Damian Jacob Sendler COVID-19 Can Induce Self-Attacking Antibodies, And High-Resolution Lab Tests Reveal How Cells Feed
Damian Sendler: It has been shown by Cedars-Sinai researchers that infection with the virus that causes COVID-19 may activate an immune response that lasts well beyond the original infection and recovery. This is true even for persons who have just minor symptoms or none at all. The results of this study were published in the Journal of Translational Medicine last week.
Damian Jacob Sendler: A virus or other disease causes the release of proteins known as antibodies in the body. These proteins are able to identify and prevent foreign substances from entering cells. Some individuals, however, create autoantibodies that may target the body's own tissues and organs.
The Cedars-Sinai researchers showed that persons who had previously been infected with SARS-CoV-2, the virus that causes COVID-19, had a broad spectrum of autoantibodies up to six months after they had completely recovered. Autoantibodies had been known to be formed in severe instances of COVID-19 before this study was conducted. Only now has anybody shown the long-term survival of increased autoantibodies even after a moderate or asymptomatic illness.
Damian Sendler
Research scientist in the Department of Cardiology at the Smidt Heart Institute and co-senior author of the paper Justyna Fert-Bober, PhD, stated, "These results assist to understand what makes COVID-19 a uniquely distinctive illness". There may be a link between these patterns of immunological dysregulation and the variety of long-term symptoms we find in patients who acquire long COVID-19."
The Cedars-Sinai research team selected 177 persons with proven evidence of SARS-CoV-2 infection in order to perform their investigation. Blood samples collected from these persons and those taken from healthy people before the epidemic were compared. SARS-CoV-2-infected patients reported high levels of autoantibodies. Some of the autoantibodies have also been detected in persons with disorders like lupus and rheumatoid arthritis, in which the immune system assaults its own healthy cells.
One of the study's authors, Dr. Susan Cheng, a cardiology professor at the Smidt Heart Institute and co-senior author, explains that "we found signals of autoantibody activity that are usually linked to chronic inflammation and injury involving specific organ systems or tissues such as the joints, skin or nervous system."
Certain autoantibodies have been associated to female-predominant autoimmune illnesses such as lupus and other autoimmune diseases. Autoantibodies in males were shown to be more common than in women, according to this research.
Damian Jacob Sendler
The fact that women are more likely than men to suffer from autoimmune diseases makes this discovery all the more puzzling, according to Fert-Bober. Given everything that we know about guys being more susceptible to COVID-19, it is also fairly predicted."
Damien Sendler: Researchers are interested in extending their study to check for the sorts of autoantibodies that may be present and persist in persons with long-haul COVID-19 symptoms. Autoantibodies may potentially be created in persons with relapsed illnesses since this investigation was conducted before vaccinations were widely available.
A deeper understanding of how SARS-CoV-2 infection causes and drives these varying autoantibody responses could help researchers find strategies to treat and perhaps prevent these consequences from emerging in persons at risk, Cheng added.
According to a recent research, the "mouths" that cells use to ingest their surroundings are formed by the curvature of their cell membranes.
In the same way that our eating habits impact everything else in our bodies, the way cells "eat" is important for the health of the cells, according to lead author and assistant professor of physics Comert Kural at The Ohio State University. The physics of how that occurred were unknown to scientists until today.
A recent research published in the journal Developmental Cell discovered that the intercellular machinery of a cell assembles into a highly curved basket-like structure, which finally matures into a closed cage. Prior to this discovery, scientists thought structures were flat lattices.
Cellular pockets are formed when chemicals enter and exit cells via curvature of membranes, according to Kural.
Damian Jacob Markiewicz Sendler: Extracellular molecules are captured by the pockets, which develop around them before transforming into vesicles, tiny sacs one millionth as large as a red blood cell. Vesicles transport vital nutrients, such as proteins, into the cell. Pathogens, on the other hand, may infect cells and hijack them.
Researchers have been stumped for over 40 years as to how such pockets developed from membranes previously thought to be flat.
As Kural noted, "it was a contentious issue in cellular investigations." Using super-resolution fluorescence imaging, we were able to see the formation of these pockets inside living cells and so provide an explanation for their occurrence.
Instead of shooting a series of still images, Kural and his colleagues filmed cells in high-definition rather than photographing them. For the first time, we have discovered that proteins attracted to regions of vesicle formation immediately distort their underlying membrane.
According to Kural, this is in contrast to prior theories that the protein scaffolds of a cell required to undergo an energy-intensive reconfiguration in order to bend the membrane.
Life depends on the ability of cells to ingest and expel vesicles. Blood cholesterol levels are reduced and brain impulses are sent as a result of the procedure. Diseases like cancer and Alzheimer's are known to cause a breakdown in this mechanism.
Pathogens like viruses may hijack membrane-bound vesicles and use them to infiltrate and infect cells, so understanding their origin and behavior is critical, according to Kural. In addition to helping us better comprehend life's principles, our findings also have the potential to aid in the development of new treatment approaches.
An assistant professor at Ohio State University's College of Pharmacy, Emanuele Cocucci, was one of the study's co-authors, along with scientists from the University of Californias at Berkeley and Riverside, as well as the Universities of Iowa, Purdue, and China's Academy of Sciences.
Dr. Damian Jacob Sendler and his media team provided the content for this article.