Approximately 5 million people worldwide suffer from a disease called lupus. immune system Attacks the contents of the cell nucleus. Scientific teams have now linked the onset of the disease to a virus that almost all humans carry. Epstein Barr (EBV). Although this link has been noticed for years, scientists at Stanford Medicine in the US say this study is the first to demonstrate the mechanism by which it occurs. The key is in a small part of your body. B cells and their changes.
“this is, the most shocking discovery It’s something that has come out of my lab throughout my career,” summarizes William Robinson, adding: “We believe that is the case in 100% of lupus cases.”. The study results are published in the journal Science Translational Medicine. The majority of humans are infected with EBV by the time they reach adulthood.
Transmitted through saliva, this infection usually occurs during childhood when people share spoons or drink water from them. Or perhaps it occurs when a kiss is exchanged during adolescence. May cause mononucleosis “Kissing disease”. “Pretty much the only way to avoid getting EBV is to live in a bubble,” Robinson said.
EBV belongs to a large family of viruses that includes: chickenpox and herpescan deposit genetic material in the nucleus of infected cells. There it remains latent but can be reactivated under certain conditions. A link between EBV and systemic lupus erythematosus has long been suspected, but so far, the authors say, Could not prove.
Among the cell types that EBV permanently resides in are immune B cells. Although latent EBV is ubiquitous in the sense that almost everyone carries it, it is present in only a small proportion of B cells, making it virtually impossible to identify infected ones and distinguish them from uninfected ones using existing methods. To move in this direction, the Stanford Medicine team High precision sequence system.
He found that fewer than 1 in 10,000 B cells in a typical EBV-infected but otherwise healthy person harbor the latent viral genome. In lupus patients, the proportion of B cells infected with EBV increases approximately 400-fold, a 25-fold difference. The researchers used a combination of bioinformatics and cell culture experiments to discover how such a small number of infected cells become infected. trigger a powerful immune attack to the organization itself.
Despite its almost complete inactivity, latent EBV is known to occasionally prompt sleeping B cells to produce a single viral protein, EBNA2. Researchers found that this protein Acts as a molecular switch — in genetic language, a transcription factor — which activates a set of previously inactive genes within the B cell genome.
At least two of the genes activated by EBNA2 are recipes for proteins that are themselves transcription factors that activate a variety of other pro-inflammatory human genes. What is the effect? B cells become highly inflammatory: Begins to stimulate other immune cells (helper T cells) that share the tendency to attack the nuclear components of the cell.
These helper T cells recruit numerous other antinuclear B cells. Once that “militia” is strengthened, it does not matter whether some of the newly recruited anti-nuclear B cells are infected with EBV (the vast majority are not). If there are enough of them, the result is a lupus flareThe author summarizes.
The vast majority of people infected with EBV do not develop lupus, but if about 95% of the population has latent lupus, why do some people develop autoimmunity? Robinson probably Only certain strains of EBV stimulate this transformation Converts infected B cells into “driver” cells.
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