Ebola outbreak circulated undetected for months, study finds

A Bundibugyo ebolavirus outbreak in Central Africa began with a new spillover from an animal reservoir and circulated undetected for at least four months, ERR reports, citing a study published in Nature Medicine.

Genetic data indicate that the first people were infected in the Democratic Republic of the Congo in January or February, although Congolese authorities declared the epidemic on May 15. The virus then spread directly from the Congo to Uganda in an uninterrupted chain of transmission.

Bundibugyo ebolavirus is one of the three most dangerous Ebola variants. There is currently no vaccine or treatment for it. People have been exposed to the virus on a larger scale only twice before, in 2007 and 2012, and roughly more than one in three infected people died.

Hospitals in the Democratic Republic of the Congo and Uganda reported a new suspected cluster this spring, but the rapid tests initially used repeatedly failed to detect the infection. The failure of standard diagnostics concealed the true scale of the outbreak.

An international team led by Placide Mbala-Kingebeni analysed samples from 22 patients in laboratories in Kinshasa and Kampala. Twenty-one samples were clean enough for research. The resulting genetic tree showed that the outbreak virus differs from earlier strains and forms a distinct new branch, indicating that people were infected by a new animal host rather than by a previously dormant outbreak.

Researchers also found a direct genetic link between cases identified in the Democratic Republic of the Congo and Uganda. All the Ugandan patients analysed belonged to the same transmission chain that began in the Congo. High population density and active migration around mining areas helped the virus spread, while national borders did little to stop it.

The researchers used changes caused by the human immune system to trace the virus’s spread. An enzyme called ADAR attacks the double-stranded RNA produced when the virus reproduces, changing its genetic code. It replaces adenosine with inosine, which the virus later copies as guanosine.

These accumulated mutations act as a biological clock. Samples from this year’s outbreak differed by 25 mutations in total, nine of which showed a clear signature of the human enzyme. Because this defence mechanism occurs only inside the human body, the number of mutations indicated that the virus had been circulating unnoticed in communities for several months before coming to the authorities’ attention.