New evidence points to why genes that make us susceptible to infections and autoimmune diseases continue to be passed down instead of being eradicated from the gene pool.
The National Science Foundation (NSF) reports that biologists conducting research funded by the NSF and the National Institute of Allergy and Infectious Diseases have discovered evidence of why mice, people and other vertebrate animals carry thousands of varieties of genes that create MHC immune-system proteins (Major histocompatibility complex) yet some of these genes make vertebrate animals susceptible to infections and to autoimmune diseases.
According to the NSF report, MHC proteins "identify invading germs, reject or accept transplanted organs and help vertebrates smell compatible mates." Once they have distinguished ‘friendly’ or similar proteins from foreign ones they activate an immune response against the ‘foreign bodies.'
The report explains that although each person carries approximately 12 varieties of the six human MHC genes, the human population has anywhere from hundreds to over 2000 types of each of the six human genes that produce MHC proteins.
Certain MHCs actually make people more vulnerable to pathogens (disease-causing viruses, bacteria or parasites) including the AIDS virus, malaria and hepatitis B and C and autoimmune diseases such as type I diabetes, rheumatoid arthritis, lupus, multiple sclerosis, irritable bowel disease and ankylosing spondylitis.
Microbes in a testtube
Scientists have proposed three theories as to why so many MHC gene variants exist in vertebrate animal populations:
One theory is that “an organism with more MHC varieties has a better immune response than organisms with fewer varieties, so over time, organisms with more MHCs are more likely to survive.”
Another is that according to past research “people and other animals are attracted to the smell of potential mates with MHCs that are ‘foreign’ rather than ‘self’ and parents with different MHC variants produce children with more MHCs and thus stronger immune systems."
The third theory is that pathogens mutate and evolve to become less recognisable by the MHCs and thus evade an immune response. Consequently, the pathogens thrive.
In their study, the scientists created emerging diseases by causing a mouse leukaemia virus to evolve in mice. This process showed how the virus adapted to specific MHC proteins.
In the NSF report biologist Wayne Potts of the University of Utah says that the results of this study explain why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated.
Potts is stated as saying:
The experiments demonstrate the first step in the antagonistic co-evolutionary dance between a virus and MHC genes. It's a model to identify what things change in viruses to make them more virulent and thus emerging diseases.
In addition to Potts and Kubinak, the paper's lead author, the paper's co-authors are James Ruff, Cornelius Whitney Hyzer, and Patricia Slev, all of The University of Utah.