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Natural flu-fighting protein discovered in human cells

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first_imgHarvard researchers report having discovered a family of naturally occurringantiviral agents in human cells, a finding that may lead to better ways to prevent and treat influenza and other viral infections.In both human and mouse cells the flu-fighting proteinsprevented or slowed most virus particles from infecting cells at theearliest stage in the virus lifecycle. The anti-viral action happenssometime after the virus attaches itself to the cell and before itdelivers its pathogenic cargo.“We’ve uncovered the first-line defense in how our bodies fight theflu virus,” said Stephen Elledge, the Gregor Mendel professor ofgenetics and of medicine at Harvard Medical School (HMS) and a seniorgeneticist at Brigham and Women’s Hospital (BWH). “The protein isthere to stop the flu. Every cell has a constitutive immune responsethat is ready for the virus. If we get rid of that, the virus has aheyday.”“When we knocked the proteins out, we had more virus infection,” saidgeneticist Abraham Brass, an instructor in medicine at HMS and Massachusetts General Hospital (MGH), who led the study first as apostdoctoral fellow with Elledge and then in his ownlab at the Ragon Institute. “When we increased the proteins, we hadmore protection,” Brass said. The native antiviral defenders are also crucial after the cells areinfected, Brass and his co-authors found. In the cells, the proteinsaccounted for more than half of the protective effect of theinterferon immune response. Interferon orchestrates a large componentof the infection-fighting machinery.“Interferons gave the cells even more protection, but not if we tookaway the antiviral proteins,” Brass said. The study is publishedin today’s early on-line edition of the journal Cell.The potent interferon response is what makes people feel so sick whentheir bodies are fighting the flu or when receiving interferons astherapy. “If we can figure out ways to increase levels of thisprotein without interferon, we can potentially increase naturalresistance to some viruses without all the side effects of theinterferons,” Elledge said.In the study, the surprisingly versatile antiviral proteins protectedcells against several devastating human viruses-not only the currentinfluenza A strains including H1N1 and strains going back to the1930s, but also West Nile virus and dengue virus. While IFITM did notprotect against HIV or the hepatitis C virus, experiments suggestedthe protein may defend against others, including yellow fever virus.The researchers do not know how the antiviral proteins deflect thisvariety of viruses, which use different mechanisms of entry into thecell. The protein family, called interferon-inducible transmembraneproteins (IFITM), was first discovered 25 years ago as products ofone of the thousands of genes turned on by interferon. Since then,not much else has been discovered about the IFITM family. Versions ofthe IFITM genes are found in the genomes of many creatures, from fishto chickens to mice to people, suggesting the antiviral mechanism hasbeen working successfully for millions of years in protectingorganisms from viral infections.In Elledge’s lab, Brass began the study as a genetic screen to learnhow the body blocks the flu. The researchers had previously runsimilar screens with hepatitis C virus and with HIV. In the screen,the researchers used small interfering RNA to systematically knockdown one gene at a time by depleting the proteins the genes weretrying to make. Then they examined what effect each blocked gene hadon a cell’s response to influenza A virus.The screen revealed more than 120 genes with potential roles indifferent stages of infection. Four of those genes, when knockeddown, allowed for a robust increase in the infection of cells byinfluenza A virus. Of these four candidate “restriction factors,” theresearch team concentrated on the IFITM3 protein because of its knownlink to interferon and found two closely related proteins in theIFITM family with similar activity.The most distinctive property of the first-line IFITM3 defense is itspreventive action before the virus can fuse with the cell, saidco-author and virologist Michael Farzan, associate professor ofmicrobiology and molecular genetics at HMS and the New EnglandPrimate Research Center. “The virus is unable to make a protein inthe cell to counteract the IFITM proteins, because the cell isalready primed against the virus,” Farzan said. “To find somethingthat hits the flu and hits it so close to the entry stage of theviral life cycle is really interesting and unusual among viralrestriction factors.”The researchers have more questions than answers about how the IFITMrestriction factors actually work, but they are excited about therange of inquiry the discovery opens up. For example, variations inthe protein from person to person may explain differences in people’ssusceptibility to flu and other viral infections, as well as itsseverity, the researchers speculate.And if scientists can understand the mechanism of action, they may beable to design new therapies with even better antiviral actions. Theproteins themselves may be useful for defending against infections inanimals, like birds and pigs, which might prevent the emergence ofnew, potentially more dangerous influenza A strains.In another potential application, if IFITM3 has a role in the chickenembryos or canine cells used to make flu vaccines, inhibiting theproteins may speed up vaccine production, which has been an issuethis year with the manufacture of the H1N1 pandemic vaccine.The research was funded by the Howard Hughes Medical Institute, thePhillip T. and Susan M. Ragon Foundation, the National Institutes ofHealth, New England Regional Center of Excellence for Biodefense,Cancer Research UK the Wellcome Trust, and the Kay Kendall LeukaemiaFoundation. BWH and MGH have filed a U.S. patent application for thistechnology that relates to the identification and use of host factorsto modulate viral replication/growth.last_img read more

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Graeme Souness slams James Maddison after Arsenal’s Ainsley Maitland-Niles is shown red card

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first_imgMaitland-Niles was not impressed with Maddison (Picture: Getty Images)Maddison and Maitland-Niles are teammates for England under-21s and held a conversation after the latter saw red, which seemed surprisingly friendly.The Leicester man went down grasping his ankle after the challenge, which Souness believed was unnecessary and influenced referee Michael Oliver.‘Where’s he hurt him there? He goes down holding what? Where’s the contact there to warrant that sort of reaction?’ Souness continued.‘The referee was right on it. The players go down with a scream as well and that’s affected the referee who’s very close to the incident. There’ll be players all around him shouting “foul” but for me that’s not a yellow card.’More: FootballRio Ferdinand urges Ole Gunnar Solskjaer to drop Manchester United starChelsea defender Fikayo Tomori reveals why he made U-turn over transfer deadline day moveMikel Arteta rates Thomas Partey’s chances of making his Arsenal debut vs Man CityArsenal are looking to move back into the top four in the Premier League with a point or more at Leicester, at least until Chelsea play Manchester United at Old Trafford later on Sunday afternoon.A point would be enough to see them leapfrog Chelsea, but defeat would leave them languishing outside of the Champions League spots with two games to play.MORE: Mesut Ozil misses Arsenal’s clash against Leicester City through injuryMORE: Watch Neymar shove fan as PSG suffer penalty shootout loss to Rennes in Coupe de France final Ainsley Maitland-Niles was shown a second yellow card for a foul on James Maddison  (Picture: Getty Images)Ainsley Maitland-Niles was unlucky to be sent off for Arsenal against Leicester and has James Maddison to blame, according to Graeme Souness.The 21-year-old was booked twice in the first half at the King Power Stadium, the first for knocking over Ben Chilwell and the second coming for a lunge on Maddison.It is the first red card of Maitland-Niles’ young career and Souness believes he should count himself unfortunate for the second yellow card, if not the first.‘This is a booking, he obstructs him, doesn’t want to get in a race with him [Chilwell] and it’s a yellow card,’ Souness told Sky Sports.AdvertisementAdvertisementADVERTISEMENT‘The second one no, I think very unlucky, Maddison’s not helped his mate here. He [Maitland-Niles] slips, briefly, there’s a lunge but there’s not a lot of contact and I think that’s really harsh on the young man.’ Graeme Souness slams James Maddison after Arsenal’s Ainsley Maitland-Niles is shown red card Phil HaighSunday 28 Apr 2019 1:18 pmShare this article via facebookShare this article via twitterShare this article via messengerShare this with Share this article via emailShare this article via flipboardCopy link85Shares Advertisement Comment Advertisementlast_img read more

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Tommy Ison – of Oldenburg

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first_imgTommy Ison, of Oldenburg, was born on June 11, 1953 in Hamilton, Ohio, a son to Everett D. and Ellen McVey Ison.  He worked at Visteon for many years and was a member of the Metamora Church of God.  Tommy enjoyed many outdoor activities, especially riding horses, hunting and fishing.  He also loved spending time with his family.  On February 14, 2020 at the age of 66, he passed away at The Christ Hospital in Cincinnati, surrounded by family.Those surviving who will cherish Tommy’s memory include his caregiver and companion, Andrea Ison; four sons, Tommy E. Ison (fiancé Emily) of Batesville, Chris (Jennifer) Ison of Oldenburg, Jeremy Ison of Greensburg and Ben Ison of Oldenburg; 13 grandchildren; 2 great-grandchildren; one brother, Wayne (Mary) Ison of Metamora; three sisters, Judy (Ron) Jolliff of Brookville, Donna Nichols of Connersville, and Sue (Herb) Halcomb of Metamora.  Also surviving are many nieces and nephews.  Besides his parents, he was preceded in death by a brother, Earl Ison, and one sister, Janie Ison.Friends may visit with the family on Monday, February 17, 2020 from 4 until 8 p.m. at Metamora Church of God, 20124 US Highway 52, Laurel.  Pastor Wayne Ison will officiate the service on Tuesday at 1p.m. at the church.  Burial will follow in Cupps Chapel Cemetery.To sign the online guestbook or to leave a personal condolence, please visit www.cookrosenberger.com.  The staff of Cook Rosenberger Funeral Home is honored to care for the family of Tommy Ison.last_img read more

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