researcher at Ohio State University ( OSU ) are working on a potential newfangled method of flu prevention that pull wires a lifelike process in the body — and is n’t a vaccine . Thestudy , publish inPLOS Pathogens , focuses on a protein found naturally in the cells that helps press viral infection , calledIFITM3(interferon - have transmembraneprotein 3 ) , which holds promise for “ halt virus at the door , ” say Nicholas Chesarino , a Ph.D. student at OSU and conduct author of the study .
With climate modification promising awetter , warmerwinter for 2015–16 in much of the U.S. , the spook of influenza season hovers on the edge of our day-by-day life , especially give that 2014 ’s vaccine wasless effectivethan in late years . When the right flu strain are include , flu vaccine can behighly effectiveat preventing or drop-off symptom of flu . But the vaccinum swear upon best guessing of grippe melodic phrase and ca n’t always keep up with virus mutations .
Flu viruses break into healthy cell by what Chesarino calls a “ two - step mental process . ” First , the virus enters the body in a form of “ compartment . ” Then it has to fuse its out membrane to the prison cell tissue layer in fiat to take over the cell . If it does n’t fuse , thanks to the body ’s ability to press it off , it gets destroyed by the consistence ’s defenses . This , he says , is where IFITM3 plays a of the essence part .
“ This protein prevents the virus from ever leaving the ' compartment , ' ” he tellsmental_floss . “ It basically intercept the virus from establishing infection . That ’s why our strategy is to increase levels of IFITM3 in jail cell . Because once the computer virus gets in , it can make G of copies of itself . But if we can foreclose that one virus getting into the jail cell , we halt the infection in its rail . ”
Normally , IFITM3 is produced in large quantities only after the influenza computer virus select hold . Chesarino and his fellow worker , led by Jacob Yount , older author and assistant prof of microbic contagion and immunity at OSU , discovered that suppress an enzyme calledNEDD4 , which is responsible for for clearing out IFITM3 in the cells ( a process known as ubiquitination ) , leaves behind high enough numbers of IFITM3 to preclude grippe contagion in mouse and human lung cells . “ This was a Brobdingnagian finding — that you do n’t need an contagion orinterferonto increase the level of IFITM3 . ”
This young therapy is still in enquiry and examination phases , but Chesarino tell the issue are encouraging : “ This is a promising way of life to forestall grippe at a universal level — something that would n’t have to modify year to year . It also protect against new and emerging viruses such asavianandswineflu that transfer to humans . ”
He is flying to place out that it wo n’t replace vaccine , but could be used in compounding to overlap what vaccine lack in their function . “ A vaccine ca n’t protect against a computer virus humans have n’t seen before , whereas this therapy could make up for that , ” he articulate .
Though his lab only studies influenza virus , Chesarino says the finding could potentially help prevent pandemics in other strong-growing viruses such as dengue , Ebola , SARS , andWest Nile .
