But that's because it is the only place researchers are looking. The major histocompatilbility complex (MHC) region remains the area under exploration, now 40 years since its initial discovery.
And they continue to get research grants from pharmaceutical companies to continue to look at the same location, because making this connection to the autoimmune theory advances drug sales.
In fact, the connection to heretability and genetics in MS is rather slim. In identical twins, genetic risk is less than 1/3 if one twin has MS.
...there is a 2% to 4% elevated genetic risk in siblings of patients with MS and a 30% greater risk in identical twins.
There was a recent story in the NY Times regarding research into a potential genetic link found in those who die due to Ebola infections. Researchers Angela L. Rasmussen and Michael G. Katze of the University of Washington found a problem with blood vessels, which were allowing immune cells open access and an overblown reaction to the virus. That's right. Death from Ebola happens because of a break down of the endothelium, or the lining of blood vessels. And there is a potential genetic link.
About two-thirds of people who die from Ebola never develop the terrifying hemorrhages that appear in others a day or two before death, in which eyes turn fiery red, gums bleed, red dots emerge on the skin as blood seeps out of capillaries, and blood appears in vomit and diarrhea. Many mice, too, die of Ebola without hemorrhages.
The mouse studies indicate the animals that hemorrhage and — by implication, humans— die because their immune systems overreact to the virus. The result is an inflammatory response that makes cells leak fluids and white blood cells, and makes tissues and organs deteriorate. Many die at that point. In those mice — or humans — that survive long enough, the researchers propose, blood eventually starts to seep out of vessels.
In fact, researchers found a genetic link to two specific genes, which were allowing for the overblown inflammatory response.
The mouse studies showed that animals that died after bleeding had an overblown inflammatory response to the virus. They also had low activity of two genes, Tie1 and Tek, that made their blood vessels more permeable. The leaky vessels allowed white blood cells to stream out, escalating the inflammatory response and causing a chain reaction of damaging immune system chemicals that destroyed organs.
She said that “a big take-home lesson from the paper” is that genetics plays a major role in determining the outcome of a mouse’s Ebola infection. By inference, she said, genetics probably plays the same role in humans.
(for those who enjoy learning more, here is a paper on how Tie1 and Tie2 (TEK) are involved in vascular permeability.)
From his abstract at the ISNVD: