Population bottlenecks caused by stark population loss due to illness or habitat destruction caused mammals' disease immunity to decline, according to a new study led by computational biologists in the Penn State School of Electrical Engineering and Computer Science. The finding comes from the first comparative study of genomic sequences - roadmaps of DNA instructions responsible for encoding how the body works - encoding immunity in 46 mammals.
The study, published in Molecular Biology and Evolution, is the first step for scientists analyzing regions of mammalian DNA that were previously inaccessible without modern biotechnology computational tools, according to team lead Yana Safonova, assistant professor of computer science at Penn State.
"Genes influence how our body works: Humans and animals have genetics predisposed to certain diseases based on DNA," Safonova said, explaining that although the same basic building blocks make up DNA across the 46 mammals assessed, the genomic sequences diverged wildly. "So, even though we might have a similar set of genes, they are different based on variations in the DNA architecture."
In the immune system, things are complicated further by something known as adaptive immunity. As opposed to the non-discriminatory defense the immune system deploys at the first hint of an infection, adaptive immunity refers to the parts of the immune system that study the specifics of a pathogen and design antibodies precisely targeted for it, should it invade again. Antibodies are produced from highly variable "template" genes encoded in the genome, Safonova explained, and this variability enables versatile immune responses through the generation of antibodies against diverse targets.
