Tag: 8/9/26

DRC’s Ebola Epidemic Could be the Worst in History: 4 Things that Could Help End it

Yap Boum, Mbarara University of Science and Technology and Marie Roseline Belizaire, Universidad de Alcalá

The Democratic Republic of Congo’s fight against Ebola has reached a tipping point. It can accelerate what it has been doing to bring the latest outbreak under control, or risk allowing it to persist as the worst Ebola epidemic ever recorded.

As at 1 September 2026, more than 6186 confirmed cases and 3007 deaths have been reported since May 2026 when it was first declared. It is the deadliest Ebola outbreak in the history of the DRC. The outbreak is being driven by the Bundibugyo strain of the virus that causes Ebola disease. There is currently no licensed vaccine or specific treatment for Bundibugyo.

The outbreak is thought to have originated in the high-mobility mining area of Mongbwalu in Ituri, north-east DRC, in late April 2026, before spreading through interconnected communities and healthcare networks to Rwampara and Bunia – health zones in the Ituri province – and subsequently Uganda.

The response to the outbreak has been nationally led by the government of the DRC, with Africa Centres for Disease Control, the World Health Organization and other partners supporting the expansion of surveillance, laboratory capacity, treatment centres, infection prevention and control, vaccination, logistics, community engagement and safe and dignified burials.

Significant progress has been achieved, including interruption of transmission in Uganda through decisive national leadership and close collaboration with communities.

However, in the DRC, insecurity, population mobility, delayed detection, gaps in financing and supplies, and insufficient community ownership have continued to sustain transmission.

The response is therefore not yet sufficient to interrupt transmission in the DRC. This underscores the need to bring surveillance, testing, treatment, vaccination and community engagement closer to the village level.

As public health experts with expertise in Ebola who have been at the forefront of containing the latest outbreak in DRC, it is our view that more is required.

What’s required is informed by the four factors that have made this epidemic difficult to control:

  • the DRC’s difficult geographical and humanitarian environment
  • highly mobile populations
  • low trust and poor community engagement
  • the incomplete scientific arsenal against the Bundibugyo virus.

The four factors

First, this is an outbreak occurring in an exceptionally difficult environment. The affected areas are vast, remote and, in many places, insecure. Short journeys can take a day or more on bad roads, particularly during the rainy season (which is now).

Second, populations are highly mobile. Mining communities, motorcycle transport, displacement and cross-border movement connect villages and health zones that are difficult to monitor. The outbreak has been concentrated in several interconnected areas, particularly in Ituri, about 2,886km from Kinshasa, the DRC capital. Bunia, the main urban hub in Ituri, is connected to surrounding transmission areas. Movement of people is important in the response.

Third, trust and community engagement remain challenges. When people are afraid, when health facilities have closed after health workers have died, or when families have experienced Ebola without seeing an effective response, they may delay or avoid getting help. This directly affects surveillance. Current investigations by our team suggest that a substantial proportion of cases are being identified outside established contact lists. The response therefore cannot depend only on traditional contact tracing.

Fourth, unlike Ebola caused by the Zaire species, the Bundibugyo virus has no licensed vaccine or specific treatment. Clinical research is therefore part of the response itself.

The DRC has launched Ebola vaccination in Kisangani. The first injections were administered to health workers and other frontline responders. More than 50 000 doses have been received. The International Coordinating Group on Vaccine Provision has approved 70 000 doses of Ervebo for use in the country. Around 20 000 doses will be used in a clinical trial to assess its effectiveness against the Bundibugyo strain.

The response thus far

It is important to recognise how much has been achieved in only three months – between 15 May and 15 August 2026.

More than 20 Ebola treatment and isolation facilities have been established or supported. At the height of the crisis in late May 2026, treatment capacity was overwhelmed, with bed occupancy exceeding 200%. In late August, occupancy had fallen to around 66%.

Laboratory capacity has expanded dramatically, with 22 laboratories operating across the five affected provinces. Before there was only one in Kinshasa with the capacity to detect Bundibugyo. This has helped reduce turnaround time between sample collection and result, from over a week to just hours.

Safe and dignified burials have also improved substantially, with the vast majority now taking place within 24 hours.

These improvements matter. They are signs that the response can change the trajectory of an epidemic when resources, coordination and technical capacity come together.

There are also encouraging epidemiological signals. The effective reproduction number has fallen substantially from the very high levels (Rt 4.0) observed in May. The average number of people that each patient infects has fallen from four to just over one.

The scale of resources mobilised for the outbreak is substantial, with approximately US$1.72 billion in pledges, including US$118.5 million committed by African countries. Around US$867 million (about half of the pledges) has reportedly been released.

The continental response plan launched on 27 June 2026 by Africa CDC and WHO was designed around a simple principle: one plan, one budget, one team, one monitoring and evaluation framework, with communities at the centre.

What’s required

The next phase must centre on the villages. Local representatives, health workers and leaders should become active partners in surveillance, early detection, referral, risk communication and community protection.

Digital tools can support this, but technology must serve the community rather than replace it.

Commercial motorcycle riders, who connect communities across enormous distances, must be engaged as partners in the response rather than being treated simply as a risk.

Vaccination must be brought closer to communities. Research must be done where the epidemic is occurring. Clinical trials of vaccines and therapeutics must proceed with urgency and scientific rigour.

Rebuilding trust

Essential health services must continue alongside Ebola control.

The same applies to the reopening of schools. This must happen with infection-prevention measures, including training teachers, providing hygiene facilities, developing clear referral mechanisms, and adapting communication about the epidemic for school children and families.

Humanitarian and Ebola responses must also be integrated. A community facing insecurity, displacement and disease cannot be expected to navigate separate systems for each crisis.

Finally, Ebola doesn’t respect borders. The collaboration between the DRC and Uganda shows what regional solidarity can look like. It’s about joint surveillance, moving diagnostic capacity closer to border communities, sharing information and coordinated action. The DRC-Uganda lessons must be extended to South Sudan, the Republic of Congo and other neighbouring countries as agreed in Bangui, Central African Republic, in mid August.

Yap Boum, Professor in the faculty of Medicine, Mbarara University of Science and Technology and Marie Roseline Belizaire, Researcher, School of Medicine, Universidad de Alcalá

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Cancer Drug Reduces Atherosclerosis Inflammation and Plaque

Source: Wikimedia CC0

A new Yale study has identified a promising therapeutic avenue for atherosclerosis, a condition caused by inflammation and plaque buildup in arteries.

Martin Schwartz, PhD, Robert W. Berliner Professor of Medicine (Cardiology) and the study’s principal investigator, investigates how the mechanical forces from blood flow and pressure affect the cells lining the arteries and how cell responses to forces contribute to cardiovascular disease. Atherosclerosis predominantly impacts regions of the arteries that bend or branch, creating disturbances in blood flow dynamics that activate cells’ inflammatory pathways and eventually lead to plaque buildup.

In a study published August 31 in Proceedings of the National Academy of Sciences, Schwartz’s team, led by associate research scientist Divyesh Joshi, PhD, has now found that a protein complex called Polycomb Repressive Complex 2 (PRC2) is associated with disturbed blood flow, and that it inhibits anti-inflammatory mechanisms in the arteries that mitigate atherosclerosis.

By blocking PRC2, the team successfully reduced harmful plaque in animal models of the disease.

“By inhibiting PRC2, we boost protective pathways that reduce inflammation and could protect people from plaque rupture in atherosclerosis,” Schwartz says.

What causes atherosclerosis?

Atherosclerotic plaques are present in nearly all adults in developed countries. They are usually asymptomatic because a protective fibrous cap forms over the plaques. But if the cap weakens and ruptures, it triggers the formation of a blood clot that can lead to a heart attack or stroke. Plaques vulnerable to rupture tend to have a thinner cap or exhibit heightened inflammation.

Scientists believe there are three types of factors driving atherosclerosis. The first are metabolic risk factors, including elevated cholesterol and blood sugar. Inflammation is another – individuals with autoimmune or other inflammatory diseases are at a higher risk for the disease.

An important but overlooked third factor, Schwartz says, is the biomechanics of blood flow through the arteries. In places where the arteries are straight tubes, the blood flow activates protective, anti-inflammatory genes. Where arteries curve sharply, disturbing blood flow, there are fewer of these protective factors and increased inflammation.

Protein complex suppresses protective genes

The cells lining the arteries, called vascular endothelial cells, have receptors that detect blood flow. Previous research in Schwartz’s laboratory has shown that blocking those receptors can inhibit inflammatory processes and enhance protective ones. In the new study, the researchers investigated the underlying mechanisms of the inflammation associated with disturbed blood flow.

First, they used previously published datasets to investigate genes that interact with anti-inflammatory genes in endothelial cells, and then identified those that promote disease. These analyses revealed that genes associated with PRC2, a protein complex that inhibits gene expression, were strongly associated with suppression of certain anti-inflammatory genes.

“PCR2 is understood to be pro-inflammatory in vascular endothelial cells,” Joshi says.

The researchers also studied gene expression in human endothelial cells exposed to normal and disturbed blood flow. These experiments confirmed that genes associated with PRC2 are upregulated during disturbed blood flow where inflammation tends to be higher.

However, when the researchers treated endothelial cells with tazemetostat, a drug that inhibits PRC2 and was previously used to treat cancer, they found that inflammatory signals were reduced. The findings suggest targeting PRC2 could be a treatment for atherosclerosis.

A new avenue for treating atherosclerosis

To explore PRC2 inhibition as a therapeutic avenue, the researchers developed animal models of the disease and tested the effects of tazemetostat. They found that the drug slowed plaque growth and reduced the amount of vulnerable plaque.

“It takes an unstable plaque and turns it into a more stable form that is no longer at risk of rupture,” Schwartz says.

Since conducting the study, the manufacturers of tazemetostat have withdrawn it from the market due to emerging evidence that patients who take the drug have a slightly increased risk of secondary cancers. But there are other PRC2-inhibiting drugs that may be similarly useful for treating atherosclerosis, the researchers note.

“This is a potential path forward to treating patients,” Schwartz says.

By Isabella Backman

Source: Yale School of Medicine

Are Antibiotics an Effective Treatment for Chronic Low Back Pain?

Photo by Sasun Bughdaryan on Unsplash

There has been considerable interest in prescribing antibiotics for chronic low back pain from disc herniation, stemming from the hypothesis that low-grade bacterial infections within spinal discs may contribute to persistent symptoms, particularly in cases involving Modic changes, which are bone marrow abnormalities visible on MRI.

A new randomised clinical trial investigated whether the antibiotic amoxicillin-clavulanate could effectively reduce chronic low back pain in patients with disc herniation. Researchers conducted a double-blind, placebo-controlled study involving 170 participants over a 12-month period to assess improvements in pain intensity and disability.

The trial found that taking amoxicillin-clavulanate for 90 days provided no significant reduction in pain or disability compared to a placebo. These findings suggest that the routine prescription of antibiotics for back issues is ineffective and potentially harmful due to the risk of side effects and the global threat of antimicrobial resistance.

Clinical experts advise against this approach, noting that current evidence does not support using these drugs even when traditional treatments have failed. Consequently, the study reinforces the need for evidence-based management and cautions against relying on unproven pharmaceutical interventions for complex spinal conditions.

Listen to the podcast for a deep dive into the results!

SAHBA 2026: Beyond Clinical Excellence

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