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Hypotheses Explaining The Development Of Autoimmune Disease Include
Share on PinterestScientists have come closer to unraveling the mystery of long COVID pain and finding treatments for it. Sabine Kriesch/EyeEm/Getty ImagesResearchers investigated how COVID-19 affects pain-signaling. They found that SARS-CoV-2—the virus that causes COVID-19—leaves a gene expression signature in neurons that relay sensory information to the brain. This signature was also seen in pain caused by other conditions.The scientists hope their findings will help drug development to treat pain in long COVID.Studies show that between 4.7% and 80% of people who have recovered from COVID-19 develop long COVID. One analysis of health records from 273, 618 COVID-19 survivors found that within six months of recovering from the initial infection:12.6% experienced chest or throat pain11.6% experienced other pain 3.24% experienced myalgiaUnderstanding how COVID-19 can lead to long-term symptoms of pain could help clinicians better treat patients with long COVID. In a recent study, researchers analyzed RNA sequencing data to unravel the biochemical effects of SARS-CoV-2 on pain signaling. They found that SARS-CoV-2 leaves a gene expression signature in the dorsal root ganglia (DRG)—neurons that relay sensory data from peripheral neurons to the spinal cord and brain for processing—that remains even after recovery.The study will be presented at the American Society for Pharmacology and Experimental Therapeutics annual meeting during the Experimental Biology (EB) 2022 meeting, held in Philadelphia from 2 – 5 April.For the study, the researchers studied hamster models of COVID-19. After contracting SARS-CoV-2, they noted that the hamsters displayed pain-like behavior as they were slightly more sensitive to touch and that this became more severe over 30 days. They also observed a second group of hamsters infected with the Influenza A virus, or the seasonal flu, to see if it triggered a similar response. Influenza A infection produced a more severe hypersensitivity reaction, but unlike SARS-CoV-2, it waned after four days. After four weeks, mice with flu displayed no signs of long-term hypersensitivity. However, after the same period, those with SARS-CoV-2 experienced higher levels of hypersensitivity. The researchers recognized this as chronic pain. RNA sequencing of the hamsters’ DRG showed that SARS-CoV-2 induced more gene expression changes that altered neuroplasticity and nerve signaling than Influenza A. It also demonstrated that these changes were similar to those on the DRG of mice experiencing inflammation or nerve injury pain. “Using Influenza A as a comparative control was a clever approach and is clearly helping to reveal how SARS-CoV-2 creates a different level of immune system driven inflammatory response that engages the peripheral nervous system, activating the long lasting hypersensitivity and pain,” John A. Pollock, Ph.D., professor and co-director of the chronic pain research consortium at Duquesne University, who was not involved in the study, told Medical News Today. The researchers also applied bioinformatic analyses to the RNA data. Their analysis predicted that SARS-CoV-2 down-regulates the activity of pain regulators and a protein called interleukin enhancer-binding factor 3 (ILF3). They thus hypothesized that mimicking the acute effects of ILF3 may alleviate pain. Using a mouse model of localized pain, the researchers administered a drug to inhibit ILF3 activity and found it was effective at treating pain.“SARS-CoV-2 induced gene changes in the DRG during active infection might be helping to tone down symptoms like myalgias,” Alex Serafini MS, an M.D./Ph.D. student at the Icahn School of Medicine at Mount Sinai in New York City, co-lead author of the paper, told MNT. “However, after the animals recover from active infection, the gene signature in the DRG starts to reflect a neuropathic state, like what we would normally see after traumatic nerve injury. Their hypersensitivity gets a lot worse over time, which aligns with these gene signatures,” he added. As the study is yet to be published, Dr. Pollock said he is limited in what he can say about it. He nevertheless noted that the researchers made an interesting observation. “In the physiology of a body, ‘disease genes’ and drug therapies are not a nail being hit with a hammer. Genes associated with a disease state are like a thread in a tapestry; one thread might add color and dimension to the scene, pulling out the wrong thread might make it all unravel.”– John A. Pollock, Ph.D.“RNA sequencing generates a very large pile of data, so my first inclination is to wonder what else they are seeing aside from ILF3. ILF3 is important, but I believe [it is] a transcriptional/translational regulator; it can influence the expression of potentially many other things,” he noted. The researchers hope their findings will help develop treatments for pain among those with long COVID. When asked about potential limitations to the research, Dr. Serafini noted that findings in hamster models might not fully translate over to humans. As their study relies heavily on RNA sequencing, he said they may have also overlooked other changes that contribute to the development of COVID-19, such as changes at the protein level. Dr. Serafini nevertheless pointed out that the current study is a positive step as it moves away from cellular models. He added that, as they have already been able to validate ILF3 as a regulator of SARS-CoV-2 pain states, they are confident that other therapeutic opportunities relevant for long COVID exist in their datasets. The researchers are now working to identify other compounds—both new and pre-existing ones—that may be able to inhibit ILF3 activity.“It is exciting to see quality research that yet again reinforces the fundamental biological connections between the immune system and the nervous system,” added Dr. Pollock. “While ILF3 expression appears to be involved in these COVID pain states, it is also regulated in a variety of normal and disease states. Exploring how altering its expression relates to other physiological systems involving the immune system—and potentially other tissue—will be important,” he concluded.
Video about Hypotheses Explaining The Development Of Autoimmune Disease Include
What are Autoimmune Diseases and How Do They Develop?
What are Autoimmune Diseases? Autoimmune Diseases are caused when the immune system attacks its own cells. This video is about autoimmunity, how autoimmune diseases develop, and the symptoms they cause. Find out how autoimmune antibodies, B-cells and T-cells get made and how they get activated. Autoimmune cells are activated via molecular mimicry, bystander activation and epitope spreading. Persistent infections can increase the stimulation of the immune system over a person’s lifetime and increase the chances of activating autoimmune cells.
Autoimmune Diseases can affect one organ, as in Type I Diabetes or many organs, as in Lupus. More than 100 autoimmune disorders affect 5-10% of people worldwide.
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CHAPTERS:
00:00 What is an Autoimmune Disease?
00:13 Types of Autoimmune Disease
00:38 Autoimmune Disease Risk
00:59 Autoimmune Disease Symptoms
01:15 Autoimmune Disease Diagnosis
01:27 Autoantibodies
01:53 Autoimmunity and Immune Tolerance
02:27 Role of Antibodies
02:33 B-Cell Development
03:14 T-cell Development
04:04 Activation of Autoreactive B & T-Cells
04:10 Molecular Mimicry
04:35 Bystander Activation
05:11 Epitope Spread
06:40 Viral Persistence
06:59 Symptoms Depend on Target Antigen
07:79 Autoimmune Disease Treatment
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