For most individuals, the IAV (influenza A virus), commonly dubbed as the flu, is removed from the body by our personal immune system. In some instances, on the other hand, the immune response turns out dysregulated and if left unregulated, the inflammation caused due to our own immune cells can result in enhanced mortality & morbidity and extensive lung tissue damage.
How can we assist our immune system to balance the 2 main host defense tactics: assaulting pathogens (dubbed as host resistance) and maintaining our own tissue (dubbed as disease tolerance)?
A group of researchers at the RI-MUHC (Research Institute of the McGill University Health Centre) in Canada has dealt with this fundamental issue and lately verified a target to reduce the hyper-active immunity to infection caused by influenza. They have verified a new function for the lipid mediator LTB4 (dubbed as Leukotriene B4) in the lung. In a research posted in Nature Microbiology, they demonstrate that the LTB4 molecule has the potential of not only lowering collateral tissue damage caused due to immune reactions but also improving host survival. These novel results have pleading clinical implications for the treatment of flu in the near future.
On a related note, instituting combination ART (antiretroviral) therapy at the premature phases of HIV infection might let the creation of functional CD8 slayer T cells and conservation of the CD4 assistant T cells that are the primary target of the virus. Researchers from the MIT, Ragon Institute of MGH, and Harvard define the outcomes of their research, performed among South African females at risk, in Science Translational Medicine.
“Logically, this research demos that restricting the level of virus the immune system faces can fuel much more strong CD8 T cell reactions, resulting in the progression of enduring immune memory,” claims senior author of the report, Bruce Walker, to the media.