Mouse study suggests viral infections can lead to autoimmune diseases

Mouse study suggests viral infections can lead to autoimmune diseases
An infected cell releases roseolovirus particles
An infected cell releases roseolovirus particles
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An infected cell releases roseolovirus particles
An infected cell releases roseolovirus particles

Evidence is mounting that seemingly innocuous viral infections can in some cases cascade into a range of more serious diseases. In a new study in mice, researchers at Washington University in St. Louis have uncovered a mechanism by which a common childhood virus could play a role in autoimmune diseases down the track.

Viral infections are extremely common throughout our lives, with most resolving without serious issue. But recent research is increasingly showing that many of these apparently benign infections could possibly, in combination with other genetic and environmental factors, trigger diseases like Alzheimer’s, multiple sclerosis, and several types of cancer. Exactly how these viruses set off these chain reactions remains unclear, but in the new study the researchers may have uncovered one possible mechanism.

Roseolovirus is a type of herpesvirus that infects almost everyone within the first few years of life. The initial illness is usually mild, involving a rash and a fever that clears up in days, but the virus itself sticks around for a lifetime, lying dormant. While it usually doesn’t cause any symptoms after that initial infection, scientists have suspected that it may play a role in autoimmune diseases.

So for the new study, the Washington researchers investigated the link. They found that the virus seems to be able to infect the thymus, the organ where T cells mature so they can recognize foreign antigens. But the thymus also eliminates T cells that are liable to attack the body’s own cells – and it’s this latter process that the virus can disrupt. With this checkpoint weakened, more defective T cells circulate and increase the risk of autoimmune diseases.

The team uncovered this mechanism in experiments in mice. They started by infecting newborn animals with a mouse version of roseolovirus, and found that 12 weeks later, all of the mice had developed autoimmune gastritis, an inflammation of the stomach.

In other tests, the researchers treated the virus to see if that had an effect on the gastritis – when antivirals were administered over the first few days of infection, the inflammation didn’t occur. But if the drugs were given eight weeks later, it was too late to stop the gastritis from developing by the 12-week mark.

While the autoimmune problems manifested in the stomachs of the infected mice, analysis revealed that the extent of the problem ran further. The team found that the mice had not only developed antibodies against proteins on stomach cells, but to a range of other proteins throughout the body, some of which are implicated in other autoimmune diseases.

It’s important to note, however, that this study was performed on mice, with a mouse virus, and the results may not necessarily translate to humans. But the team says that the human roselovirus is very similar to that found in mice, so it at least warrants further investigation as a potential cause. Even so, it must only be one piece of the puzzle, due to how common the virus is.

“Human autoimmune disease also may occur via viral infection that gets cleared but leaves damage that can cause autoimmunity,” said Wayne Yokoyama, senior author of the study. “But if so, there has to be some other factor that we don’t understand yet that makes some people more susceptible to the autoimmune effects of roseolovirus infection, because almost all people are infected, but most people do not get autoimmune diseases. That is a really important topic for further investigation.”

The research was published in the Journal of Experimental Medicine.

Source: Washington University in St. Louis

Nice article Michael!
You really have to respect Washington Unersity in StL. The science behind these findings (in mice) are solid, we have suspected this process for several years now and it is good to have proof in peer reviewed journals. While we in medicine like to point out that non-human studies - no matter how well performed on extremely similar species - much of their physiology is very similar to ours - this is a mouse study and we cannot ABSOLUTELY draw anything more than a possible correlation from these results. (wink, wink).

Can't wait for the studies that narrow down the cause of Type I diabetes, Rheumatoid arthritis, and lupus. Many other auto-immune illnesses abound, but those three afflict many who remain partially functional in our world. If we determine the trigger and how the trigger affects the immune system in humans - we can develop a block that may eliminate these outcomes without destroying the life of the patient!
This has implications for ME / CFS /SEID (myalgic encephalitis / chronic fatigue syndrome / systemic exertion intolerance disease), often linked with Epstein-Barr virus (EBV), and for long COVID, which is very similar to chronic fatigue syndrome.