Hazard information profile: Bundibugyo virus 

Ebola virus disease (EVD) (formerly known as Ebola haemorrhagic fever) is a severe, often fatal human illness caused by infection with viruses of the genus Orthoebolavirus (formerly Ebolavirus) within the Filoviridae family. To date, there are six known species of orthoebolaviruses: Ebola virus (EBOV, and formerly called Zaire ebolavirus), Sudan virus (SUDV), Reston virus (RESTV), Taï Forest virus (TAFV), Bundibugyo virus (BDBV), and Bombali virus, with the latter first identified in 2018. Among them, Reston and Bombali orthoebolaviruses have not yet been associated with human disease.

BDBV was first identified in 2007 during an outbreak in Bundibugyo District, in the Western part of Uganda, where molecular investigation showed that the virus was genetically distinct from previously known orthoebolaviruses (Towner et al., 2008).

Historically, the main documented BDBV outbreaks in humans occurred in Uganda (2007–2008) and the Democratic Republic of the Congo (2012), with limited outbreak-specific evidence on the original animal source.

In April 2026, a new outbreak of Ebola virus disease caused by BDBV was detected in Democratic Republic of the Congo, with imported cases subsequently reported in Uganda. As of 22 July 2026, 2,905 human cases had been confirmed in the Democratic Republic of the Congo (1,269 deaths), 20 in Uganda (2 deaths), and one imported case in France (U.S. Centers for Disease Control and Prevention, 2026).

The source of infection for the primary case(s) remains under investigation. To date, national authorities having not yet identified a specific animal species or exposure event responsible for the initial human infections.

Wildlife reservoir and host susceptibility to BDBV

Compared to Ebola virus (EBOV), which was discovered in 1976, the evidence for the presence of BVDV in animals remains extremely limited. To date, no field studies have demonstrated natural BDBV infection, shedding or maintenance of the virus in any wild or domestic animal population in Africa.

A longitudinal study conducted in African straw-coloured fruit bats (Eidolon helvum) in Cameroon between 2018 and 2019 showed antibodies reactive to BDBV antigens, indicating prior exposure to an ebolavirus antigenically related to BDBV (Djomsi et al., 2022). However, given the substantial cross-reactivity of antibodies to different orthoebolaviruses, these findings cannot reliably confirm BDBV circulation in this species.

In experimental settings, rhesus macaques have been shown to be susceptible to BDBV infection (Mire et al., 2013). Nonetheless, BDBV is less uniformly lethal than EBOV in this species, w ith survival associated with earlier activation of adaptive immune responses(Woolsey et al., 2021; Mire et al., 2013).

Domestic animal susceptibility to BDBV

To date, there is no confirmed evidence that domestic animals have played a role in BDBV outbreaks. However, experimental studies suggest that some domestic species may be susceptible to infection.

Studies in domestic pigs have shown that BDBV can establish a productive infection with tissue dissemination and viral shedding despite the absence of clear clinical signs (Lewis et al., 2022, 2024). Experimentally infected pigs developed detectable viral loads in the respiratory tract, suggesting that the respiratory mucosa may be an important route of virus excretion into the environment. A later immune-profiling study confirmed that BDBV infection in pigs is mostly subclinical but induces a strong adaptive response in the lungs and tracheobronchial lymph nodes (Kim et al., 2025).

Overall, these findings suggest that pigs could act as subclinical hosts with a possible role in viral amplification or environmental contamination. However, the epidemiological relevance of these observations for BDBV transmission under natural field conditions remains uncertain and requires further investigation.

Ferrets are considered a highly relevant mammalian model for studying orthoebolaviruses infectivity, pathogenesis and transmission because they are susceptible to infection with wild-type viruses and develop clinical signs that closely resemble those observed in humans.

Ferrets experimentally infected with clinical BDBV isolates became viraemic by day 4 and died between days 8 and –9, exhibiting rash, thrombocytopenia, lymphopenia, organ injury and uncontrolled virus replication in major organs (Kozak et al., 2016).. Additionally, Cross et al. (2016) demonstrated that wild-type BDBV is lethal in ferrets with systemic viral replication, confirming high susceptibility in this mammalian model. Infection leads to viremia and multiorgan involvement, particularly of the liver and spleen, with disease progression similar to non-human primates.

Evidence on potential animal reservoirs and hosts for other orthoebolaviruses

Wild animals

While the natural reservoir and spillover pathways for BDBV remain uncertain, studies of other orthoebolaviruses provide important ecological insights. Among bats and wild apes, the evidence is strongest for EBOV, considerably weaker for SUDV and extremely limited for TAFV. The only confirmed virological detections in putative reservoir hosts have been reported for EBOV, with viral ribonucleic acid (RNA) detected in three African fruit bat species and serological evidence identified in additional frugivorous and insectivorous bats.

Also for EBOV, wild apes and duikers (family Bovidae) are best understood as clinically susceptible, dead-end hosts rather than natural reservoirs (Leroy et al., 2005; Judson et al., 2016; Riesle-Sbarbaro et al., 2024).

Additional studies have also explored the potential roles of small rodents. One study detected anti-orthoebolavirus IgG antibodies in bats and rodents from samples collected in the Democratic Republic of the Congo in 2021 (van Vredendaal et al., 2024).

Domestic animals

Available evidence suggests that domestic animals play a more limited role in the ecology and transmission of human-pathogenic orthoebolaviruses.

Natural infection to ebolaviruses has been documented in dogs through serological studies. However, infections appear to be subclinical, and there is no evidence that dogs transmit the virus to humans (Allela et al., 2005; Olson et al., 2012; Haun et al., 2019; Fischer et al., 2020).

Among domestic animals, pigs have a clearer evidence of susceptibility to orthoebolaviruses infection and of viral shedding under experimental conditions. Field studies from East and West Africa have provided serological evidence consistent with infection to EBOV- or SUDV-like viruses, although natural infection with EBOV itself has not been documented (Atherstone et al., 2021; Fischer et al., 2018, 2020; Ogawa et al., 2022; Grayo et al., 2024). To date, natural infection in pigs has been demonstrated only for Reston virus in swine (Barrette et al., 2009).

Evidence of infection in small ruminants seems limited to a single study conducted in Gabon, in which goats and sheep showed a low seroprevalence of anti-EBOV antibodies but no detectable viral RNA. These findings are more consistent with environmental exposure than with active infection (Ndong Mebaley et al., 2025). 

Animal-to-animal transmission of BDBV

Lewis et al. (2024) reported limited evidence of potential pig-to-pig transmission of BDBV, based on seroconversion of a naïve animal co-housed with an experimentally infected pig. However, no active virus was detected in that contact animal.

Evidence on animal-to-animal transmission pathways for other orthoebolaviruses

Modes of EBOV transmission between forest-dwelling animal species are poorly documented but some studies have suggested that spillover from bats to non-human primates, duikers and other mammals may occur through the feeding of fallen fruits potentially contaminated by the spat and guano of bats (Gonzalez et al., 2007).

One study also reported bat predation by monkeys (Tapanes et al., 2016), suggesting another potential route for Ebola spillover into non-human primate populations. Chimpanzees are also known to hunt bush pigs which may provide an opportunity for EBOV transmission between infected pigs and chimpanzees (Atherstone et al., 2015).

In smallholder pig production systems in Uganda, domestic pigs often roam freely and regularly interact with wildlife around shared resources such as fruiting trees and feeding sites, increasing opportunities for cross-species pathogen exposure (Ouma et al., 2014).

Experimental studies have shown that pigs (Sus scrofa) are susceptible to EBOV infection and can transmit virus directly to in-contact naïve pigs and indirectly to non-human primates (cynomolgus macaques) (Kobinger et al., 2011; Weingartl et al., 2012).

Field observations during the 2017 Bas-Uélé outbreak in the Democratic Republic of the Congo reported unexplained pig mortality in villages within the outbreak area, raising the hypothesis of possible spillover into domestic pigs. However, no virological confirmation was obtained and alternative causes, such as African swine fever, could not be excluded.

Animal-to-human transmission of BDBV

The animal sources of the BDBV outbreaks that occurred in 2007, 2012 and, more recently, in 2026 remains uncertain, with only limited or conflicting information on suspected wildlife exposure.

An anthropological mission conducted during the BDBV outbreak in 2012 in the Democratic Republic of the Congo identified several potential risk factors for human exposure, including large movements of fruit bats, bat feeding in mango trees, the collection by residents of partially eaten fallen fruits, and possible contamination of palm wine collection containers by bats (Epelboin A., 2012).

Evidence on animal-to-human transmission pathways for other orthoebolaviruses

Based on current knowledge of orthoebolavirus ecology and previous outbreaks, groups at increased risk of exposure include hunters, bushmeat handlers, wildlife traders, forest workers, miners, people entering caves or bat roosting sites, farmers working near fruiting trees, and communities collecting or consuming fruit contaminated by animals.

Human serological studies conducted in Uganda among people with frequent wildlife contact found reactivity to SUDV, EBOV and BDBV antigens. Reported risk factors included touching duikers, hunting primates, and touching or consuming cane rats, although these associations were not BDBV-specific (Smiley Evans et al., 2018).

Similarly, a study in the Democratic Republic of the Congo indicated that visits to the forest, hunting activities, and exposure to rodents or duikers predicted a higher likelihood of EBOV seropositivity (Mulangu et al., 2018).

The active role of domestic dogs in the epidemiology of Ebola remains unclear. However, dogs and cats could potentially carry the virus and act as fomites after feeding on infected carcasses and moving contaminated animal remains closer to human populations.

A summary of the evidence for exposure, infection and transmission of BDBV is summarized in Table 1. Despite recent advances, many fundamental gaps remain regarding BVDV epidemiology, many of which also apply to other orthoebolaviruses.

Key evidence gaps include:

• Natural reservoirs remain unknown. To date, BDBV has not been isolated from wildlife. There is no confirmed evidence of animal infection in the wild. Serological signals in bats are difficult to interpret due to cross-reactivity with other ebolaviruses.
• Limited understanding of host range and susceptibility in wildlife and domestic animals.
• Unknown transmission dynamics between animals.
• Serology and diagnostics limitations, with cross-reactivity.
• Outbreak ecology, spillover pathways and spatial drivers remain poorly defined.
• Anthropological drivers to disease spillover into human populations.

Table 1. Summary of evidence of exposure, infection and transmission of Bundibugyo virus BDBV in different animal groups.

Animal group	Evidence of exposure	Evidence of infection	Evidence of transmission within or to other groups	Operational interpretation
Fruit bats	Serological reactivity reported though potential cross-reactivity with other orthoebolaviruses.	Natural infection not confirmed.	Unknown.	Consider as part of interface-focused investigations, but avoid assuming confirmed reservoir status.
Non-human primates	Experimental susceptibility in rhesus macaques. None in field.	Experimental infection demonstrated. None in field.	Unknown.	Relevant mainly for comparative susceptibility and wildlife event investigations.
Domestic pigs	Experimental infection and shedding reported. None in field.	Experimental infection with viral shedding demonstrated. None in field.	Limited experimental evidence consistent with pig-to-pig transmission. None in field.	Investigate only in risk-based contexts; do not imply confirmed natural role.
Ferrets	Experimental susceptibility.	Severe experimental infection demonstrated.	Unknown. Not relevant as natural host evidence.	Experimental model only.
Dogs/cats	Unknown.	Unknown.	Unknown.	Consider fomite/interface risk cautiously, not as confirmed transmission hosts.

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