Chimpanzee models for human disease and immunobiology.

Chimpanzees have greater than 98% genomic sequence homology with humans but have significantly more favorable responses to human immunodeficiency virus (HIV)-1 and hepatitis B virus (HBV) and an apparently low incidence of epithelial malignancy. Although there are few shared major histocompatibility complex (MHC) alleles between human and chimp, there is considerable overlap in binding repertoires for epitopes of HIV-1 and HBV. This indicates that differences in viral handling may be due to involvement of cells other than T lymphocytes. Similar mechanisms may be involved in host response to dysplastic or malignant cells. In seeking to understand these differences, most attention has been focused on comparing and contrasting well-characterized steps in immune response. As an additional possibility, alterations in cell-cell interactions dependent upon sialic acid binding proteins known to be involved in immune responses should also be considered. The lack of a particular sialic acid structure (N-glycolyl neuraminic acid, or Neu5Gc) in humans, due to a gene mutation in an essential synthetic enzyme, has potentially altered the kinetics of cellular responses dependent upon these lectins. The absence of Neu6Gc represents the only known major biochemical difference between humans and chimpanzees.