A worldwide collaboration of researchers report solving the complete genome of Brugia malayi, one of the worms that cause elephantiasis.
“Filarial diseases are treatable, but the current treatments were discovered decades ago,” says Anthony S. Fauci, M.D., director of the NIAID, funded the work. “There is an urgent need for new discoveries in this area because of the limitations of the current drugs, including toxicities and the development of resistance.”
The research team analyzed the 90 million base pair genome of B. malayi. From the sequence analysis, they predicted approximately 14,500–17,800 protein coding regions in the B. malayi genome. These results are in agreement with previous estimates.
Comparative analysis of the B. malayi genome with that of C. elegans revealed that more than 20% of the predicted proteins in B. malayi are specific to the parasite.
The investigators believe their findings will be helpful for the discovery of more targeted and effective drug therapies. They identified several metabolic pathways containing dozens of gene products. These include pathways involved in molting, nuclear receptor responses, collagen processing, neuronal signaling, protein phosphorylation, and host and endosymbiont metabolism.
When the researchers compared the sequences of proteins of B. malayi to that of interleukins, chemokines, and other immune signaling molecules from humans, they found a number of candidates which they think are responsible for allowing the worm to evade immune detection.
Along with NIAID scientists, the study involved researchers from 11 Universities across Europe, Australia, and the U.S., New England Biolabs, Divergence, Cambria Biosciences, the J. Craig Venter Institute, New York Blood Center, and the Hospital for Sick Children, Ontario. The study is published in the September 21 issue of Science.