-Bokalanga, Email: tonywawinab@yahoo.fr.
Placide Mbala-Kingebeni, Email: mbalaplacide@gmail.com.
Supplementary information
The online version contains supplementary material available at https://doi.org/10.1038/s41467-026-77542-9.
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Associated Data
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Supplementary Materials
Data Availability Statement
The full-length genome sequences from this work are available in the Pathoplexus SeqSet https://doi.org/10.62599/PP_SS_3268.1. These sequences have also been deposited in the NCBI GenBank repository under the following accession numbers: PZ867529, PZ867530, PZ867531, and PZ867532.