Study: Reveals How Viral Infection Turns Your Joints into Source of Chronic Pain
Washington - (Saba):
A recent scientific study has revealed that the mysterious mechanism by which the chikungunya virus causes chronic joint pain closely resembles autoimmune diseases, such as rheumatoid arthritis.
Although most cases resolve spontaneously within one to two weeks, approximately 30-40% of patients may suffer from chronic joint pain that lasts for months or even years, with some potentially developing rheumatoid-like arthritis.
Chikungunya virus is the virus that causes chikungunya disease (CHIKV), an acute infection transmitted to humans through the bites of Aedes aegypti and Aedes albopictus mosquitoes, the two species responsible for transmitting dengue fever. The disease is characterized by the sudden onset of symptoms, including a high fever and severe joint pain, particularly in the extremities, accompanied by a rash, muscle pain, and headache.
The results of a new study, published in the journal Cell Reports Medicine, pave the way for a deeper understanding of the complex relationship between this viral infection and autoimmune diseases.
The study, conducted by a team from the La Jolla Institute for Immunology, analyzed blood samples from patients exposed to chikungunya in Colombia. The researchers tracked the behavior of immune cells, particularly CD4+ helper T cells, in combating the virus.
What surprised the research team was the discovery that these cells—and not CD8+ killer T cells, as expected—led the fight against the virus and persisted in the body for years after the infection cleared.
The data show that 87% of patients retained these cells in their blood six years after the initial infection, while killer cells were detected in only 13% of cases. Even more striking is that these helper cells switch to a "monofunctional" pattern, essentially secreting the inflammatory molecule TNF-alpha continuously, even after the virus has been eliminated.
This abnormal behavior of immune cells closely resembles what we see in autoimmune diseases, where the immune system attacks healthy body tissue.
"We would normally expect to see this pattern of immune response in autoimmune diseases such as rheumatoid arthritis, not in viral infections," says Dr. Daniela Weisskopf, lead researcher of the study. This discovery provides a compelling scientific explanation for why many patients suffer from chronic joint pain that can persist for years after contracting the virus.
These findings are particularly important in light of the widespread spread of the virus in more than 110 countries, and the similarity of its symptoms to other conditions such as "long COVID" and the long-term effects of dengue fever.
They also open the door to developing more precise treatments that target these specific inflammatory pathways, and perhaps the use of TNF-alpha inhibitors, which have proven effective in some autoimmune diseases.
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Study: Reveals How Viral Infection Turns Your Joints into Source of Chronic Pain
Washington - (Saba): A recent scientific study has revealed that the mysterious mechanism by which the chikungunya virus causes chronic joint pain closely resembles autoimmune diseases, such as rheumatoid arthritis. Although most cases resolve spontaneously within one to two weeks, approximately 30-40% of patients may suffer from chronic joint pain that lasts for months or even years, with some potentially developing rheumatoid-like arthritis. Chikungunya virus is the virus that causes chikungunya disease (CHIKV), an acute infection transmitted to humans through the bites of Aedes aegypti and Aedes albopictus mosquitoes, the two species responsible for transmitting dengue fever. The disease is characterized by the sudden onset of symptoms, including a high fever and severe joint pain, particularly in the extremities, accompanied by a rash, muscle pain, and headache. The results of a new study, published in the journal Cell Reports Medicine, pave the way for a deeper understanding of the complex relationship between this viral infection and autoimmune diseases. The study, conducted by a team from the La Jolla Institute for Immunology, analyzed blood samples from patients exposed to chikungunya in Colombia. The researchers tracked the behavior of immune cells, particularly CD4+ helper T cells, in combating the virus. What surprised the research team was the discovery that these cells—and not CD8+ killer T cells, as expected—led the fight against the virus and persisted in the body for years after the infection cleared. The data show that 87% of patients retained these cells in their blood six years after the initial infection, while killer cells were detected in only 13% of cases. Even more striking is that these helper cells switch to a "monofunctional" pattern, essentially secreting the inflammatory molecule TNF-alpha continuously, even after the virus has been eliminated. This abnormal behavior of immune cells closely resembles what we see in autoimmune diseases, where the immune system attacks healthy body tissue. "We would normally expect to see this pattern of immune response in autoimmune diseases such as rheumatoid arthritis, not in viral infections," says Dr. Daniela Weisskopf, lead researcher of the study. This discovery provides a compelling scientific explanation for why many patients suffer from chronic joint pain that can persist for years after contracting the virus. These findings are particularly important in light of the widespread spread of the virus in more than 110 countries, and the similarity of its symptoms to other conditions such as "long COVID" and the long-term effects of dengue fever. They also open the door to developing more precise treatments that target these specific inflammatory pathways, and perhaps the use of TNF-alpha inhibitors, which have proven effective in some autoimmune diseases. Whatsapp Telegram Email Print more of (International)
