Üks Life4me+ peamiseid eesmärke on uute HIVi- ja muude sugulisel teel levivate nakkuste juhtumite, nagu ka C-hepatiiti ja tuberkuloosi nakatumise ennetamine.

Nutirakendus aitab luua kontakti arstide ja HIV positiivsete inimeste vahel. Nutirakendus aitab mugavalt organiseerida ravimite võtmise aegu, seadistada ainult Teile arusaadavad ja personaalseid meeldetuletusi, võimaldab saada arstilt tagasisidet ning panna aega vastuvõtule või analüüsidele.

Tagasi
7 veebruar 2018, 10:59
3248

New insight into how some viruses establish a chronic infection

New insight into how some viruses establish a chronic infection - pilt 1

A study from McGill University has provided new insight into how a virus causes a chronic infection New Atlas reports. The previously undiscovered molecular mechanism explains how certain viruses, including HIV and hepatitis C, can actively make immune cells less functional, allowing an infection to spread ahead of the body's immune response.

The research focused on a type of immune cell called CD8+ T cells. The activity of these cells is modulated by a cytokine chemical called IL-10. It was discovered that some viruses can increase the production of IL-10, which in turn alters the key glycoproteins on the surface of the CD8+ T cells. It is these glycoproteins that allow the killer T cells to attach to their viral targets. In disrupting this process the virus can make the immune response less effective resulting in the pathogen gaining valuable time to establish a chronic infection.

"When it comes to viruses that lead to chronic infection, immune cells receive the wrong set of marching orders, which makes them less responsive," says Martin Richer, senior author on the study.

The relationship between cytokine IL-10 and CD8+ T cells has been previously studied and explained, but this new research offers a unique insight into the way a virus can hijack that process in order to establish a chronic infection. Uncovering this molecular mechanism offers researchers new possible targets for drug therapies that can control infections by increasing the efficacy of our own immune response.

"We might be able to take advantage of the pathways induced by these signals to fight chronic viral infections by making the immune system more responsive," says Richer. "The findings might also prove useful for diseases like cancer and autoimmunity, where T cells function is poorly regulated."

Autor: Olga Moiseeva

Jaga suhtlusvõrkudes