The World Health Organization (WHO) estimates that onchocerciasis–an eye and skin infection more commonly known as river blindness–currently affects an estimated 18 million people worldwide, predominantly in sub-Saharan Africa.
Scientists have now sequenced the genome of the parasitic worm responsible for causing this condition, gaining valuable insight into the workings of the parasite and identifying proteins that potentially could be targeted for medical countermeasure development.
In a pair of research papers published this week in Nature Microbiology, the scientists describe sequencing the complete genomes of O. volvulus worms gathered from Ecuador, Uganda and West Africa. Additionally, they reconstructed the genetic makeup of Wolbachia, the symbiotic bacteria that lives within the worms.
River blindness is commonly treated using the anti-parasitic medication ivermectin. However, a complete cure can require decades of treatment, and some researchers are concerned that widespread use of ivermectin may cause the worms to develop resistance to the drug. Additionally, ivermectin can cause severe side effects in patients who also have Loa loa, another parasitic worm infection.
By examining the genomes of the worms and their symbiotic bacteria, the researchers were able to identify genes that coded for common proteins and molecular reactions essential to infection. 16 of the newly discovered proteins look promising as targets for existing drugs not currently used as treatments for river blindness, adding to the potential new medications for the disease. Further, the authors note, the protein data will accelerate development of new treatments for river blindness as well as other diseases associated with parasitic worm infections.
The research was conducted in part by scientists employed or supported by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. Additional funding for one of the studies was provided in part by NIH’s National Human Genome Research Institute.