Un consorzio internazionale di ricercatori, coordinati dal National Institute of Allergy and Infectious Diseases (NIAID), dalla Rockefeller University (New York) e dalla Università di Parigi, ha descritto il ruolo essenziale degli interferoni nella corretta risposta immunitaria alla malattia: soggetti che presentano anticorpi che neutralizzano tali molecole (autoanticorpi) o difetti genetici che ne condizionano l’espressione tendono a sviluppare forme particolarmente gravi di malattia. I risultati contribuiscono anche a spiegare la ragione per cui i soggetti di età più avanzata sono più suscettibili alle forme più severe di COVID-19.

I risultati dello studio, pubblicati su due lavori apparsi oggi sulla prestigiosa rivista Science Immunology, potranno avere importanti ricadute anche nella gestione clinica della malattia.

Cells translate their genetic material at rapid rates with exquisite precision to reproduce, repair damage or even combat disease. But the process can deregulate and give rise to disease. Byproducts of errant processes can build up like gunk in the gears, especially around neurons, breaking down the repair mechanisms and causing further damage and even neurodegenerative disorders such as Alzheimer’s disease.

Now, an international research team may have found that a protein implicated in tumor growth may be able to help regulate awry cellular translation and protect against neuronal decay. They published their results on July 13 in the Cell Reports.

“Researchers have begun to understand that age-related neurodegenerative diseases may be caused by slow but steady accumulation of toxic peptide products, which leads to death of neurons, such as beta-amyloid plaques causing Alzheimer’s disease,” said lead paper author Katsura Asano, professor in Hiroshima University’s Graduate School of Integrated Sciences for Life and also in Division of Biology, Kansas State University. “Repeat-associated non-AUG (RAN) translation is one of the mechanisms that generates such toxic products.”