About five million people worldwide suffer from lupus, a disease that affects the body Immune system Attacking the contents of the cell nucleus. Now, a scientific team links the development of this disease to a virus that almost everyone carries: Epstein Barr (epf). This connection has been observed for years, but this study is the first, according to scientists from Stanford University of Medicine (USA), to clarify the mechanism by which it occurs: the key is found in a small part of B cells and their changes.
“This is it The most shocking discovery that have come out of my laboratory throughout my career,” sums up William Robinson, adding: “We believe this applies to 100% of lupus cases.”. The results were published in the journal Science Translational Medicine. By the time adulthood is reached, the vast majority of humans have been infected with EBV.
The infection, which is transmitted through saliva, usually occurs in childhood when sharing a spoon or drinking from it, or perhaps during adolescence when kissing. This can cause mononucleosis, “The kissing disease”. “The only way to not get EBV is to live in a bubble,” Robinson says.
EBV belongs to a large family of viruses, including those responsible for… Chicken pox and herpeswhich can deposit its genetic material in the nucleus of infected cells. There, it remains dormant, although it can be reactivated under certain conditions. The relationship between EBV and systemic lupus erythematosus has long been suspected, but until now, according to the authors, It cannot be proven.
Among the cell types in which EBV permanently resides are immune B cells. Although latent EBV is ubiquitous, meaning almost everyone carries it, it is only present in a small fraction of B cells, so it has been nearly impossible to identify infected cells and distinguish them from uninfected cells with current methods. To advance in this direction, the Stanford University Medicine team has developed… High precision sequencing system.
He found that fewer than 1 in 10,000 B cells from an EBV-infected but healthy person contained a latent viral genome. In lupus patients, the proportion of B cells infected with EBV increases to about 1 in 400, a 25-fold difference. In collaboration with bioinformatics and cell culture experiments, the researchers discovered how such a small number of infected cells could do this Provoking a strong immune attack against the tissue itself.
It is known that latent EBV, although not nearly fully active, sometimes prompts the B cell in which it was dormant to produce a single viral protein, EBNA2. The researchers showed that this protein Acts as a molecular switch – In genetic parlance, a transcription factor – which activates a series of genes in the B cell genome that were previously inactive.
At least two of the genes activated by EBNA2 are recipes for proteins that are themselves transcription factors that activate a variety of other human proinflammatory genes. The effect is that The B cell becomes hyperinflammatory: It begins to stimulate other immune cells (helper T cells) that share a tendency to attack the nuclear components of cells.
These helper T cells recruit a large number of other antinuclear B cells. When this “militia” is reinforced, it does not matter whether any of the newly recruited antinuclear B cells are infected with EBV or not (the vast majority are not). If there are enough of them, the result is a lupus flarethe authors summarize.
The vast majority of people infected with EBV never develop lupus, but if about 95% of the population has latent lupus, why do some of them develop autoimmunity? Maybe, Robinson expects Only certain strains of EBV induce this transformation From infected B cells to “motor” cells.
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