Geneticists at the American Museum of Natural History trace the evolution of St. Louis encephalitis

Solving the mystery of disease origins

Before West Nile virus arrived in this country, we had (and still have) a home-grown relative of this pathogen. An epidemic of unknown origin exploded around St. Louis, Missouri in the autumn of 1933, a disease that is now known to be transmitted by mosquitoes from birds to people. Now, a new analysis of the genome of St. Louis encephalitis completed at the Sackler Institute for Comparative Genomics at the American Museum of Natural History (AMNH) is shedding light on the evolution of this virus.

Under the direction of Susan Perkins, Assistant Curator of Microbial Genomics, postdoctoral fellows Gregory Baillie, Sergios-Orestis Kolokotronis, and Eric Waltari sequenced the entire genetic code of 23 strains of the virus that cause St. Louis encephalitis, all from the genus Flavivirus. Previous research had found that recombination (the cutting and pasting of strands of genetic material, in this case RNA) explained the evolution of this virus, but these studies sequenced just a single gene of the virus. Because the whole-genome approach turned a microscope on the entire set of instructions for St. Louis encephalitis, the AMNH researchers were able to determine that a single mutation in the coding for an envelope protein rather than recombination most likely caused changes that made the virus pathogenic to humans. “Recombination is important for disease; it makes novel proteins or genes that the immune system has never seen before,” explains Perkins. “But in this case, it was population dynamics combined with slight changes in the form of point mutations that have been important in the evolution of this virus.”