1Department of Anthropology, University of Massachusetts at Amherst, MA, 2Department of Pathology, University of Massachusetts Medical School, Worcester, MA, 3Department of Medicine, University of Massachusetts Medical School, Worcester, MA
Saturday 2:15-2:30, Parlors
Due to the inactivation of the α1-3 galactosyltransferase (GT) gene approximately 28 MYA, the carbohydrate αGal is not expressed on the cells of Catarrhini, but is expressed in all other mammals. Viruses can utilize host cell carbohydrates in various ways such as binding receptors or attachment proteins. We found that susceptibility to certain viral infections is tied to the presence or absence of αGal on the surface of host cells. We show that Sindbis virus (Alphavirus) replicates well in αGal-positive cells but herpes simplex viruses (HSV-1 and HSV-2) preferentially grow in cells lacking αGal. In both cases, differences in infection levels result from the ability of the virus to successfully initiate infection. This points to a role for αGal in the early stages of viral infections. We also show that GT knockout mice infected with HSV-2 have higher viral load and greater pathology compared to WT B6 mice that naturally express αGal. This is clear evidence that the presence or absence of αGal in cells or animal hosts has an effect on the course of viral infections. Our results have implications for the evolution of resistance to viral infections in catarrhines. Pathogens exert great selective pressure on their hosts, and it is possible that a pathogen, able to exploit αGal, could have helped shape primate lineage evolution during the Oligocene.
This material is based upon work supported by the National Science Foundation SBE DDRIG Grant No. 0925717 to IAR and LRG.