Roseolovirus particles emerge from an infected immune cell (above). Studying mice, researchers at Washington University School of Medicine in St. Louis have discovered that roseolovirus can trigger autoimmunity in a previously unknown way: by disrupting the process by which immune cells learn to avoid targeting their own body's cells and tissues.
Credit: Bernard Kramarsky
Researchers at Washington University School of Medicine in St. Louis have discovered how a virus can probably make our immune system turn against us to create autoimmune diseases such as arthritis, lupus and type I diabetes, long after infection by the virus.
In the wackadoodle world of Creationism, this means that the viruses in question were designed specifically to produce that outcome since, being omniscient, the designer knows exactly what the outcome will be and so designs them for that exact function.
The fact that it does this to use a system it supposedly designed to protect us from the parasites like viruses and bacteria it designs to harm us with, is not seen as a reason to doubt the intelligence or sanity of this supposed designer!
It is very hard to find the culprit of a crime that was never even at the scene of the crime. As clinicians, we often look directly in the diseased tissue, and if we find no virus we conclude that the disease was not caused by a virus. But here we have a situation in which a virus is doing its damage someplace else entirely. This virus goes to the thymus, which is where T cells undergo a process to select those cells useful for immune defense but also get rid of T cells that are too likely to damage the body’s own tissues. And what we find is that this whole process, which is called central tolerance, is affected. T cells that shouldn’t leave the thymus get out, and they manifest months later in the stomach, causing an autoimmune disease in a location that was never infected with the virus.
Human autoimmune disease also may occur via viral infection that gets cleared but leaves damage that can cause autoimmunity, 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.
What the researchers discovered is that a key process of the immune system that occurs in the thymus gland is disrupted by a virus. The problem is that some viral proteins can closely resemble the body’s own proteins and so some T cells produce antibodies against those proteins as well as against the viral proteins. The disrupted process in the thymus normally identifies and destroys any T cells which have this self-destructive capability. This allows rogue T cells to escape into the body and start attacking cells, setting up an autoimmune disease long after the virus itself has been eliminated. In effect, these naturally occurring rogue T cells become agents of the virus. Human autoimmune disease also may occur via viral infection that gets cleared but leaves damage that can cause autoimmunity, 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.
Professor Wayne M. Yokoyama, MD, senior author.
The Sam J. Levin and Audrey Loew Levin Professor of Arthritis Research.
Washington University School of Medicine in St. Louis
St. Louis, MO, USA
The Sam J. Levin and Audrey Loew Levin Professor of Arthritis Research.
Washington University School of Medicine in St. Louis
St. Louis, MO, USA
The team, led by Professor Wayne M. Yokoyama, used mice which were infected with the murine roseolovirus - a close relative of the human roseolovirus, both members of the herpesvirus family. Viruses in this family can result in life-long infections by remaining hidden from the immune system until reactivated by some environmental trigger, but the human roseolovirus rarely causes a problem after the initial infection. Most human children will be infected by this ubiquitous virus before starting school and symptoms of infection may be a rash and a mild fever, which subsides within a few days.
We don’t think the autoimmune gastritis is the result of molecular mimicry because we observed such a broad autoantibody response. The observation that infected mice produced diverse autoantibodies, in addition to the anti-stomach autoantibodies, suggested that murine roseolovirus infection early in life was inducing a wide-ranging defect in the body’s ability to avoid targeting its own proteins. This is why we focused our studies on the impact of infection on central tolerance rather than molecular mimicry.
Baby mice were infected then divided into three batches - those that were treated with antiviral drug treatment in the first few days, those treated 8 weeks later, after the virus infection had been resolved, and those given no treatment. Those treated 8 weeks later and those not treated at all went on to develop the autoimmune inflammatory stomach condition in mice, gastritis, 3 months later. Those treated promptly did not develop the disease. No virus particles were present in the stomach.Dr. Tarin Bigley, MD.
Department of Pediatrics
Division of Rheumatology
Washington University School of Medicine,
St. Louis, MO, USA
Department of Pediatrics
Division of Rheumatology
Washington University School of Medicine,
St. Louis, MO, USA
From the Washington University School of Medicine press release:
Scientists already knew that viral infections can lead to autoimmunity if some of the virus’s proteins happen to resemble normal human proteins. Antibodies meant to target the virus end up also reacting with normal human cells. The researchers found that the mice with gastritis had developed antibodies against proteins on stomach cells. But they also had developed antibodies against a wide array of normal proteins associated with other autoimmune conditions. In addition, they had many T cells that targeted the body’s own normal proteins, and other changes to the T cell population that biased the immune system toward autoimmunity.The team's results are published, open access in the Journal of Experimental Medicine:
Graphical Abstract
Infections with herpesviruses, including human roseoloviruses, have been proposed to cause autoimmune disease, but defining a causal relationship and mechanism has been difficult due to the ubiquitous nature of infection and development of autoimmunity long after acute infection. Murine roseolovirus (MRV) is highly related to human roseoloviruses. Herein we show that neonatal MRV infection induced autoimmune gastritis (AIG) in adult mice in the absence of ongoing infection. MRV-induced AIG was dependent on replication during the neonatal period and was CD4+ T cell and IL-17 dependent. Moreover, neonatal MRV infection was associated with development of a wide array of autoantibodies in adult mice. Finally, neonatal MRV infection reduced medullary thymic epithelial cell numbers, thymic dendritic cell numbers, and thymic expression of AIRE and tissue-restricted antigens, in addition to increasing thymocyte apoptosis at the stage of negative selection. These findings strongly suggest that infection with a roseolovirus early in life results in disruption of central tolerance and development of autoimmune disease.I wonder how much longer it is going to take before religious fundamentalist Creationists dupes realise what they've been fooled into believing. The Discovery Institute and its hirelings have, maybe inadvertently, but in all probability, for right-wing political purposes not connected with worship of any assumed god, come up with a notion which, while appealing specifically to those with little understanding of science or evolutionary biology, portrays what they think of as an all-loving, benevolent creator god, as the pestilential, mendacious, sadist these many examples of the amoral design stupidity that abound in nature, show any designer of such things to be.
Bigley TM, Yang L, Kang LI, Saenz JB, Victorino F, Yokoyama WM.
Disruption of Thymic Central Tolerance by Infection with Murine Roseolovirus Induces Autoimmune Gastritis. Journal of Experimental Medicine. (2022); 219 (3): e20211403; DOI: 10.1084/jem.20211403
Copyright: © 2022 The authors. Published by Journal of Experimental Medicine
Open access
Reprinted under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 Internationallicense (CC BY 4.0)
Certainly, I have so far found none willing to debate the many examples to be found in my illustrated book, The Malevolent Designer: Why Nature's God is not Good, in an adult style or without resort to the religious superstation about some assumed 'fall' that gives the game away that ID is just religious fundamentalism dressed in a grubby lab coat in order to fool American legislators.
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