Articles, Blog

Demystifying Medicine 2016: Ebola, MERS, and Likelihood of More Epidemics

March 3, 2020


THE INTENT OF THIS COURSE IS TO REALLY EXCITE YOU IN THE THINGS GOING ON IN THE BASIC BIOLOGICAL SCIENCES, AND ALSO IN CLINICAL WORK. DISEASE-RELATED. AND SO THE WHOLE THING IS AN EXERCISE IN BRIDGE BUILDING, AND I TRUST MANY OF YOU BUT PERHAPS NOT ALL RECOGNIZE THIS AS THE MOST FAMOUS BRIDGE IN THE WORLD, PARTICULARLY IF YOU GREW UP NEAR NEW YORK CITY, THIS IS THE BROOKLYN BRIDGE. THE REASON WHY WE USE THIS AS A LOGO FOR THE COURSE IS FOR TWO REASONS. ONE, IT SORT OF EXEMPLIFIES THE CHALLENGE THAT PEOPLE HAVE IF YOU’RE WELL TRAINED IN IT BASIC MORE REDUCTIONIST BIOLOGY ON ONE HAND, OR MORE IN CLINICAL TRANSLATIONAL KIND OF WORK ON THE OTHER. THE BIG CHALLENGE IS TO BRIDGE THE GAP IN THE SENSE, THE EAST RIVER, TO BE ABLE TO COMMUNICATE WITH ONE ANOTHER, AND THAT’S ONE OF THE MAIN PURPOSES OF HAD COURSE. THE OTHER THING IS THAT LIFE IS NEVER THE SAME ON EITHER SIDE ONCE YOU BUILD A BRIDGE. SO THAT’S THE INTENTMENT SO WE ENCOURAGE YOU TO ASK QUESTIONS IF YOU DON’T FOLLOW WHAT’S GOING ON, PLEASE DON’T HESITATE TO SPEAK UP. THERE WILL BE QUESTIONS AFTER EACH SPEAKER AND ALSO AT THE END, BUT YOU CAN INTERRUPT. THOSE WHO ARE SPEAKING ABOUT MORE CLINICAL-RELATED THINGS, WE URGE THEM TO AVOID MEDICAL JAR COJARGON AND SO FORTH, BUT IF SOMEBODY LATCHES AND USES IT IS TERMS THAT DON’T REGISTER WITH YOU, SPEAK UP. EVERYBODY WOULD LIKE TO DO THE RIGHT THING OR COMMUNICATE WELL. NOW, WHEN POSSIBLE, AND IT’S USUALLY ABOUT HALF THE SESSIONS, WE BEGIN WITH A LIVE PATIENT WHO AS ONE PH.D. POSTDOC TOLD ME IS THE HIGHLIGHT THE OF THE COURSE BECAUSE IT PUTS A HUMAN FACE ON A DISEASE. SO THAT INDIVIDUAL BRIEFLY DESCRIBES WHAT THEIR DISEASE IS LIKE, WHICH IS SOMETHING THAT MOST PEOPLE WORKING IN A LABORATORY HAVE LITTLE COMMUNICATION WITH. AND THEN THERE IS AN INDIVIDUAL, USUALLY A PHYSICIAN OR MD PH.D. FOR THE MOST PART WORKING HERE AT THE CLINICAL CENTER WHO TALKS IN TERMS THAT ARE FOR A BROAD AUDIENCE, THINGS IT LIKE EPIDEMIOLOGY, CHANGING PATTERNS OF A IT DISEASE, HOW PEOPLE KNOW IF THEY HAVE IT AND THINGS LIKE THAT. IT’S NOT INTEND ITE INTENDED TO
INUNDATE WITH YOU A MEDICAL SCHOOL KIND OF LECTURE. AND WHAT ARE THE CHALLENGES, WHERE ARE WE. AND THEN THE BASIC SCIENTIST, DISCUSSES NOT LAST WEEK’S SEMINAR, BUT WHAT DO WE UNDERSTAND IN TERMS OF BASIC MECHANISMS, AND AGAIN, WHAT ARE THE CHALLENGES AND WHERE DO THESE THINGS COME TOGETHER? SO I HOPE THAT YOU FIND THIS ENJOYABLE AND THAT YOU COME TO AS MANY SESSIONS AS POSSIBLE. NOW I TOOK THE LIBERTY OF DID — ONE OF THE GENERAL THEMES THAT’S BOUND TO EMERGE THIS AFTERNOON IS THAT THE ORGANISMS, VIRUS, BACTERIA AND SO FORTH WHICH ARE RESPONSIBLE FOR EPIDEMICS THAT POP UP ALL THE TIME, THERE ON ONE SIDE OF A FENCE, AND OUR ABILITY OH DO SOMETHING ABOUT IT, RECOGNIZE, RECEIPT, UNDERSTAND AND SO FORTH, THE OTHER. SO THIS CARTOON FROM A DUTCH ARTIST, DO YOU RECOGNIZE HIM? THAT’S AN ORIGINAL GRUCH. SO THIS IS THE THEME, PROBLEMS WORTHY OF ATTACK PROVE THEIR WORTH BY HITTING BACK. THIS IS A GOOD THING. SO YOU MIGHT JUST GIVE A LITTLE THOUGHT TO WHAT ARE ALL THESE THINGS, ALL THESE INCREDIBLE NAMES, AGENTS, WHAT DO THEY HAVE IN COMMON? WELL, ONE OF THE THINGS IS THEY ALL COME OUT OF THE TROPICAL RAIN FOREST. AND THAT’S THE DEEP RESERVOIR OF LIFE, IT CONTAINS MOST OF THE WORLD’S PLANTS AND ANIMAL SPECIES AND VIRUSES, AND AS YOU KNOW, ALL LIVING THINGS CONTAIN VIRUSESMENES. VIRUSES CAN COME FROM OTHER SOURCES, BUT IT SEEMS AS IF ALL THE ONES ON THAT PREVIOUS LIST SOMEHOW EMERGE FROM THE TROPICAL RAIN FOREST. SO MAYBE WE’LL HEAR SOMETHING ABOUT HOW, WHY THAT HAPPENS. BACTERIA, BY AND LARGE, HAVE A DIFFERENT SOURCE AND IT’S MORE COMPLEX THAN I INDICATED HERE, IT EVEN INCLUDES A SCHOOL OF THOUGHT WHICH AT ONE POINT WAS VOICED BY JOSH LEDDERBERG THAT BACTERIA MAY ACTUALLY HAVE HAD THEIR ORIGIN FROM OUT OF SPACE. SO WE’RE GOING TO HAVE TWO EXTRAORDINARY SPEAKERS THIS AFTERNOON, AND I WILL BRIEFLY INTRODUCE THEM TO YOU SO WE WON’T INTERRUPT FURTHER. SO FIRST DR. FAUCI, TONY FAUCI, THE DIRECTOR OF NIAID WILL SPEAK. HE’S BEEN THE DIRECTOR HERE SINCE 1984. HIS JOB IS EXTRAORDINARY. HE OVERSEES IN AN EXTENSIVE RESEARCH PORTFOLIO DEDICATED TO PREVENTING, DIAGNOSING AND TREATING INFECTIONS AND IMMUNE MEDIATED DISEASES NOT ONLY IN THIS COUNTRY BUT AROUND THE WORLD. IN ADDITION, TONY IS THE CHIEF OF THE LABORATORY OF IMMUNOREGULATION, WHICH HAS BEEN RESPONSIBLE FOR MANY, MANY, MANY MAJOR DISCOVERIES, PARTICULARLY IN THE HIV/AIDS FIELD, AND HE’S PROBABLY — HE’S CERTAINLY ONE OF THE MOST CITED SCIENTISTS IN THAT FIELD. IN ADDITION, HE’S BEEN AN ADVISOR TO THE PRESIDENT, TO THE WHITE HOUSE, THE DEPARTMENT OF HEALTH AND HUMAN SERVICES, ON GLOBAL ISSUES, PRIMARILY RELATED TO AIDS BUT ALSO IN RELATION TO EMERGING INIT FEKTIOU INFECTIOUS
DISEASES, PARTICULARLY INFLUENZA. I THINK IF YOU WERE TO ASK THE GENERAL PUBLIC WHAT DO THEY KNOW OR WHOM DO THEY RECOGNIZE AT THE NIH, I SUSPECT THAT TONY FAUCI’S NAME WILL BE AT THE TOP OF THE LIST BECAUSE OF HIS VERY EFFECTIVE PRESENTATION TO PUBLIC AUDIENCES AS WELL TO CARRY THE MESSAGE OF WHAT SCIENCE AND INFECTION IS ABOUT. HE WAS ONE OF THE PRINCIPAL AR TECTS OF THE PRESIDENT’S EMERGENCY PLAN FOR AIDS RELIEF, WHICH HAS HAD A MAJOR EFFECT AND PROBABLY SAVED MILLIONS OF LIVES IN THE DEVELOPING WORLD. NOW IN RECOGNITION OF THIS, HE’S ONLY ACQUIRED 42 HONORARY DEGREES AND HAS AUTHORED MORE THAN 1200 SCIENTIFIC PAPERS. HE’S A MEMBER OF THE NATIONAL ACADEMY, AND HE’S RECEIVED MANY AWARDS, PROBABLY AMONG THE MOST PRESTIGIOUS, THE NATIONAL MEDAL OF SCIENCE, THE LASKER AWARD FOR PUBLIC SERVICE, AND THE PRESIDENT IT DENGS MEDAL OF FREEDOM. THE — THE PRESIDENTIAL MEDAL OF FREEDOM. THAT’S NOT BAD FOR A DAY’S WORK. OUR SECOND SPEAKER IS A NEW ARRIVAL AT THE NIH, VINCENT MUNSTER, FROM HOLLAND. HE RECEIVED HIS PH.D. DEGREE FROM ERASMUS UNIVERSITY IN ROTT IT ERDAM, WHERE HE STUDIED ECOLOGY, EVOLUTION AND PATHOGENESIS OF AIF VAN INFLUENZA VIRUSES. HE CAME HERE IN 2009 AND IN 2013 AS A PRINCIPAL INVESTIGATOR, ESTABLISHED THE VIRUS ECOLOGY UNIT, WHICH HAS ITS PURPOSE TO ELUCIDATE THE ECOLOGY OF EMERGING VIRUSES AND DRIVERS OF ZOONOTIC AND CROSS-SPECIES TRANSMISSION. NOW HE WORKS IN THE ROCKY MOUNTAIN LABORATORY, WHICH IS A PART OF NIH THAT’S IN GOD’S COUNTRY OUT IN MONTANA, BUT IT ALSO CONTAINS STATE OF THE ART HIGH AND MAXIMUM CONTAINMENT FACILITIES BECAUSE OF THE AGENTS HE WORKS WITH. BUT NOT CONTENT TO BE ONLY IN MONTANA, HIS WORK CARRIES HIM ALL OVER THE WORLD, WHERE MAJOR INFECTIONS HAVE OCCURRED LIKE EBOLA AND, MORE RECENTLY, MERS. SO VINCENT IS GOING TO TALK ABOUT ZOO NO I ZOONOTIC
TRANSMISSION, CROSS-SPECIES TRANSMISSION. WHERE DO THESE VIRUSES COME FROM, AND HOW DO THEY GET INTO MAN, AND MAYBE WHERE DO THEY GO FROM THERE. AT ANY RATE, IT’S A GREAT PLEASURE TO HAVE BOTH OF YOU HERE TODAY, AND PERHAPS, TONY, YOU WOULD BEGIN. THANK YOU. [APPLAUSE]>>THANK, IT’S A REAL PLEASURE TO BE HERE WITH YOU THIS EVENING. AS YOU HEARD, I’M GOING TO TALK ABOUT THIS TOPIC OF — HE ASKED ME TO MAKE THAT TITLE, I WOULD HAVE NEVER MADE A TIE EL IT LIKE THAT. TITLE LIKE THAT. IT’S NOT NEAT. SO IT’S EBOLA, MERS AND — I’M REALLY GOING TO TALK ABOUT EMERGING INFECTIOUS DISEASES, INCLUDING THESE IMPORTANT ONES THAT HAVE BEEN ON OUR RADAR SCREEN MOST RECENTLY. SO WHEN ONE THINKS OF EMERGING INFECTIOUS DISEASES, I THINK IT REALLY IS IMPORTANT AND ENJOYABLE TO PUT IT INTO A BROAD HISTORICAL PERSPECTIVE, BECAUSE THE ISSUE OF PLAGUES AND OUTBREAKS HAVE REALLY TRANSFORMED CIVILIZATIONS OVER THE CENTURIES, AND THERE ARE A COUPLE OF REALLY GREAT BOOKS I’M SURE YOU’RE FAMILIAR WITH THEM BY JARED DIAMOND AND WILLIAM MCNEILL AND OTHERS THAT HAVE SHOWN THE INFLUENCE OF DISEASES, HOW THEY’VE TRANSFORMED EVERYTHING FROM POLITICAL TO ECONOMIC SITUATIONS THROUGHOUT THE WORLD. SO THIS IS SOMETHING THAT’S NOT NEW WITH US, IT’S AN INHERENT PART OF OUR CIVILIZATION, IS THE EE MEEMERGENCE AND RE-EMERGENCE
OF PLAGUES. IN FACT, IF YOU LOOK HISTORICALLY GOING BACK TO THE 14TH CENTURY WITH THE VERY WELL RECOGNIZED BUBONIC OR BLACK PLAGUE, WHICH WAS YERSINIA PESTIS, THROUGH THE PLAGUES SHOWN ON THE SLIDE, AND I WON’T GO THROUGH EACH AND EVERY ONE OF THEM, ONE OF THEM IS IN THE RELATIVELY MODERN ERA THAT YOU’VE HEARD A LOT ABOUT AND I’LL GET BACK OH THAT, AND THAT IS THE SO-CALLED SPANISH INFLUENCE IS A, WHICH AT THE TIME KILLED BETWEEN 50 AND 100 MILLION PEOPLE, WHICH IN THE POPULATION RELATIVE TO TODAY WOULD BE EQUIVALENT TO SEVERAL HUNDREDS OF MILLIONS OF PEOPLE IF WE HAD THE 1918 INFLUENZA TODAY. SO THESE ARE THINGS AGAIN THAT CONTINUE TO TRANSFORM. NOW WHAT HAS HAPPENED OVER THE YEARS, THOUGH, IS THAT THERE HAVE BEEN AN AMAZING AMOUNT OF PROGRESS IN THE CONTROL OF INFECTIOUS DISEASES. SHOWN ON THE SLIDE, EVERYTHING FROM THE GERM THEORY, RECOGNIZING THAT MICROBES CAUSE DISEASES, THERE HAVE BEEN CHANGES AND IMOF PROVEMENTS IN SANITATION, HYGIENE, IMPORTANTLY VECTOR CONTROL, THE ALL IMPORTANT DISCOVERY OF ANTIMICROBIALS, THE DEVELOPMENT OF VACCINES, THE IMPLEMENTATION OF VACCINE PROGRAMS AND OUR ABILITY TO MONITOR AND DETECT INFECTIONS AS THEY OUTBREAK. AND BECAUSE OF ALL OF THIS, WHAT WE HAVE SEEN OVER THE YEARS IS A DRAMATIC DECREASE IN THE MORTALITY RATE DUE TO INFECTIONS, AND IF YOU TAKE THE UNITED STATES AS AN EXAMPLE, IT GOES ALL THE WAY DOWN TO WHAT YOU SEE HERE. BUT THIS IS STILL A VERY IMPORTANT NUMBER. BUT WHEN YOU LOOK GLOBALLY, IT’S MUCH DIFFERENT. NOW YOU MIGHT ASK, WHAT IS THIS IT SPIKE HERE? I REMEMBER YEARS AGO, WHEN I WAS PRESENTING BEFORE THE CONGRESS ABOUT THE IMPORTANCE OF WHAT VACCINES HAVE DONE FOR INFECTIOUS DISEASES, I WANTED TO IMPRESS THEM WITH THIS, AND THEY KEPT ON FOCUSING ON THAT. THAT WAS THE PANDEMIC FLU OF 1918. WHICH ACTUALLY WAS PRETTY GOOD BECAUSE IT GOT ME AN EXTRA $20 MILLION FOR INFLUENZA. BUT OTHER THAN THAT, IT WAS A GOOD SLIDE. ANYWAY, WHAT’S HAPPENED IS THAT THERE HAVE BEEN SOME UNDERSTANDABLE BUT NONETHELESS INAPPROPRIATE UTTERANCES BY PUBLIC OFFICIALS OVER THE YEARS THAT THE AREA OF INFECTIOUS DISEASES WAS OVER. ONE PERSON IN PARTICULAR, AIDAN COCKBURN IN 196 IT TI THREE SAID, SINCERELY, WE CAN LOOK FORWARD TO CONFIDENCE TO IT A CONSIDERABLE DEGREE OF FREEDOM FROM INFECTIOUS DISEASES AT A TIME NOT TOO DISTANT IN THE FUTURE, AND THAT — I LOVE THIS — ALL THE MAJOR I
INFECTIONS WILL HAVE DISAPPEARED.” YOU’RE LOOKING FOR ONE THAT WORKS. DID YOU FIND ONE THAT WORKS? DON’T WORRY ABOUT IT. NO BIG DEAL. SO THE PROBLEM WITH THIS IS THAT IT IS INACCURATE FROM THE STANDPOINT OF WHAT’S GOING ON BECAUSE HE SAID THIS IN ’63, WHEN THERE WERE 2 MILLION DEATHS OF TUBERCULOSIS AND A MILLION DEATHS OF MALARIA, AND IT IS NOT ONLY A COMPLETE PROVINCIAL CRAZINESS, HOW CAN YOU SAY THAT IN THE UNITED STATES, WHEN MILLIONS OF PEOPLE ARE DYING FROM INFECTIOUS IT DISEASES AROUND THE REST OF THE WORLD, BUT IT IS WHAT IT IS, AND PEOPLE WERE SAYING THAT. IF YOU LOOK AT THE REALITY, INFECTIOUS DISEASES, ALTHOUGH THEY’VE GONE DOWN IN THE UNITED STATES, ARE STILL A MAJOR CAUSE OF DEATH WORLDWIDE. THERE ARE 55 MILLION DEATHS A YEAR IN THE WORLD, ABOUT 16 TO 18% OF THEM ARE DUE TO INFECTION. NOW, IF YOU LOOK AT WHAT’S CALL CALLED DISABILITY ADJUSTED LIFE YEARS, A COMBINATION OF DEATH AND DISABILITY, AND YOU RANK THEM IN THE WORLD, THE INFECTIOUS DISEASES ARE STILL THE LEADING CAUSE OF DALYs FROM PEOPLE FROM BIRTH TO I AGE 49. SO INFECTIOUS DISEASE, THERE ARE ABOUT 16 TO 18%, AND IT REALLY IS VERY IMPORTANT. SO WE’RE GOING TO TALK A LITTLE BIT ABOUT INFECTIOUS DISEASES IN GENERAL. SO I IT TEND TO LIKE TO CATEGORIZE THINGS INTO DIFFERENT BUCKETS TO MAKE THEM A BIT MORE CLEAR TO PEOPLE WHEN I’M TALKING TO THEM ABOUT IT. SO YOU TALK ABOUT ESTABLISHED INFECTIOUS DISEASES, NEW INFECTIOUS DISEASES AND REEMERGING INFECTIOUS IT DISEASES. SO LET’S TAKE A LOOK FIRST AT ESTABLISHED INFECTIOUS DISEASES. MY DEFINITION IS ONE THAT YOU CAN REASONABLY ACCURATELY PREIT DICTIONARY THE GLOBAL MORBIDITY AND MORTALITY FROM YEAR TO YEAR. LET ME SHOW YOU AN EXAMPLE. FOR EXAMPLE, IF YOU LOOK AT RESPIRATORY ILLNESSES, IT KILLS ABOUT 2 MILLION PEOPLE A YEAR. THAT DOESN’T CHANGE MUCH FROM YEAR TO YEAR. DIARRHEAL DISEASES, ABOUT 1.8 MILLION. IT’S INTERESTING THAT HIV/AIDS USED TO BE A NEWLY EMERGING DISEASE BUT IT’S GRADUATED AFTER 34 YEARS INTO AN ESTABLISHED INFECTIOUS DISEASE. BUT THERE’S TB, HEPATITIS, MALARIA. WE KNOW ALL ABOUT THOSE THOSE ARE ESTABLISHED. BUT WHAT WE’RE GOING TO FOCUS ON FOR THE PURPOSE OF TODAY’
TODAY’S DISCUSSION IS BOTH NEWLY EMERGING AND REEMERGING INFECTIOUS DISEASES. WHEN I GAVE MY FIRST TESTIMONY BEFORE CONGRESS IN 1984, THE FIRST YEAR THAT I WAS DIRECTOR, I WANTED TO IT MAK MAKE THE
POINT TO THE CONGRESS THAT NEW DISEASES EMERGE, SO I SKETCHED A LITTLE MAP MYSELF AND THEN I HAD AN ARTIST DO IT, AND I SAID, LOOK THE AT WHAT WE HAVE HERE. WE HAVE HIV AS A NEW DISEASE. SO I’VE BEEN TESTIFYING NOW FOR 31 YEARS, AND EVERY YEAR, I ADD ONE OR TWO AND SOMETIMES THREE NEW DISEASES TO THE MAP SO IT DOESN’T BORE THEM. THEY GET A NEW MAP EVERY YEAR. THIS IS WHAT THE MAP LOOKS LIKE RIGHT NOW, WITH A VARIETY OF THINGS. NOW WE OBVIOUSLY DON’T HAVE TIME TO GO THROUGH EACH AND EVERY ONE OF THOSE, BUT I WANT TO DANCE THROUGH A FEW OF THEM TO GIVE YOU AN EXAMPLE OF THE DIFFERENCE BETWEEN NEWLY EMERGING, RE-EMERGING AND THEN I HAD TO PUT DELIBERATELY BECAUSE THAT’S WHEN WE HAD THE ANTHRAX ATTACK, YOU MIGHT REMEMBER BACK IN THE FALL OF 2001, RIGHT AFTER THE 9/11 ATTACK IN NEW YORK AND THE PENTAGON. SO THIS IS JUST AN EXAMPLE OF A FEW OF THE NEWLY EMERGING INFECTIOUS DISEASES AND RE-EMERGING INFECTIOUS DISEASES THAT HAVE OCCURRED ONLY IN THE YEAR 2015 THROUGH THIS MONTH IN 2016. EVERYTHING YOU REMEMBER, THE MEASLES OUTBREAK IN CALIFORNIA, DRUG-RESISTANT TB AND MALARIA, THE BIRD FLUS, MERS, CHIKUNGUNYA, ET CETERA, ET CETERA, ET CETERA. WE COULD SPEND AN ENTIRE LECTURE ON EACH AND EVERY ONE OF THESE, BUT THEY’RE ALL REAL EMERGING AND RE-EMERGING INFECTIOUS DISEASES. SO LET’S TAKE A LOOK AT SOME OF THE ISSUES THAT GET INVOLVED IN THIS. WHY DO YOU GET EMERGING AND RE-EMERGING INFECTIOUS DISEASES? I THINK VINCENT IS GOING TO TELL YOU PROBABLY MORE ABOUT THAT THAN I WILL, BUT THERE ARE THINGS GENERALLY, I WERE TO TAKE THESE SEVEN BULLETS AND PUT THEM INTO ONE, IT’S HOW WE PERTURB OUR ENVIRONMENT. ONE WAY OR THE OTHER. THE DEMOGRAPHY AND BEHAVIOR, TECHNOLOGY AND INDUSTRY, ECONOMIC DEVELOPMENT, TRAVEL, PUBLIC HEALTH MEASURES, ECOLOGY, MICROBIAL ADAPTATION. ALL OF THESE HAVE AN IMPACT. NOW IT, ONE ONOW, ONE OF THE
THINGS YOU’RE GOING TO HEAR FROM ONE OF THE WORLD’S EXPERT ON THIS NOW IS THE ISSUE OF WHERE THESE INFECTIONS COME FROM. 75% OF THE NEW INFECTIONS THAT AFFLICT MANKIND ARE ZOONOTIC. MAINLY, THEY’RE FUNDAMENTALLY ANIMAL VIRUSES THAT JUMP SPECIES AND ULTIMATELY ADAPT THEMSELVES TO HUMANS. WHEN THEY ADAPT THEMSELVES WELL TO HUMANS, THE WAY INFLUENZA HAS DONE, THE WAY HIV HAS DONE, THEY BECOME OUTBREAKS AND SOMETIMES PANDEMICS. SOMETIMES THEY’RE JUST CURIOSITIES WHEN THEY JUMP SPECIES AND A HANDFUL OR MORE OF PEOPLE GET INFECTED. IT’S STILL A ZOO INTO TICK, BUT
ZOONOTIC B
UT IT ISN’T A MAJOR OUTBREAK. AIR TRAVEL, THIS IS ONE OF THOSE SCHEMATIC ITS THAS THAT SHOW
YOU, FOR EVERY GREEN LINE IS A FLIGHT THAT TOOK OFF TODAY THROUGHOUT THE WORLD. AND IF YOU JUST TAKE A LOOK AT THE CONNECTIVITY BETWEEN DIFFERENT COUNTRIES, IF YOU GET A GOOD FLIGHT, THERE’S NO PLACE IN THE WORLD THAT’S MORE THAN 19 HOURS AWAY. YOU GET A DIRECT FLIGHT FROM HERE OVER TO CHINA OR JAPAN, WHICH IS DIRECTLY ON THE OTHER SIDE OF THE WORLD, THAT’S ABOUT AN 18 TO 19 HOUR FLIGHT. SO THAT’S PRETTY GOOD COMPARED TO WHAT WAS MANY DECADES AGO. SO LET’S TAKE A LOOK AT NEWLY EMERGING INFECTIONS. SO HIV IS THE MOTHER OF ALL NEW EMERGING INFECTIONS. WHY? BECAUSE RIGHT NOW THERE HAVE BEEN, AS YOU KNOW, AS I’M GOING OH SHOW YOU, 70 MILLION INFECTIONS. SO THAT’S NOT A BLIP ON THE RADAR SCREEN. THAT RANKS IN THE SHORTLIST OF A HANDFUL OF THE WORST PANDEMICS EVER. SO IF YOU WANT TO LIST THEM, THE BUBONIC PLAGUE, INFLUENZA OF 1918, MEASLES, ET CETERA, HIV IS RIGHT THERE IN A SMALL HANDFUL, WHICH IS I KIND OF THINK INTERESTING FOR THOSE WHO ARE INTERESTED IN INFECTIOUS DISEASES, BECAUSE AS INFECTIOUS DISEASE PEOPLE, WE’RE LIVING THROUGH ONE OF THE WORST PANDEMICS IN THE HISTORY OF MANKIND. WE TEND TO KIND OF FORGET THAT BECAUSE WE GET USED TO IT. SO IT ALL STARTED OFF THE WAY THESE OUTBREAKS DO, WITH A SEEMINGLY INCOCONSPICUOUS REPORT THAT CAUGHT MY ATTENTION 34 1/2 YEARS AGO WHEN I WAS IN MY LABORATORY, WHICH WAS INTERESTING, IT WAS FIVE GAY MEN FROM LOS ANGELES WHO PRESENTED WITH KNEW KNO PNEUMOCYSTIS
PNEUMONIA. I HAVE A PARTICULAR EMOTIONAL INTEREST IN THIS MMWR BECAUSE IT CHANGED MY LIFE. WHEN I SAW THAT MMWR, I DIDN’T BELIEVE THE FIRST ONE WITH FIVE GAY MEN, BUT WHEN THE SECOND ONE CAME OUT A MONTH LATER OF 26 MEN, ALSO ALL GAY, NOT ONLY FROM L.A. BUT FROM SAN FRANCISCO AND NEW YORK, I SAID, OH, MY GOD, THIS IS A BRAND NEW DISEASE, AND I STOPPED WHAT I WAS DOING AND IT DID EVERYTHING AND STARTED ADMITTING THESE PEOPLE WHO WE DIDN’T EVEN KNOW WHAT THE NAME OF THE DISEASE WAS, WE WERE CALLING IT GRID. FAST FORWARD 34 YEARS, AND LOOK WHAT YOU HAVE. THERE ARE NOW 37 MILLION PEOPLE LIVING WITH HIV, 1.2 MILLION IT DEATHS, AND 2 MILLION NEW INFECTIONS EACH YEAR. THE SCIENCE HAS BEEN INCREDIBLE. IF THERE’S EVER ONE DISEASE IN WHICH THE SCIENTIFIC COMMUNITY RESPONDED WITH AN EXTRAORDINARY AMOUNT OF ACCOMPLISHMENT, IT’S BEEN HIV. BELIEVE IT OR NOT, THIS IS A PICTURE OF ME MAKING ROUNDS IN 1981. AND I SHOW IT NOT BECAUSE I WANT TO SHOW A PICTURE OF MYSELF, BECAUSE IT REMINDS ME THAT ALL ABOUT FIVE TO SEVEN YEARS OF MY LIFE, I WAS KIND OF — I WOULDN’T SAY DEPRESSED, THAT’S CLIB CALCLINICAL, I WASN’T
FEELING TOO GOOD BECAUSE EVERY ONE OF MY PATIENTS DIED. I HAD HUNDREDS AND HUNDREDS OF PATIENTS A YEAR BECAUSE WE FILLED UP A 52-BED WARD ON THE 11TH FLOOR AND THEY ALL DIED. THE MEDIAN LIFE EXPECTANCY WAS 8 MONTHS TO A YEAR AND A HALF. BUT WHAT HAPPENED BECAUSE OF THE SCIENCE IS THAT WE NOW HAVE MORE THAN 30 DRUGS WHICH WE USE IN COMBINATION OF THREE AND SOMETIMES FOUR, WE’VE COMPLETELY TRANSFORMED THE LIVES OF HIV-INFECTED INDIVIDUALS. SUCH THAT IF A PERSON COMES IN TO THIS SAME CLINIC NOW AND IS 20 YEARS OLD AND NEWLY INFECTED AND WE START THEM ON AN ANTIRETROVIRAL, YOU CAN PREDICT THAT THEY’LL LIVE AN ADDITIONAL 50, 5-0, YEARS. I TELL YOU THAT BECAUSE WE TEND TO TAKE IT FOR GRANTED NOW. AND WHEN NEW FELLOWS OM IN AND ROTATE THROUGH MY SERVICE, THEY TAKE IT FOR GRANTED. SOMEBODY COMES IN, YOU GIVE THEM A ABOUT PILL, BOOM, IT’S DONE, YOU’RE GOOD. BUT THEY DON’T KNOW OR HAVE THE EXPERIENCE THAT EVERY PATIENT BEFORE THIS CAME ALONG DIED, AND NOW THEY HAVE A NORMAL LIFE EXPECTANCY. WHICH AGAIN GOES DOWN HISTORICALLY AS I THINK ONE OF THE MOST IMPORTANT ACCOMPLISHMENTS IN BIOMEDICAL RESEARCH. ON SUNDAY, SOME OF YOU MAY HAVE READ, I WROTE AN EDITORIAL IN THE “WASHINGTON POST,” AND IF YOU HAVEN’T HAD A CHANCE TO CLICK ONLINE, READ IT, BECAUSE IT REALLY EXPLAINS IN DETAIL WHAT I DON’T HAVE TIME TO DO RIGHT NOW, IS THAT WE HAVE NO EXCUSES WHATSOEVER NOT TO END THE AIDS EPIDEMIC, BECAUSE WE HAVE ALL THENES THE NECESSARY TREATMENTS AND PREVENTION. YOU CAN ACTUALLY STOP THE EPIDEMIC IN ITS TRACKS AND IT BECOMES AN IMPLEMENTATION ISSUE. DO WE HAVE THE POLITICAL WILL GLOBALLY TO GO OUT, SEEK OUT, TEST, TREAT AND GET PEOPLE INTO CARE, WHICH WE’RE NOT DOING VERY WELL AT. OKAY. LET’S MOVE IT T TO ANOTHER NEW
VIRUS. IN 1976, EBOLA WAS A NEWLY EMERGING DISEASE. THE EBOLA THAT WE EXPERIENCED RECENTLY THAT I’M GOING TO TELL YOU A LITTLE BIT MORE ABOUT IS A RE-EMERGING DISEASE, BUT THE FIRST TIME WE RECOGNIZED IT WAS IN SOUTHERN AFRICA, IN ZAIRE AND IN SOUTH AFRICA, IN WHICH THERE WAS A NEW IT DISEASE THAT WAS DISCOVERED, EBOLA WAS THE FIRST TIME WITH EXPERIENCED IT AND SINCE THEN, THERE HAVE BEEN ABOUT 24 OUTBREAKS, USUALLY ANYWHERE FROM TWO OR THREE PATIENTS UP TO A COUPLE HUNDRED PATIENTS. WE’LL GET BACK TO EBOLA AS A RE-EMERGING DISEASE. SARS WAS AN INTERESTING NEW EMERGING DISEASE. IT STARTED OFF, AS YOU KNOW, THINKING THE CHINESE EITHER THOUGHT OR DIDN’T WANT TO LET ANYBODY KNOW THAT IT WAS INFLUENZA IN GUANGDONG PROVINCE. SOMEBODY WENT FROM THERE TO HONG KONG, BROUGHT THE INFECTION WITH THEM, AND DID SOMETHING WHICH IS AN EPIDEMIOLOGIST’S DREAM, IF YOU WANT TO CALL IT THAT. THAT SOUNDS SORT OF MORBID, BUT IT IS. SOMEBODY WENT INTO A HOTEL IN HONG KONG, INFECTED A NUMBER OF PEOPLE WHO THEN WENT OFF FROM THE HOTEL INTO DIFFERENT PARTS OF THE WORLD AND SPREAD THE INFECTION. TORONTO GOT HIT PRETTY BADLY, THE UNITED STATES REALLY NOT SO MUCH. AND WHAT HAPPENED VERY QUICKLY IS THAT WE WENT FROM A HANDFUL OF CASES TO MORE THAN 8,000 CASES AND ABOUT 775 DEATHS. NOW AS WE WERE SCRAMBLING TO DEVELOP VACCINES AND THEIR IT PETHERAPEUTICS, GOOD BASIC LOW TECH NOT ROCKET SCIENCE PUBLIC HEALTH MEASURES COMPLETELY PUT AN END TO THE EPIDEMIC. THINGS LIKE I’D IF FIX,
IDENTIFICATION, ISOLATION, SOME QUARANTINE, AND THAT WAS THE END OF THAT. SO IT WAS A REASONABLY GOOD PUBLIC HEALTH STRUCTURE THAT IT DID IT. INTERESTINGLY, WE DEVELOPED A VACCINE FOR SARS BUT WE NEVER HAD TO USE IT. NOW, THEN CAME MERS CORONA VIRUS. INTERESTING THAT SARS IS A CORONA I VIRUS AND MERS IS A CORONA VIRUS. IF YOU GO TO YOUR MICROBIOLOGY CLASS BEFORE THESE TWO, CORONA VIRUS WAS A WIMPY LITTLE VIRUS THAT CAUSES THE COMMON COLD, BUT IT OBVIOUSLY ISN’T, BECAUSE THERE ARE SOME CORONA VIRUSES THAT ARE PRETTY DANGEROUS, LIKE THIS ONE. SO MERS CAME ALONG AND THEN WHAT WE HAD IS WE THIS I HAD IT
SPRINGING UP IN THE MIDDLE EAST, YOU’LL PROBABLY HEAR MORE FROM VINCENT, THERE ARE NOW OVER 1600 CASES, ABOUT 584 DEATHS. THESE COUNTRIES HERE ARE NOT PRIMARY INFECTIONS. THE INFECTIONS ORIGINATE IN THE MIDDLE EAST AND HAVE GONE BECAUSE PEOPLE TRAVEL TO OTHER COUNTRIES INCLUDING A COUPLE IN THE UNITED STATES. THE COUNTRY THAT REALLY GOT HIT WAS SOUTH KOREA. AND IT WAS INTERESTING BECAUSE IT’S A PRIME EXAMPLE OF SOMEONE WITH AN INFECTIOUS DISEASE THAT’S TRANSMISCIBLE THAT WHEN YOU DON’T REALIZE WHAT YOU’RE DEALING WITH, YOU CAN HAVE A REAL PROBLEM THE WAY THE SOUTH KOREANS HAVE, BECAUSE A PERSON CAME FROM THE MIDDLE EAST TO SOUTH KOREA AND WAS VISIBLY ILL AND WENT TO A COUPLE OF EMERGENCY ROOMS AND NO ONE PUT TWO AND TWO TOGETHER AND IMPLEMENTED WHAT YOU LEARN IN MEDICAL SCHOOL. WHAT YOU LEARN IN MEDICAL SCHOOL IS SOMEONE COMES IN WITH AN INFECTIOUS DISEASE, YOU ASK THEM, WHERE HAVE YOU TRAVELED LATELY. SO IF THEY HAD ASKED THIS PERSON, WHERE HAVE YOU TRAVELED LATELY, AND HE SAID QATAR OR JORDAN, YOU WOULD THINK, BINGO, MAYBE IT WAS MERS, BECAUSE MERS WAS ALL OVER THE NEWSPAPER. UNFORTUNATELY THAT DIDN’T HAPPEN. BUT WE IT DI DID MOBILIZE THE SCIENTIFIC COMMUNITY. THIS WAS AN EARLY VACCINE CANDIDATE THAT WAS DEVELOPED HERE IN THE VACCINE RESEARCH CENTER BY BONNIE GRAHAM, AND THEN THERE ARE RE-EMERGING INFECTIOUS DISEASES, WHICH ARE MANY MORE PLENTIFUL THAN NEWLY EMERGING INFEK SHOUL INFECTIONS,
SUCH AS MULTIPLE AND EXTENSIVELY DRUG RESISTANT TUBERCULOSIS. WE JUST HAD A BIG MEETING DOWNTOWN THAT I PARTICIPATED IN WITH TOM FRIEDEN FROM THE CDC AND PEOPLE FROM USAID ON THE PRESIDENT’S INITIATIVE ON COMBATING MULTI- PEL DRUG RESISTANT I TB. INTERESTING FACT, IT COST $17,000 TO TREAT A CASE OF GARDEN VARIETY TB. IT COSTS ABOUT $100,000 TO TREAT A CASE OF MULTIPLE DRUG RESISTANT IT TB. IT COSTS $435,000 TO TREAT A CASE OF EXTENSIVELY DRUG RESISTANT TB, BECAUSE IT TAKES AT LEAST A COUPLE OF YEARS TO TREAT THEM, THE PEOPLE ESSENTIALLY HAVE TO BE IN THE HOSPITAL FOR MONTHS AND MONTHS. THEN THERE’S DRUG RESISTANT MALARIA. WE’RE STARTING TO SEE THE EMERGENCE OF RESISTANCE. BAD NEWS BECAUSE IT’S ONE OF THE BEST DRUGS WE HAVE EVER HAD FOR MALARIA, AND NOW WE’RE STARTING TO GET DRUG RESISTANT MALARIA. THEN THERE’S THE FAMOUS ANTIMICROBIAL RESIST IT TANS WHICH WE’RE FACING RIGHT HERE ON THIS CAMPUS, FOR THOSE WHO MIGHT REMEMBER, WITH THE EPIDEMIC THAT WE HAD AT THE CLINICAL CENTER A FEW YEARS AGO, WHERE WE HAD 18 CASES AND 11 DEATHS. THAT’S A RE-EMERGING INFECTION. DRUG RESISTANCE IS RE-EMERGING. AND THEN WEST NILE. SO ONE OF THE WAYS YOU RE-EMERGE IS IF YOU OWE KU YOU OCCUR IN A
DIFFERENT GEOGRAPHIC LOCATION THAN YOU’VE EVER SEEN THE VIRUS BEFORE. BECAUSE WEST NILE VIRUS FOR CENTURIES HAS EXISTED IN THE MIDDLE EAST, PARTICULARLY ISRAEL, AND MOSTLY IN THE WEST NILE AREA OF AFRICA. AND YET WE’VE NEVER SEEN IT IN THE UNITED STATES UNTIL IT EMERGED ABOUT 12, 15 YEARS AGO, IN THE UNITED STATES, BECAUSE SOMEBODY OR SOMETHING, A MOS, A MOSQUITO, A PERSON OR SOMETHING ON A PLANE LANDED AT KENNEDY AIRPORT UNTIL WE END UP WITH THE VIRUS. THAT HAPPENED IN 1999, AND WE KEPT ON GETTING ASKED, DO YOU THINK WE HAVE A WEST NILE OUTBREAK IN THE UNITED STATES AND I SAID, OBVIOUSLY, OF COURSE. THEY SAID HOW COULD YOU BE SO SURE? IT’S BECAUSE WE HAVE THE THREE THINGS THAT WEST NILE NEEDS. WE HAVE PEOPLE, WE HAVE MOSQUITOES, AND WE HAVE BIRDS. AND THAT’S EXACTLY WHAT THE WEST NILE EPIDEMIC NEEDED. AND NOW WE HAVE THIS. SO HERE’S WHERE I TOLD THEM IT WOULD HAPPEN AND THEY SAID YOU’RE CRAZY, FAUCI, YOU’RE JUST AN INFECTIOUS DISEASE GUY THAT WANTS MORE MONEY FOR YOUR INSTITUTE. THAT’S TRUE BUT IT’S UNRELATED TO THIS. AND NOW ALL OF A SUDDEN IT’S HAPPENED. WE’RE HAVING VARYING DEGREES, DEPENDING ON THE SEASON, THE MOSQUITOES, THE WEATHER, ALL THINGS LIKE THAT. SO WE WENT AHEAD AND TRIED TO DEVELOP A VACCINE FOR WEST NILE AND WE’RE ACTUALLY QUITE SUCCESSFUL. I’M TELLING YOU THIS VACCINE STORY BECAUSE WE’VE DEVELOPED A VACCINE FOR ALMOST EVERY OUTBREAK THAT HAS OCCURRED, AND THE PHARMACEUTICAL COMPANIES HAVE A PROBLEM WITH MAKING A MAJOR INVESTMENT BECAUSE WHO ARE YOU GOING TO VACCINATE FOR WEST NILE? EVERYBODY IN THE UNITED STATES? UNLIKELY. SO THERE’S NO BIG MARKET. THE SAME THING WITH MERS. THERE’S NOT A BIG ENTHUSIASM ABOUT THIS IN THE UNITED STATES. YOU’LL SEE THE SAME THING WITH A NUMBER OF OTHERS THAT I’M GOING TO SHOW YOU. THEN THERE’S DENGUE. AGAIN, DENGUE HAS BEEN IN ASIA AND IN AFRICA FOREVER. AND THEN IT COMES OVER TO THE AMERICAS. IN BRAZIL NOW, DENGUE IS AN EPIDEMIC. IT’S MORE THAN AN EPIDEMIC, IT’S A PAN IT DEMIC BECAUSE THERE’S A NUMBER OF OTHER CASES. THE SAME THING HAPPENED WITH DENGUE. DENGUE IS AN AMAZING DISEASE. BECAUSE IF YOU LOOK AT THE TROPICAL BELT ACROSS THE GLOBE, THERE ARE ABOUT 400 MILLION INFECTIONS. THAT’S A LOT OF INFECTIONS. IT DOESN’T KILL A LOT OF PEOPLE BUT IT DOES KILL SOME. BECAUSE YOU HAVE SOME COMPLICATIONS OF DENGUE. HEMORRHAGIC FEVER AND OTHERS ASSOCIATED WITH DENGUE. AND AGAIN, WE HAVE A PROBLEM NOW BECAUSE AS YOU MIGHT EXPECT, THERE ARE NOW AN OUTBREAK, NOT A MAJOR BUT A PRETTY GOOD OUTBREAK IN HAWAII OF DENGUE. SO NOT ONLY IT DID COME TO THE AMERICAS, IT COMES WAY OUT TO ONE OF OUR STATES IN THE PACIFIC. NOW, DENGUE VACCINES ARE MOVING ALONG, THERE’S A DENGUE VACCINE THAT WAS APPROVED, THE SANOFI CANDIDATE, NOW APPROVED IN MEX COULD, BRAZIL AND THE PHILIPPINES, AND RIGHT HERE NE NIH AND NIAID, WE HAVE A VACCINE CANDIDATE THAT’S GOING INTO PHASE 3 TRIAL IN BRAZIL. SO THE SCIENCE OF DEVELOPING A VACCINE FOR AN INFECTION THAT THE BODY MAKES A PRETTY GOOD IMMUNE RESPONSE AT ISN’T THAT CAN DIFFICULT. WE HAVE DIFFICULTIES WITH VACCINES THAT THE BODY DOESN’T MAKE A GOOD RESPONSE IN, LIKE MALARIA AND HIV AND TUBERCULOSIS. THAT’S THE REASON WHY WE DON’T HAVE IT. IT WOULD BE WON IT DER FULL TO HAVE A VACCINE FOR ALL OF THOSE BECAUSE EVERYBODY WOULD WANT IT. PEOPLE AREN’T THAT INTERESTED IN VACCINES THAT THEY’RE NOT GOING OH BE ABLE TO USE. HERE AGAIN, YOU CAN JUST GO ON AND ON, IT’S VERY EXCITING TO ME BUT IT CAN ALMOST GET BORING, YET ANOTHER ONE, IS CHIKUNGUNYA. SO CHIKUNGUNYA WAS KIND OF A FUN INFECTION WHEN I WAS IN MEDICAL SCHOOL BECAUSE NO ONE COULD PRONOUNCE IT VERY WELL. WE USED TO GO IN THE BOOKS. BUT AS A MATTER OF FACT, IT, AGAIN, WAS A IT DISEASE THAT WAS IN ASIA AND IN AFRICA, AND THEN ALL OF A SUDDEN, IT LANDS IN THE WESTERN HEMISPHERE, IN THE CARIBBEAN, AND NOW IT’S A MAJOR OUTBREAK IN THE CARIBBEAN, WHICH IS WREAKING HAVOC ON THE TOURIST TRADE IN PLACES LIKE THE VIRGIN ISLANDS AND PUERTO RICO. SO THIS WAS THE GLOBAL DISTRIBUTION OF CHIKUNGUNYA BEFORE THE OUTBREAK IN THE WESTERN HEMISPHERE. THEN WHAT HAPPENED, THE FIRST LOCALLY ACQUIRED CASES WERE SEEN IN 2013, AND THEN, BOOM, ALL OF A SUDDEN NOW, WE HAVE BRAZIL, MEXICO AND THE CARIBBEAN HAVE A PANDEMIC OF CHIKUNGUNYA WITH OVER A MILLION 300,000 CASES LAST YEAR. AGAIN, WE HAVE VACCINES THAT WE’RE DEVELOPING RIGHT HERE AT THE VRC WITH JULIE AND BONNIE AND OTHERS AS WELL AS SOME OF OUR EXTRAMURAL PEOPLE. NOW LET’S GET BACK TO EBOLA BECAUSE I’M GOING TO SPEND A LITTLE TIME ON EBOLA. SO EBOLA, I TOLD YOU, IN 1976 STARTED OFF AS A NEWLY EMERGING INFECTION. IN 2013, 14, 15, I SAY 13 BECAUSE THE FIRST CASE WAS IN DECEMBER. IN 2014 AND 15, IT BECAME A NEWLY EMERGING DISEASE, AND IT’S A VERY INTERESTING STORY BECAUSE IF YOU LOOK AT THE TOTAL NUMBER OF CASES OF EBOLA FROM 1976 IT TO THE PRESENT TIME, EXCLUDING THIS OUTBREAK, THERE WAS ABOUT 2400 CASES WITH ABOUT 12,000 DEATHS. SO NOW THIS EPIDEMIC IS MULTIPLE FOLD MORE THAN ALL OF THE OTHER COMBINED. AND THE REASON FOR THATS WAS THAT IT TOOK PLACE NOT IN A REMOTE REGION BUT IN THE REGION THAT HAD A CERTAIN CHARACTERISTICS. POROUS BORDER, HIGH POPULATION, BIG CITIES, NO IT HEALTH INFRASTRUCTURE, WHICH IS JUST EXACTLY WHAT AN EP DEIT MIC
EPIDEMIC REALL
Y LIKES TO SEE IF YOU WANT TO SPREAD. THERE ARE MULTIPLE DIFFERENT SUBTYPES OF EBOLA. THE ONE THAT WE WERE DEALING WITH WAS EBOLA ZAIRE, WHICH WAS SAID TO HAVE A 50 TO 90% FATALITY RATE. BUT WE KNOW NOW IF YOU CAN GIVE INTENSIVE CARE TO IT PEOPLE, THE FATALITY RATE IS MUCH, MUCH, MUCH LOWER THAN THAT. BUT WHEN YOU’RE OUT IN THE FIELD TRYING TO TAKE CARE OF PEOPLE WITH NO CAPABILITY, THEN IT BECOMES VERY HIGH. IT’S GOT AN ENZOOTIC AND EPIZOOTIC CYCLE. VINCENT HAS BEEN STUDYING THAT. IT ISN’T PARTICULARLY CLEAR WHAT THE DETAILS OF THAT ENZOOTIC CYCLE IS. IT’S PRETTY CLEAR, ONCE IT GETS INTO MAN, EITHER BY TOUCHING OR GET INVOLVED WITH A DEAD ANIMAL, A BAT OR A CHIMP OR APRIL OR WHAT HAVE YOU, THAT IT’S SPREAD FROM MAN-TO-MAN BY BODILY FLUIDS, BY OBJECTS SUCH AS FOMITES, NAMELY CLOTHING YOU HAVE MATERIAL ON. IT’S VOMIT, IT’S FECES, IT’S A VARIETY OF OTHER THINGS WHEN SOMEONE IS REALLY VERY SICK, AS WELL AS INFECTED ANIMALS. AND IT HAS A VERY, I THINK, WELL DESCRIBED IT TYPICAL COURSE NOW. YOU GET EXPOSED, ABOUT EIGHT TO 10 DAYS OR 2 IT TO 21 DAYS LATER, YOU GET SICK. NOW THAT WE’VE SEEN THOUSANDS OF PEOPLE, THIS IS PRETTY TIGHT. THE INCUBATION PERIOD THAT SAYS 2 IT TO 21, IT REALLY IS VERY TIGHT, AROUND 8 TO 10 DAYS, THAT WE HAVE THE GOOD EPIDEMIOLOGY. THEN YOU GET WEAKNESS, FEVER AND INFLUENZA-LIKE SYMPTOMS. SO THAT’S THE CONFUSION OF WHAT IT IS UNTIL YOU START MAKING THE RIGHT DIAGNOSIS IT. THEN YOU HAVE PROTRACTED VOMITING, DIARRHEA, DEHYDRATION, CONFUSION, AND THEN IF YOU DON’T GET REPLENISHMENT OF FLUID, YOU WIND UP GETTING HYPOVOLY MIC SHOCK AND ORGAN SYSTEM FAILURE. I WAS A LITTLE BIT INCORRECT IN WHAT I WAS THINKING ABOUT THE ABILITY TO REPLACE FLUID UNTIL I TOOK CARE OF EBOLA PATIENTS AND THEN THAT BECAME VERY CLEAR IT TO ME THAT IT WAS A LITTLE BIT DIFFERENT THAN WHAT I THOUGHT, AND I’LL EXPLAIN TO THAT IN A SECOND. SO IN MARCH OF 2014, THE GUINEA MINISTRY OF HEALTH REPORTED AN OUTBREAK IN GUINEA. ACTUALLY, IT RELATED TO A CHILD, A PATIENT, A 2-YEAR-OLD IN GUINEA WHO WAS INFECTED AND IT WAS NOT PROPERLY RECOGNIZED, AND THROUGH THE TYPICAL WAY WE KNOW, FAMILY MEMBERS TAKING CARE OF SOMEONE, FUNERAL PROCESSES WHERE YOU WASH AND EMBRACE THE BODY, A WHOLE BUNCH OF PEOPLE IN GUINEA GOT INFECTED. AND THEN IT WAS ONLY WHEN YOU CAME INTO MARCH OF 2014, DID WE START WITH THIS. AND THIS WAS A SCARY THING. SO RED INDICATES THE PROVINCE WHERE THE INFECTION ARE NOW. THE INTERESTING THING IS IF YOU KNOW A LITTLE ABOUT THE GEOGRAPHY OF WEST AFRICA, NOTICE THAT GUINEA WRAPS IT SELF AROUND LIBERIA AND SIERRA LEONE. SO THESE COUNTRIES ARE LIKE ONE COUNTRY. AND THERE ARE BIG CITIES LIKE MONROVIA AND FREETOWN THAT GOT DEEPLY INVOLVED, UNLIKE BACK IN THE 70s AND 80s, WHEN LITTLE VILLAGES IN UGANDA WOULD HAVE A MINI OUTBREAK AND YOU COULD EASILY TAKE CARE OF IT. NOT WHEN YOU HAVE SITUATIONS IN THE CITY. THEN IT WENT LIKE THIS, MAY 2014, JULY 2014, OCTOBER 2014, FEBRUARY ’15, JUNE 2015, AND THEN ALL OF A SUDDEN IS TURNED AROUND AND SHUT OFF. IT DIDN’T SHUT OFF BECAUSE OF THE VACCINE, IT DIDN’T SHUT OFF BECAUSE OF A THERAPY, IT SHUT OFF BECAUSE PEOPLE STARTED DOING WHAT THEY SHOULD HAVE BEEN DOING IN THE BEGINNING. NAMELY, IDENTIFY, ISOLATE, CONTACT TRACE, AND WATCH OUT FOR FUNERAL SERVICES SO THAT YOU DON’T EXPOSE A LOT OF PEOPLE AT THE FUNERAL. AND THAT’S EXACTLY WHAT HAPPENED. NOW, WHAT ARE THE FACTORS THAT FACILITATE THE SPREAD, I HAVE SAID PUBLICLY A LOT ON TELEVISION AND IN THE NEWSPAPERS, THAT WE WOULD NOT HAVE AN OUTBREAK OF EBOLA IN THE UNITED STATES. AND THE REASON WE WOULDN’T HAVE IT IS NOT BECAUSE WE’RE SO PRESUMPTUOUS ABOUT IT, IS THAT IF YOU HAVE A HEALTHCARE SYSTEM THAT’S ABLE TO IDENTIFY, ISOLATE AND CONTACT TRACE, LU HAVE AN OCCASIONAL CASE. OF COURSE SOMEONE IS GOING TO COME FROM WEST AFRICA, BE THAT A HEALTHCARE WORKER OR SOMEONE THAT JUST SLIPS THROUGH THE SCREENING, BUT YOU’RE NOT GOING TO HAVE AN OUT ITBREAK, BECAUSE THESE ARE THE THINGS THEY HAD IN WEST AFRICA: POOR INFRASTRUCTURE, THEY NEVER SAW EBOLA BEFORE. DO YOU KNOW IN LIBERIA, IT’S AMAZING, THERE’S ONE PHYSICIAN FOR EVERY 70,000 PEOPLE IN THE COUNTRY. SO THAT MEANS, I DID THE MATH, THERE ARE MORE PHYSICIANS ON K STREET IN WASHINGTON, D.C. THAN THE ENTIRE COUNTRY OF LIBERIA, AND THEY NEED PHYSICIANS. ANYWAY, YOU HAVE REGIONAL CONFLICTS, THEY DIDN’T TRUST US WHEN WE WENT THERE BECAUSE THEY HAD JUST HAD CIVIL WARS AND A LOT OF DISRUPTION. I WROTE AN ARTICLE IN — ONLINE IN AUGUST BUT IT WAS PRINTED IN SEPTEMBER, SAYING EXACTLY WHAT I’M SAYING RIGHT NOW, THAT THE REASON THERE’S AN OUTBREAK BECAUSE OF A IT DISPARITY OF HEALTHCARE, IF THEY HAD A HEALTHCARE SYSTEM THAT WAS ABLE TO DO THE IDENTIFICATION, THEY WOULDN’T HAVE THIS IT. SO LET’S TAKE A LOOK AT WHAT WE IT DID, JUST VERY QUICKLY. I THINK TALKING ABOUT EMERGING INFECTIONS, IT’S ALSO IMPORTANT TO EMPHASIZE HOW YOU RESPOND TO THEM. SO FIRST OF ALL WITH VACCINES, RIGHT HERE IN THE CLINICAL CENTER, WE IT DID THE FIRST PHASE ONE TRIAL OF THE CHIMP ADENOVECTOR EBOLA VACCINE THAT WAS ONE OF THE TWO COMPONENTS OF THE VACCINES THAT WERE USED. WE DID A PHASE 2 TRIAL IN LIBERIA. WE WERE GOING TO DO A PHASE 3 TRIAL BUT AS WE WERE DOING THE TRIAL, THE INFECTIONS DISAPPEARED ON THEIR OWN AND THERE WERE NO MORE PEOPLE TO DO THE TRIAL ON. GOOD NEWS, PEOPLE ARE GETTING BETTER, BAD NEWS, BAD THAT YOU CAN’T PROVE THE VACCINE WORKS. EVEN THE ONE IN GUINEA, THE DATA ON THAT ARE STILL A LITTLE SOFT AS TO REALLY HOW EFFECTIVE IT IS. THERE WERE THERAPEUTICS, ONE OF THE MOST IMPORTANT OF WHICH WAS THE Z MAP, WHICH IS A TRIPLE ANTIBO IT DEAGAINST THE EBOLA GLYCOPROTEIN THAT WAS DEVELOPED BY A CAN COMPANY AND THEN HAD SOME COLLABORATIONS AND WE IT DID A STUDY WHICH IS ACTUALLY STILL ONGOING. WE’RE GOING TO CALL THE STUDY OFF PROBABLY IN TWO WEEKS BECAUSE THERE ARE NO MORE CASES, BUT IT WAS DOING OPTIMUM CARE VERSUS OPTIMUM CARE FOR Z MAP. IT’S THE ONLY RANDOMIZED STUDY OF ANY THERAPEUTIC IN THE ENTIRE EBOLA OUTBREAK. EVERYTHING ELSE WAS JUST GIVEN DRUGS TO PEOPLE THINKING IT MIGHT WORK OR NOT, WHICH IS NOT THE WAY TO DO THINGS BECAUSE YOU’LL NEVER GET AN ANSWER WITH THAT. THEN I WANT TO TELL YOU A LITTLE ABOUT OUR OWN PERSONAL EXPERIENCE HERE BECAUSE IT TELLS ME SOMETHING ABOUT EBOLA WITHOUT GOING OUT INTO THE FIELD. SO WE HE NIH, THE BETHESDA CAMPUS HERE, WAS ONE OF THE THREE DES IT IG NATEED EBOLA TREATMENT FACILITIES TOGETHER WITH EMORY AND NEBRASKA. AND YOU ALL KNOW THE GREAT PUBLICITY THAT WENT WITH OUR TAKING CARE OF AND DISCHARGES NINA FAMILIAR FAM, ONE OF THE
TWO NURSES WHO GOT INFECTED FROM TEXAS, THE OTHER WAS AMBER VINCENT. THEY SHIPPED AMBER TO EMORY, THEY SHIPPED NINA TO US HERE. SHE DID VERY WELL, BUT TO BE HONEST, SHE WASN’T EVER CRITICALLY ILL IN THAT SHE WAS IN DANGER OF DYING. HERE’S HER GETTING DISCHARGED BY OUR INCREDIBLE TEAM OF STUDY NURSES WHO WERE INVOLVED IN TAKING CARE OF HER. BUT THE REAL CHALLENGE CAME, AND SOMETHING YOU CAN DIDN’T HEAR
DID DIDN’T H
EAR ABOUT, BECAUSE IT WAS A PATIENT THAT DID NOT WANT TO BE IDENTIFIED EXCEPT TO SAY THAT HE WAS A HEALTHCARE WORKER THAT WAS WORKING IN PAUL FARMER’S UNIT OF PARTNERS IN HEALTH IN SIERRA LEONE, AND HE GOT INFECTED BUT HE IT DIDN’T WANT ANYBODY TO KNOW WHO HE WAS, SO IT DIDN’T GET THE PUBLICITY THAT NINA PHAM GOT. BUT IT WAS ONE OF THE MOST INCREDIBLE EXPERIENCES WE HAD AT THE CLIN CAN CAL CENTER BECAUSE THIS IS HIM COMING IN TO THE SIDE ENTRANCE OFF THE CLINICAL CENTER, AND HERE WE ARE, THIS IS DAN CHUR TO YOU AND MYSELF GETTING READY TO GO IN AND SEE THE PATIENT. YOU GET A GOOD FEEL FOR WHAT IT WAS LIKE TO TAKE CARE OF PEOPLE, BECAUSE WHEN YOU PUT THAT SUIT ON, YOU REALLY CAN’T STAY IN IT FOR ANY MORE THAN TWO HOURS. EVEN WITH AN AIR CAN CONDITIONED ROOM. BECAUSE YOU WIND UP JUST GOING ALMOST CLOS TRA PHOBIC WITH THIS HORRIBLE THING YOU GOT TO WEAR WHEN YOU’RE TAKING CARE OF A REALLY, REALLY SICK PERSON, THAT YOU HAD TO INTUBATE, THAT YOU HAD TO PUT A CENTRAL LINE IN, SO IT WAS VERY, VERY STRESSFUL TO DO THAT. AND THE REASON I SAY THAT IS BECAUSE THAT WAS ONE OF THE REASONS WHY SOME OF THE HEALTHCARE WORKERS GOT INFECTED THERE, BECAUSE THEY GET SO TIRED, THEY GET INFECTED AS THEY TAKE OFF THEIR PPE. OBVIOUSLY NOT AS THEY PUT THEM ON. AND A LOT OF PEOPLE GOT INFECTED THERE. SO THAT’S US TALKING ABOUT GOING IN. THE ROTATION WAS ONE INFECTIOUS DISEASE PERSON, ONE INTENSIVIST, .WE WOULD JUST ROTATE IN EVERY COUPLE OF HOURS AND WE HAD A TOTAL OF ABOUT 15 OF US. SO THAT’S DAN GETTING READY TO GET DRESSED, HERE’S MEE GETTING DRESSED, PUTTING ALL THIS EQUIPMENT ON, AND THAT’S DAN AND I IN WITH THE PATIENT. NOW, THE REASON I SHOW THIS IS THAT THERE WASN’T A SINGLE MINUTE WHEN HIS BLOOD PRESSURE WAS BELOW NORMAL. SO WE WERE ALWAYS SAYING THAT ALL YOU’VE GOT OH DO I TO DO IS
KEEP SOMEBODY’S BLOOD PRESSURE NORMAL AND THEY WON’T HAVE ORGAN FAILURE. WE WERE WRONG. THERE’S A CERTAIN SUBSET OF PEOPLE WHO, EVEN IF YOU KEEP THEIR BLOOD PRESSURE NORMAL, THEY WIND UP GETTING — WHILE WE HAD PERFECT CONTROL OF HIS FLUID VOLUME AND HIS ELECTROLYTES, HE PROGRESSIVELY WENT INTO RESPIRATORY FAILURE, RENAL FAILURE, CARDIOVASCULAR COLLAPSE AND MENINGOENCEPHALITIS, AND HE STILL LIVED BECAUSE HE WAS IN A REALLY GOOD INTENSIVE CARE UNIT, TAKEN CARE OF BY PEOPLE WHO UNDERSTOOD INTENSIVE CARE. WE UNDERSTOOD INFECTION BUT THE INTENSIVE CARE GUYS AND LADIES ARE THE ONES THAT BROUGHT HIM THROUGH. HE WALKED OUT OF THE HOSPITAL WELL, FEELING GREAT, WITH A NICE NIH SWEATSHIRT THAT WE BOUGHT HIM. [LAUGHTER] OKAY. NOW, THE OTHER STUDY THAT WE HAVE IS A SURVIVOR STUDY, I’M GOING TO BE LIKELY, DEPENDING ON THE TRAVEL ARRANGEMENTS, TO GO TO LIBERIA ON SATURDAY WITH CLIFF LANE AND CHECK UP ON THIS SURVIVOR STUDY WHICH WE’RE FINDING SOME VERY INTERESTING LONG-RANGE COMPLICATIONS IN IT PEOPLE WHO HAVE RECOVERED FROM EBOLA. AND AGAIN, THE OTHER THING THAT’S OCCUPYING A LOT OF MY TIME RIGHT NOW, ZIKA, THIS IT ONE IS A SURPRISE LIKE ALL OF THE OTHERS. FORMERLY, ZIKA WAS A DISEASE THAT WAS IN ASIA AND AFRICA. ISN’T THAT KIND OF A RECURRING THEME? ASIA, AFRICA. HERE, VARIETY OF REASONS, BECAUSE THIS IS AN — IT’S A FLAVI VIRUS. IT WAS FIRST DESCRIBED IN 1947 IN THE ZIKA FOREST IN UGANDA, FIRST CASE IN 1952. IT’S SPREAD BY AEDES AEGYPTI AND THAT IS THE LINK. WE HAVE AEDES IN SOUTH AMERICAN, IN THE CAR CARIBBEAN, AND IN THE UNITED STATES. SO THE UNITED STATES, AS YOU KNOW FROM YOUR TIME HERE IN THE SUMMER, HAS A LOT OF MOS
MOSQUITOES. IT’S GENERALLY A MILD DISEASE. INCUBATION PERIOD 3 TO 12 DAYS, 4 TO 5 INDIVIDUALS ARE REALLY ASYMPTOMATIC WHEN YOU GET SICK, YOU GET FEVER, CONJUNCTIVITIS, MYALGIA, ET CETERA. SO THESE WERE THE COUNTRIES THAT HAD ZIKA PRIOR TO 2015. THIS IS WHAT’S GOING ON RIGHT NOW, AN EXPLOSIVE PANDEMIC IN BRAZIL, MEXICO, COLOMBIA, AND A NUMBER OF PLACES IN SOUTH AMERICA. NOW, AS WITH MANY VIRUSES, YOU CAN GET GILLIA GILLIAN BA
RSMARRE. THERE WAS AN OUTBREAK IN POLYNESIA, BUT NOW WE’RE STARTING TO SEE SOMETHING THAT’S REALLY SCARY, THAT IS MICROCEPHALY IN BABIES BORN OF WOMEN WHO WERE PREGNANT DURING THE OUTBREAK. NOW, WE DON’T KNOW DEFINITIVELY IF ZIKA IS RELATED TO MICROCEPHALY IN KIDS. WHO WERE BORN WHEN THEIR MOTHER WAS PREGNANT DURING THE OUTBREAK. BUT WE DO KNOW SOMETHING THAT’S EPIDEMIOLOGICALLY STRIKING, AND THAT IS THESE ARE THE NUMBER OF ZIKA CASES, EXCUSE ME, MICROCEPHALY, 2010, 11, 12, 13, 14, AND THIS IS NOW A 20 FOLD IT INCREASE IN THE NUMBER OF THE MICROCEPHALY CASES IN BRAZIL TO THE POINT NOW, EVEN THOUGH THERE’S NO DEFINITIVE PROOF THAT THE BRAZILIAN HEALTH OFFICIALS ARE TELLING PREGNANT WOMEN TO BE INCREDIBLY METICULOUS ABOUT PUTTING ON MOSQUITO REPELLENT, BUT ALSO EVEN AVOIDING GETTING PREGNANT. THAT’S A PRETTY BIG DEAL FOR HEALTH AUTHORITIES TO BE TELLING THE POPULATION TO IT AVOID GETTING PREGNANT BECAUSE OF THIS. SO THIS IS A WORK IN PROGRESS, IT REMAINS TO BE SEEN WHAT THIS IS GOING TO BE. FOR THOSE WHO FOLLOW ONLINE, I JUST LOOKED AT THE GALLEY, I HAVE A PAPER COMING OUT TOMORROW OR THURSDAY IN THE NEW ENGLAND JOURNAL ON ZIKA THAT SORT OF SUMMARIZES A LOT OF THE STUFF THAT I’M SPEAKING HERE. SO LET ME CLOSE UP AND LEAVE SOME TIME FOR QUESTIONS. WHAT THIS TELLS US IS THAT WE ARE LIVING IN A DELICATE BALANCE BETWEEN THE AMAZING CAPABILITY OF MICROBES TO EMERGE, TO RE-EMERGE, AND O TO PERSIST, BALANCED AGAINST OUR ABILITY TO IMPLEMENT PUBLIC HEALTH MEASURES TO DO RESEARCH AND TECHNOLOGICAL ADVANCES. THERE WILL ALWAYS BE EMERGING MICROBES. WHEN I TELL THAT TO LAY AUDIENCES, PARTICULARLY THE CONGRESS, I’M NOT GOING TO SAY GUESS WHAT, GIVE ME ENOUGH RESOURCES AND THERE WON’T BE ANY MORE EMERGING MICROBES. NO, GIVE ME MORE RESOURCES AND WE’LL RESPOND BETTER TO EMERGING MICROBES BUT YOU’RE NEVER, EVER GOING TO STOP MY KROAP MICROBES
FROM EMERGING, THEY JUST HAVE AN EVOLUTIONARY CAPABILITY IN A WAY OF ADAPTING WHICH ALLOWS THEM TO EMERGE. THIS IS MY LAST SLIDE, WITH DAVID MY COLLEAGUE AND GREG, THAT WE WROTE A REVIEW ARTICLE IN LANCET INFECTIOUS DISEASES ABOUT EIGHT YEARS AGO, AND WE ENTITLED IT “EMERGING INFECTIOUS DISEASES, A PE PERPETUAL CHALLENGE.” BECAUSE JUST AS EMERGING INFECTIONS WILL, IN FACT, CONTINUE TO GO, WE’RE GOING TO CONTINUE TO BE CHALLENGED BECAUSE WE’RE NEVER GOING TO BE TOTALLY PREPARED FOR THEM. SO FOR THOSE OF YOU WHO ARE LOOKING FOR A JOB THAT YOU WILL NEVER GET FIRED, GO INTO INFECTIOUS DISEASES. THANK YOU. [APPLAUSE]>>THANK YOU VERY MUCH. SO WE HAVE TIME FOR QUESTIONS, AND WE’D APPRECIATE IF YOU WOULD SPEAK INTO THE MICROPHONE, WHICH WE WILL GIVE YOU, BECAUSE THERE’S A LOT OF PEOPLE ONLINE.>>HOW COME THE IVORY COAST WAS SPARED?>>THEY CLOSED THE BORDER.>>WHAT ABOUT THE ANIMALS THAT DON’T KNOW ABOUT THAT?>>NO, NO, BUT THE ANIMALS CONTINUE TO GET SICK WITH EBOLA. IT’S WHEN THE ANIMALS GET EXPOSED TO THE HUMANS. SO WE DON’T ACTUALLY KNOW WHAT THE REAL TRUE RESERVOIR IS OF EBOLA. WE KNOW APES GET INFECTED AND WE KNOW YOU CAN FIND IT IN BATS, BUT THAT ENZOOTIC CYCLE IS NOT PARTICULARLY WELL WORKED OUT. BUT THE REASON THE COUNTRIES AROUND — THEY WERE ACTUALLY CLOSED OFF, THEY WERE VERY CAREFUL OF NOT LETTING THEM IN.>>THANKS FOR THAT TALK, TONY. I’M RICK WITH NIMHD. SO I SPENT THREE MONTHS LAST SUMMER WORKING WITH — AND OTHERS IN DNA AND JUST HAVE A QUESTION ABOUT THE IS A TU
STATUS OF VACCINES AND THE THERAPEUTIC Z MAP BECAUSE NO PATIENTS, SO HOW IS THAT GOING TO PLAY OUT IN TERMS OF WHAT HAPPENS THE NEXT TIME?>>OKAY, SO WHAT WILL LIKELY HAPPEN, BECAUSE OF THE POSITIVE THOUGH NOT DEFINITIVE RESULTS FROM THE GUINEA RING TRIAL, THAT AT LEAST CSV, IF WE HAVE ANOTHER OUTBREAK, WILL LIKELY BE GIVEN IN A COMPASSIONATE WAY, NOT AN ACCELERATED APPROVAL BECAUSE THERE’S NOT ENOUGH DATA TO APPROVE IT BY THE FDA. THE WHO WILL LIKELY ASK TO DEPLOY IT ON AN EMERGENCY BASIS. SIMULTANEOUS WITH THAT, AND WE HOPE THERE NEVER IS ANOTHER OUTBREAK TO DO IT, BUT IF THERE IS, THAT WILL HAPPEN. SUBSEQUENT TO THAT, OR AT THE SAME TIME, WE’RE GOING TO DO A NON-INFERIORITY IMMUNOGENIC U.S. DID DI. WE’RE GOING TO LOOK AT THE IMMUNE RESPONSE TO VSV COMPARED OH THE IMMUNE RESPONSE TO CHIMP ADENO AND HUMAN ADENO VECTOR AND DETERMINE IF THEY’RE THE SAME SO YOU’LL HAVE MORE THAN ONE VACCINE THAT MIGHT BE AVAILABLE. BUT THE Z. MAP, WE HAVE — THE DID DSMV KEEP LOOKING AT THE DATA AND IT WASN’T GOOD ENOUGH OR BAD ENOUGH TO STOP THE STUDY, BUT IT STILL MAY BE THAT IF YOU LOOK AT THE DATA AFTER YOU DO FORMALLY STOP IT BECAUSE THERE ARE NO NEW INFECTIONS, THAT YOU CAN ACTUALLY SAY THERE WAS A BENEFIT IN DECREASING HOSPITAL DAYS OR QUICKNESS TO THE DECREASE IN VIREMIA, I DON’T THINK IT’S GOING TO BE A SLAM DUNK RESULT ON MORTALITY. OTHERWISE THEY WOULD HAVE STOPPED THE STUDY IF THERE WAS.>>I WONDER IF YOU CAN COMMENT ON THE TREATMENT OF THE MOSQUITOES, BECAUSE WE HAD SOME SIGNIFICANT DECREASE IN MALARIA WHEN DDT WAS SPRAYED IN CERTAIN PARTS OF THE WORLD, AND THEY’RE BACK WITH VENGEANCE, WITH DRUG-RESISTANT MALARIA TO THE ZIKA.>>WELL THERE’S AN ONGOING ARGUMENT THAT THE STOPPING OF AGGRESSIVE MOSQUITO CONTROL WITH DDT WAS A MISTAKE, EVEN THOUGH THERE WAS FEELING THAT THERE WAS A LOT OF ENVIRONMENTAL REASONS TO DO THAT. THERE ARE STILL GOOD WAYS TO CONTROL MOSQUITOES. YOU CAN CONTROL MOSQUITOES, BUT WITH MALARIA, IN SOME COUNTRIES, JUST BED NETS AND INDOOR SPRAYING HAVE DECREASED MALARIA DRAMATICALLY IN CERTAIN COUNTRIES.>>A QUICK FOLLOW-ON TO THE Z MAP STUDY QUESTION. ARE THERE GOING TO BE LONGITUDINAL STUDIES OF THOSE WHO ARE — OF YOUR CASE CONTROL STUDY TO LOOK AT THE LONG TERM REPERCUSSIONS AND IF THAT HAS A POSITIVE EFFECT?>>YES. THE Z MAP RECIPIENTS ARE PART OF THE SURVIVOR STUDY. SO WE WILL BE ABLE TO LOOK AT SEE MAP SURVIVORS COMPARED TO PEOPLE WHO DIDN’T GET Z MAP. GOOD QUESTION.>>CAN YOU SUMMARIZE FOR US, TONY, WHAT’S THE STATUS NOW OF THE DEVELOPMENT OF PUBLIC HEALTH MEASURES IN WEST AFRICA AND THE UNDERDEVELOPED WORLD? IS THERE ANY — IS IT BEING TAKEN SERIOUSLY AND ARE THERE VENTURES, I MEAN, OTHER THAN GATES OR SOMETHING, WHAT ABOUT INTRINSICALLY, DO YOU SEE A MORE –>>WELL, EVERY TIME SOMETHING LIKE THIS HAPPENS WHEN THERE’S A BIG SURGE OF ENTHUSIASM, PEOPLE WRITE BLOG, PEOPLE WRITE ARTICLES, WHO MAKES STATEMENTS, AND THEN WHEN IT GOES OFF THE RADAR SCREEN, NOTHING HAPPENS. AND THE REASON IS THAT COUNTRIES THEMSELVES HAVE TO MAKE THE COMMITMENT THAT HEALTH INFRASTRUCTURE IS AN IMPORTANT PART OF THEIR BUDGETARY AGENDA. EVEN THOUGH WHEN THEY DON’T HAVE A LOT OF MONEY, BECAUSE SOME OF THESE KUN RIS DON’T PUT ANYTHING INTO HEALTHCARE INFRASTRUCTURE. NOW THE OUTSIDE RICH WORLD CAN COME IN AND HELP. WHAT WE’RE DOING A LITTLE BIT DIFFERENTLY IS THAT AT LEAST WE HAVE MADE A COMMITMENT THAT WHEN YOU GO IN AND HELP IN AN EMERGENCY SITUATION, YOU DON’T LEAVE UNLESS YOU LEAVE SOME SUSTAINABLE HEALTHCARE INFRASTRUCTURE. AND WHEN CLIFF LANE WENT OVER AND SPENT A LOT OF TIME IN LIBERIA SETTING UP THE VACCINE AND THE THERAPY TRIALS, HE TOOK A LOT OF THE MONEY THAT WAS GIVEN US IN THE SUPPLEMENTARY BUDGET AND WE RENOVATED A NUMBER OF THE CLINICS IN REDEMPTION HOSPITAL AND JFK HOSPITAL IN MONROVIA SO THAT WHEN WE GET OUT OF THERE, THEY WILL HAVE AT LEAST SOME DEGREE OF INFRASTRUCTURE. WE’VE TRAINED THEM, YOU KNOW, HEINZ AND VINCENT WENT OVER AND TRAINED A LOT OF THEIR PEOPLE HOW TO DO THE DIAGNOSTIC TESTS, SO YOU’VE JUST GOT TO MAKE A COMMITMENT. YOU’RE NOT JUST GOING TO COME IN AND GO OUT. YOU’RE GOING TO TRY AND LEAVE A SUSTAINABLE INFRASTRUCTURE.>>DR. FAUCI, THE QUESTION I HAVE IS ONE OF THE LAST EXAMPLES DISCUSSED ABOUT EBOLA, THE MARCH 2015 CASE WHERE YOU SAID THAT THERE WERE ORGAN FAILURES, SO IS IT ONLY RELATED TO THAT PATIENT OR YOU GET THAT AS A GENERAL TREND WITH ALL PATIENTS AND –>>NO, GO AHEAD, FINISH. I’M SORRY.>>AND THEN IS IT SOMETHING THAT IS RELATED TO THE VIRUS ITSELF OR HAS TO DO WITH THE STATE OF THE PATIENT IN WHICH THE PATIENT IS TAKEN INTO CARE?>>OKAY, THAT WAS A GREAT QUESTION. SO BASED ON EXPERIENCE THAT OUR PEOPLE HAVE HAD, PEOPLE LIKE DAN CHURTOW, SPENT A CONSIDERABLE AMOUNT OF TIME THERE TAKING CARE OF PATIENTS. IT IS OUR GENERAL IMPRESSION AND IT ISN’T 100% BUT IT’S A PRETTY STRONG IMPRESSION THAT IF YOU LOOK AT ALL PEOPLE WHO GET EBOLA, AND THERE MAY BE WHAT THE INITIAL — WHAT YOUR IMMUNE RESPONSE IS, THEY’RE GOING TO BE MAYBE 20% OF PEOPLE WHO GET SICK WHO DON’T REALLY HAVE A LOT OF PROBLEMS, DON’T NEED SERIOUS REHYDRATION. SO MAYBE ANOTHER 20% WHO CAN GET BY WITH ORAL HYDRATION. THERE MAY BE ANOTHER 40% OR SO WHO WILL NEED INTRAVENOUS CENTRAL LINE TYPE OF REPLENISHMENT OF FLUID. IF YOU DO THAT, THEY WILL BE FINE. THEN THERE’S ABOUT ANOTHER 20%, MAYBE 15 TO 20% OF PEOPLE THAT NO MATTER WHAT YOU DO WITH REPLENISHMENT OF FLUID, THE VIRUS WILL ATTACK THEIR ORGAN SYSTEM. SO THERE’S ORGAN SYSTEM FAILURE ASSOCIATED WITH HYPOVOLEMIC SHOCK, AND THEN THERE’S ORGAN SYSTEM DAMAGE DUE TO DIRECT DAMAGE OF THE VIRUS. THOSE 20% OR SO, MAYBE IT’S 15, MAYBE IT’S 20, IF THEY’RE NOT IN AN INTENSIVE CARE SETTING, YOU CAN GIVE THEM ALL THE FLUID YOU WANT, THEY’RE GOING TO DIE. AND THE REASON OUR PATIENTS SURVIVE WAS BECAUSE WE HAD THEM MONITORED 24 HOURS A DAY FOR THE 12 DAYS THAT HE WAS ACUTELY ILL. AND HE CAME IN REASONABLY WELL, I MEAN, I GREETED HIM AT THE DOOR AND BROUGHT HIM IN, PUT HIM IN BED, GOT HIM UNDRESSED AND ALL THAT, TALKING TO HIM, THEN ALL OF A SUDDEN, OVER A PERIOD OF A DAY OR TWO, HE JUST COMPLETELY CRASHED. AND HE CRASHED WITH A CENTRAL LINE IN WITH OUR MONITORING HIS BLOOD PRESSURE THAT IT THAT IT NEVER, EVER WENT BELOW A LEVEL THAT YOU’D BE CONCERNED. SO THAT’S DEFINITIVE PROOF THAT IT WAS THE VIRUS THAT DID THAT, NOT FLUIDS.>>HI, ANOTHER QUICK QUESTION. REGARDING INFRASTRUCTURE BUILDING IN DEVELOPING NATIONS. IF WE WERE GOING TO BE DIRECTING FUNDS TOWARDS ANY PARTICULAR PROJECT, WHAT WOULD YOU SEE AS THE MOST VALUABLE IN IT PREVENTING THE EMERGENCE AND SPREAD OF THESE INFECTIOUS DISEASES?>>TRAINING NURSES. TRAINING NON-PHYSICIAN HEALTHCARE PROVIDERS. THERE WILL NEVER BE ENOUGH DOCTORS TO DO IT ALL. BUT YOU KNOW, IF YOU LOOK NOW AT SOME OF THE COUNTRIES THAT WE GIVE PEPFAR AID TO, WE HAVE PEOPLE WHO ARE NOT PHYSICIANS AND NOT EVEN NURSES OUT IN THE COMMUNITY IMPLEMENTING THE PEPFAR PROGRAM, WHICH IS WORKING TERRIFICALLY WELL.>>THAT MIGHT ALSO HELP THE U.S. AS WELL. ONE MORE QUICK QUESTION WITH REGARD TO SPECIFICALLY THE MANAGEMENT OF THAT PATIENT WHO HAD ORGAN SYSTEM FAILURE. IS THERE A POSSIBILITY THAT MAYBE NOT DUE TO THE FACT THAT THERE’S HYPOVOLEMIA BUT THAT THE EBOLA VIRUS MIGHT ACTUALLY ATTACK RED BLOOD CELLS AND CAUSE HEMO LYSIS, WHICH COULD PRESUMABLY CAUSE ORGAN SYSTEM DAMAGE, IS THAT A POSSIBILITY WITH REGARD TO THE CAUSE?>>I DON’T THINK SO BECAUSE TO MY KNOWLEDGE, EBOLA DOESN’T DIRECTLY ATTACK RED BLOOD CELLS, I DON’T THINK SO. NO, IT DOESN’T.>>THE BLEEDING IS NOT FROM RED BLOOD CELLS –>>THAT’S NOT ATTACKING, THAT’S AN ENDOTHELIAL CELL PROBLEM, THAT’S NOT A RED CELL PROBLEM.>>YOU MENTIONED THAT THE PATIENT YOU HAD HERE IN VERY CRITICAL CARE WAS ABLE TO SURVIVE BECAUSE HE WAS BEING CONSTANTLY MONITORED FOR THE ENTIRE TIME HE WAS THERE, THEY HAD A WHOLE TEAM DEDICATED TO HIS CARE. IF YOU HAD A LARGER NUMBER OF PATIENTS COME IN, SORT OF AT THAT CRITICAL LEVEL AT THE SAME TIME, DO YOU THINK YOU WOULD BE ABLE TO MANAGE THE SAME VERY POSITIVE SURVIVAL OUTCOMES THAT YOU SAW IN THE PATIENT –>>THAT’S A GOOD QUESTION. WE KIND OF MODELED THAT, WE FELT HA WITH THE STAFF THAT WE HAD, THAT WE COULD MANAGE TWO VERY SICK PERSONS AND ONE NOT SO SICK PERSON, BUT NO MORE THAN THREE TOTAL. THAT’S WHAT WE MODELED THAT, WE COULDN’T CAN DO ANY MORE THAN THREE. IT WOULD BE PHYSICALLY IMPOSSIBLE. WE WERE ALMOST EXHAUSTED WITH ONE, WE WOULD HAVE BEEN REALLY EXHAUSTED WITH TWO, AND THAT’S WHY THE THIRD ONE WOULD HAVE TO BE NOT SO SICK.>>WELL, THANK YOU VERY MUCH.>>YOU’RE WELCOME. [APPLAUSE]>>CAN EVERYBODY HEAR ME? GREAT. A LITTLE BIT OF UNGRATEFUL SPOT TO FOLLOW IN THE FOOTSTEPS OF DR. FAUCI, SO I TRY TO DO MY BEST AND I PUT SOME SLIDES TOGETHER TO GET A LITTLE IDEA OF WHAT I’M WORKING ON AND PERSONAL EXPERIENCE. AND I KIND OF MOVED FROM FLU, WHICH I HAVE A COUPLE OF INTERESTING SLIDES ON TO MERS AND I’LL FINALIZE WITH EBOLA VIRUS. AND AS DR. FAUCI ALREADY SAID, MOST OF THESE EMERGING OR RE-EMERGING VIRUSES HAVE WHAT WE CALL A RESERVOIR IN WILD ANIMALS. WE’RE TAUBING ABOUT NON-HUMAN PRIMATES, WATER FOWL FOR INFLUENZA VIRUSES, RODENTS, AND MARBURG VIRUS, EBOLA VIRUS ORIGINATE FROM BAT AS WELL. FROM THESE NATURAL RESERVOIRS, THESE VIRUSES CAN SOMEHOW TRANSMIT INTO THE HUMAN POPULATION, BUT WHAT IS VERY IMPORTANT TO POINT OUT IS WE HAVE WHAT WE CALL AMPLIFYING RESERVOIRS. FOR INSTANCE, POULTRY IN THE CASE OF AVIAN INFLUENZA IS ONE OF THE MOST PREDOMINANT AMPLIFYING HOSTS, GETS INTRODUCED INTO POULTRY AND THEN IT ACTUALLY STARTS MUTATING INTO HIGHLY PATHOGENIC VIRUSES, AND THESE BECOME DANGEROUS FOR HUMANS. SIMILAR TO SWINE, WE HAD THE H1N1 OUT ITBREAK. THE INTRODUCTION OF NEPA VIRUS INTO THE SWINE POPULATION IN MALAYSIA IN 1999 AND SUBSEQUENT, AND THAT OUTBREAK HAD A CASE OF AROUND 90%, SO VERY, VERY HIGH CASE FATALITY RATE. SO WHAT I’M TRYING TO DO IN MY LAB IS COMBINE KNOWLEDGE ON DIFFERENT LEVELS TO SEE WHAT WE CAN FIND OUT ABOUT THESE OUTBREAKS AND HOW THESE VIRUSES CROSS THE SPECIES BARRIERS WE CALL IT, SO TRYING TO IT USE GENETIC AND PROTEIN INFLAMMATION TO SOMEHOW PREDICT POST SPECIES TROPISM OF THESE VIRUSES, MOVING TO THE INDIVIDUAL HOST, THE NATURAL RESERVOIR. IN HAD CASE IT’S A VERY PRETTY — PROVED THAT WITH BATS IN AFRICA. MOVING INTO THE INTERMEDIATE RESERVOIR WHICH I POINTED OUT, IN THIS CASE FO FOR MRSA, AND
THEN OF COURSE THE CIRCULATION OF THESE VIRUSES IN A LARGE POPULATION, TYING THAT ALL TOGETHER TO IT TRY TO UNDERSTAND WHY THESE VIRUSES CROSS THE SPECIES BARRIER. I THINK THIS IS A REALLY NICE SLIDE ON INFLUENZA A VIRUSES. EACH AND EVERY BOX IN THIS TREE IS A DIFFERENT POPULATION, SO THE ONE THAT STANDS OUT IS IN LIGHT BLUE, THAT’S THE HUMAN POPULATION, AND THEN WE HAVE HERE AVIAN, WILD WATER FOWL, SO A COUPLE THINGS STAND OUT, THAT THE EVOLUTION IN DIFFERENT POPULATIONS IS DIFFERENT. SO WE SEE IN HUMANS VERY NICE PUNCTUATED EVOLUTION, KIND OF COINCIDES WITH THE DRIFT BUT THIS IS NOT ONE OF THE PROTEINS ON — THEN WE SEE THE EVOLUTION, NICELY SEPARATED IN THE RESERVOIR, WHICH IS WILD WATER FOWL. WHAT YOU CAN SEE IS THAT AVIAN INFLUENZA IN NORTH AMERICA IS DIFFERENT FROM THOSE IN EURASIA. KIND OF NICELY SHOWN OVER HERE. SO BASICALLY DIFFERENT HOST POPULATION EXERT DIFFERENT EVOLUTIONARY PRESSURES ON THE VIRUS. ANOTHER LEVEL OF LOOKING AT THAT IS TRYING TO UNDERSTAND HOW TRANSMISSION OCCURS. THIS IS, AGAIN, INFLUENZA VIRUS. I’VE BEEN LOOKING A LOT IN DABBLING DUCKS, AND IF YOU SAMPLE — AND WHAT YOU SEE, IT’S PREDOMINANTLY VIRUS — WHICH, OF COURSE, MAKES FOR A VERY NICE ROUTE OF TRANSMISSION, THESE, THEY FEED UP END IN THE WATER IT, SO IF YOU DEFECATE IN THE WATER, IT’S VERY EASY FOR THE VIRUS TO TRANSMIT TO THE SECOND ONE. THIS IS ACTUALLY NOT TRUE FOR GEESE. AND HERE WE SEE WHITE FRONT GEESE, SO IF YOU KIND OF KNOW WHAT GEESE DOES, SO IF WE GO OUT TO THE MALL AND YOU SEE ALL THESE GEESE THERE, YOU SEE ALL THE TURRETS LYING ON THE GROUND, RIGHT? SO THIS DOESN’T WORK FOR GEESE. SO THE INFLUENZA VIRUS HAS TO DO SOMETHING DIFFERENT, AND IT ACTUALLY DOES. SO IF YOU LOOK AT WHERE THE VIRUS IS PREDOMINANTLY POUND IN THESE GEESE, IT’S ACTUALLY THE RESPIRATORY TRACT SIMILAR TO HUMANS. SO THESE VIRUSES CAN ACTUALLY CHANGE ON THE BEHAVIOR OF THE HOST. HERE’S ANOTHER THING, WHAT KIND OF EFFECT DOES A VIRUS IN THE NATURAL RESERVOIR HAVE? PEOPLE THINK WELL, IT’S A NATURAL RESERVOIR SO IT DOESN’T HAVE ANY PATHOGENIC EFFECT. THAT’S KIND OF COMMON KNOWLEDGE. I ALWAYS THINK LIKE, WELL, IT’S KIND OF SIMILAR TO IT CHILDHOOD DISEASES, EVEN THOUGH LIKE EVERYBODY — NOW THEY GET VACCINATED FOR MOST OF THEM, EVEN THOUGH THE MORTALITY RATE MIGHT NOT BE THAT HIGH, BUT IT DEFINITELY HAS LIKE AN IMPACT. SO AGAIN WE’RE LOOKING AT BASICALLY THIS IS HOW WE KEPT THEM, SO YOU HAVE THESE CANNONS, AND YOU SHOOT A NET OVER THEM. THEN OVER HERE YOU SEE — HERE IS WHERE I’M SAMPLING. THIS IS IN THE TOP OF THE NORTHERN PART OF THE NETHERLANDS. THIS IS WHAT I STILL DO. BUT THE MOST INTERESTING THING IS, WHAT HAPPENS IF YOU START COMPARING INFECTED ANIMALS FROM NON-INFECTED ANIMALS. I WAS ACTUALLY WORKING TOGETHER WITH ECOLOGISTS WHO WERE VERY INTO THE PHYSIOLOGY OF MIGRATION. SO THESE ARE MIGRATORY ANIMALS. SO WHAT I ACTUALLY MEADE TO DO, WHEN THEY’RE IN THE NETHERLANDS, HE NEED TO FATTEN UP, THEY NEED TO START — YOU CAN ACTUALLY MEASURE THAT. SO YOU CAN ACTUALLY — HERE WHERE YOU HAVE LABELED THESE ANIMALS WITH ASSET LIGHT TRANSMISSION COLLAR, AND YOU CAN ACTUALLY LOOK WHAT THEY CALL THE ABDOMINAL PROFILE INDEX, HOW BIG THIS ANNAL IS GETTING. THESE GUYS ARE ACTUALLY LOOKING AT THOSE ANIMALS FOR A DURATION OF TIME, THEY ACTUALLY COUNT THE NUMBERS OF DROPPINGS THEY ACTUALLY PUT DOWN IN AN HOUR AND THEY CAN ACTUALLY MEASURE THE EFFICIENCY OF TAKING OUT NUTRIENTS. I DIDN’T KNOW THIS, I WAS JUST A VIROLOGIST OF. SO THEN I STARTED LOOKING AT THE ONES INFECTED WITH A VERY BENIGN AVIAN INFLUENZA VIRUS, AND YOU CAN SEE ALL THE MEASUREMENTS WERE UP, BUT MOST STRIKING IS WHEN THEY START MIGRATING ALL THE HELP — MIGRATING, WHEN WAS THE TIME. HOWEVER, THE SICK ONES STAYED AROUND FOR A LONG TIME. SO WHAT KIND OF IMPACT DOES IT GO? IF YOU GO TO YOUR BREEDING GROUNDS, YOU WANT TO BE THE FIRST BECAUSE YOU WANT TO PICK THE BEST START — IF YOU COME TOO LATE, THE BEST SPOTS ARE GONE SO WE’LL HAVE — BACK TO YOUR OFFSPRING BUT ALSO THESE ANIMALS CAN MAKE A CONSCIOUS DECISION, WELL, MAYBE NOT THIS YEAR, BREEDING IS NOT GOOD FOR ME. SO THEY ACTUALLY CAN MAKE A COMPETENT DECISION. I THINK EVERYBODY KIND OF KNOWS ABOUT SEASONAL INFLUENZA OR HUMAN INFLUENZA AND AVIAN INFLUENZA AND THE KIND OF RECEPTORS THEY USE SO THEY HAVE WHAT THEY CALL HUMAN RECEPTORS, THE AVIAN RECEPTOR, SO IT’S KIND OF A DISKNOW MER, BECAUSE ROUX MANS HAVE THE AVIAN RECEPTOR BUT NOT WHERE NORMAL SEASONAL INFLUENZA REPLICATES, WHICH IS IN THE UPPER — SO VERY IMPORTANT FOR BOTH APPLICATION OF SEASONAL INFLUENZA AND ALSO SUBSEQUENT TRANSMISSION, SO IF YOU GO THROUGH THE RESPIRATORY TRACT, DEEP DOWN, YOU COULD SEE THE ABUNDANCE OF THE RECEPTOR AND THE ABILITY FOR THE FIRES TO BIND THERE IS DECREASING, SO IT ACTUALLY EXPLAINED WHY SEASONAL INFLUENZA PREDOMINANTLY DUPLICATES IN THE UPPER RESPIRATORY TRACT AND DOESN’T NORMALLY CAUSE DEVEER DISEASE, WHEREAS — DOESN’T REALLY REPLICATE IN THE RESPIRATORY TRACT BUT GOES DEEP DOWN AND CAUSES SEVERE PNEUMONIA. SO I THINK INFLUENZA SET THE STAGE QUITE NICELY, MOVING TO MERS, AND DR. FAUCI ALREADY QUITE NICELY INTRODUCED IT, WAS IDENTIFIED IN A PATIENT IN SAUD
SAUDI ARABIA IN 2012. THE MOST INTERESTING THING IS IN THIS TREE WHERE IT ACTUALLY — VERY CLOSELY TO SEQUENCES OF — FROM BACKGROUND VIRUSES. ANOTHER ONE, THE KNOW TORE YAS ONE IS IN THIS GROUP TOO. SO IT ACTUALLY, FOR A LOT OF PEOPLE, SAW RINGING ALARM BELLS. THIS IS AN INTERESTING VIRUS, WE REALLY NEED TO SEE WHAT’S GOING ON HERE. THEN OF COURSE THE SOUTH KOREAN SITUATION, WHERE YOU HAD A LOT OF — TRANSMISSION AND SUPER SPREADER EVENT, WHICH IS ALSO NEW FROM SARS. SO IT’S IMPORTANT TO KEEP IN MIND, THAT’S GOING TO BE IMPORTANT. SO ALTHOUGH IT WAS POINTED OUT THAT THIS MIGHT BE SIMILAR, THIS IS ACTUALLY WHAT — IT MIGHT NOT BE THAT WELL-KNOWN BUT AROUND, I WOULD SAY, 80 TO 90% OF THE CASES GET INFECTED IN THOSE SETTINGS SO THE ACTUAL TRANSMISSION FROM RESERVOIR INTO THE HUMAN POPULATION SEEMS TO BE FAIRLY MINIMAL. SO FIRST THING WE IT DID WAS KIND OF WHAT WE CALL PROVING THE — SEE WHERE THE INFECTIOUS AGENT THEY ISOLATED ACTUALLY CROSSES THESE. SO YOU HAVE TO ADAPT IT A LITTLE BIT, SO THE IDEA IS YOU PUT THAT VIRUS IN THIS CASE IN A NON-HUMAN PRIMATE MODEL AND IT NEEDS TO REPLICATE, YOU NEED TO BE ABLE TO IT RE-ISOLATE THAT VIRUS. SO WHAT WE IT NICELY SEE HERE IS THAT THE VIRUS CAUSES LOWER SURGERY TRACT INFECTION AND YOU CAN SEE IT REPLICATING HERE, THE LUNGS ARE NORMALLY — THE ALVEOLI IS WHERE — TAKES PLACE SO IT’S A NICE OPEN SPACE, TYPE 1 AND TYPE 2 PNEUMOSTIETS, SO IT KIND OF LOOKS LIKE THIS, WHERE EVERYTHING IS FILLED — EDEMA, CELLS, INFLUX OF NUTRAFILLS, THAT’S NOT GOOD. HERE WE ACTUALLY ARE ABLE TO SHOW REPLICATION OF THE VIRUS IN THE LOWER RESPIRATORY TRACT BY HUE MON HISTOCHEMISTRY, AND THEN IF YOU DO COSTAINING, YOU CAN ACTUALLY SEE THAT THIS VIRUS REPLICATES IN THE TYPE 1 AND TYPE 2 — EXPLAINS WHY IT IS A VIRUS-CAUSED DISEASE. SO IT IS KIND OF IMPORTANT THAT — BECAUSE THE VIRUS — UP TO NOW, THERE’S NO HUMAN PATHOLOGY DAY A OF THIS VIRUS, WHICH IT’S KIND OF UNDERSTANDABLE IF YOU SEE WHERE THE VIRUS ORIGINATES FROM, WHICH IS THE MIDDLE EAST, AND POSTMORTEMS ARE NOT COMMONLY DONE THERE. HOWEVER, I WOULD HAVE EXPECTED, DUE TO THE SOUTH KOREAN OUTBREAK, WHICH WAS AROUND MAY OF LAST YEAR, THAT THIS INFORMATION WOULD BE AVAILABLE, BUT I HAVEN’T SEEN IT SO FAR. SO WE’RE STILL RELYING ON NON-HUMAN PRIMATE DATA. SO GETTING A LITTLE BIT INTO — YOU HAVE A WHOLE LOAD OF PATIENTS WITH ALL THESE KIND OF CO-MORBIDITIES, AND I THINK THAT EXPLAINS WHY THIS VIRUS IS SO EFFICIENT IN THIS KIND OF SETTING AND NOT IN THE NORMAL POPULATION. I THINK IT’S KIND OF LIKE NOT REALLY WELL EXPLAINED TO THE GENERAL AUDIENCE THAT THE GENERAL PUBLIC IS NOT REALLY AT RISK FOR THIS PARTICULAR VIRUS. HOWEVER, IF YOU INTRODUCE IT IN A HEALTHCARE SETTING, THAT’S WHERE THE PROBLEMS ARISE. SO WHAT WE DID HERE IS WE ACTUALLY TREATED NON-HUMAN PRIMATES WITH A COMBINATION WHICH COMPLETELY SUPPRESSES THE IMMUNE SYSTEM, AND NOT SURPRISINGLY, WE SEE VERY HIGH REPLICATION IN THE LOWER TRACT IN THE LUNGS. SO NORMALLY IF YOU SEE THESE KIND OF PATIENTS IN THE BEGINNING HA DON’T REALLY SHED THAT MUCH VIRUS. HOWEVER, IF THEY GET MORE PROGRESSING IN THE DISEASE THEY START SHEDDING MORE VIRUSES, WHICH ALSO EXPLAINS WHY THIS VIRUS IS SO EASILY TRANSMITTED IN THESE HEALTHCARE SETTINGS. SO GETTING BACK TO THE NATURAL RESERVOIR, SO WE DID SOME EXPERIMENTS WHICH SHOW THAT THE RECEPTOR FOR A VA VITAL OF
VARIETY OF ANIMALS, THE MRSA A WAS ABLE TO BIEND TO THE RECEPTOR OF COMMON LIVE DK STOCLIVESTOCK SUCH AS
CAMELS, THIS IS IN SAUDI ARABIA AND THIS IS SEROLOGY, BUT WE DON’T SEE IT IN ANY OF THE OTHER SPECIES LIKE HORSE, GOAT AND SHEEP. WE ALSO SET UP SURVEILLANCE IN JORDAN AND THESE ARE MY VETERINARY COLLEAGUES IN JORDAN, SO THIS IS NOT HOW YOU SAMPLE DROMEDARY CAMELS. BUT YOU KIND OF EXPECT WHAT HAPPENED HERE IT DID HAPPEN, SO THIS ANIMAL WAS DEFINITELY NOT HAPPY AND KICKED HIM. I WAS SANDING WITH A VERY IMPRESSED — YOU’RE SUPPOSED TO MAKE THEM KNEEL DOWN AND THEN YOU SAMPLE THEM. SO THEY’RE KIND OF MOODY ANIMALS. THIS IS A LITTLE BIT ABOUT THE DROMEDARY CAMEL. SO IT’S BEEN DOMESTICATED AROUND 5,000 YEARS AGO. THIS IS DISTRIBUTION SO ALL DOM DRI CAMELS ARE DOMESTICATED. THIS IS THE NORMAL DISTRIBUTION RATE. WE SEE SERO PREVALENCE FROM MAUI UP TO KENYA AND TANZANIA, MIDDLE EAST, AS FAR AS IN BANGLADESH, WE HAVE NOW INFORMATION THAT ALSO THE DROMEDARY CAMELS IN BANGLADESH ALSO ARE SER O-POSITIVE — AND THEN THERE’S A LARGE FERRELL POPULATION THAT’S ZERO-NEGATIVE IN — IT ACTUALLY ORIGINATED FROM THE AMERICAS. SO WE USED TO HAVE DROMEDARY CAMELS HERE, IF YOU GO TO L.A., YOU STILL SEE FOSSILIZED REMAINS OF DROMEDARY CAMELS, HOWEVER, THE CAMEL HAS CROSSED THE BEARING STREET INTO THE OLD WORLD, BUT OF COURSE — WHICH ARE ALL CAMELITES. SO I WANTED TO KNOW WHAT YOU COULD ACTUALLY — WHAT THE DISEASE WOULD LOOK LIKE IN A DOM DRI CAMEL. SO I THIS TO EXPLAIN TO DR. PFAU CHEEK THAT THE NIH WAS THE PROUD OWNER OF THREE DROMEDARY CAMELS. I ACTUALLY BOUGHT THESE FOR MY STARTUP BUDGET, BUT THIS IS SOMETHING WE CANNOT DO AT NIH. SO I HAVE COLLABORATION WITH COLORADO STATE UNIVERSITY, WHO HAS A VET SCHOOL, A LARGE ANIMAL FACILITY, THIS IS ME AND THIS IS DICK BOWEN, MY COLLABORATOR, WHERE WE DID AN INOCULATION OF THREE DROMEDARY CAMELS, AND THIS IS WHAT IT LOOKED LIKE. IT’S A COMMON CALL FOR A DROMEDARY CAMEL. THEY GET AN UPPER RESPIRATORY TRACT INFECTION, NASAL DISCHARGE, THEY DON’T GET ELEVATION TEMPERATURE, THEY GET MOODY BECAUSE WE SWAB THEM ALL THE TIME, THEY DON’T REALLY LIKE THAT. BUT IF YOU LOOK AT THE SHEDDING, WE SEE VERY HIGH TITERS COMING FROM THE NOSE. REALLY KIND OF EXPLAINING WHY THIS IS — THIS IS KIND OF SIMILAR TO WHAT WE SEE WITH AVIAN INFLUENZA VERSUS SEASONAL INFLUENZA. IN THE DROMEDARY CAMEL, IT REPLICATES IN THE NASAL VAF IT,
CAVITY, BUT THE DEEPER YOU GET DOWN, WE DON’T SEE REPLICATION ANYMORE, HOWEVER — IN THE ALVEOLI. SO THIS IS ANOTHER THING LIKE AT NIH, OF COURSE WE’RE VERY WELL-KNOWN WITH THE CONCEPT OF VACCINATION OF HUMANS. SO HOW ABOUT VACCINATION OF DROMEDARY CAMELS TO PREVENT ZOONOTIC TRANSMISSION. WHICH IS KIND OF INTERESTING BECAUSE IT’S NOT A PROBLEM FOR A DROMEDARY CAMEL SEW WE DON’T REALLY KNOW HOW IT’S GOING TO IT PLAY OUT. LET’S START WITH PROOF OF PRINCIPAL FIRST. WE USED ONE OF THEIR VACCINES, WE VACCINATED THEM, WE HAD TWO GROUPS, WE HAD DROMEDARY CAMELS AND WE HAD HAD ALPACAS. AND WE CHALLENGED THEM. IT DIDN’T WORK WELL INTO CAMELS, SO THESE WERE THE VACCINATED CAMELS AND THESE WERE THE UNVACCINATED CONTROL, AND YOU CAN SEE IT DOESN’T REALLY PROTECT THAT WELL. WE DIDN’T REALLY SEE ANY VERY GOOD — RESPONSE EITHER, BUT THESE WERE ALL AIT DULT MALE DROMEDARY CAMEL, SO WE THINK THERE MIGHT BE SOMETHING THAT WE NEED TO WORK ON TO GET THEM BETTER. HOWEVER, YOU LOCK AT THE EL PA KAS, IT WORKED REALLY WELL, BUT THERE’S DEFINITELY OPPORTUNITY TO PROTECT ANIMALS FROM AN UPPER RESPIRATORY FACT, HOWEVER WE NEED TO WORK A LITTLE BIT MORE ON THE CORE LETS OF IMMUNITY OR A NEW PROTECTION FOR THIS PARTICULAR VIRUS. SO I THINK THIS IS WHERE IT COMES TOGETHER FOR — UPPER RESPIRATORY TRACT, RELATIVELY — TRANSMISSION FROM DROMEDARY CAMEL TO HUMANS, BUT INEFFICIENT TRANSMISSION FROM HUMAN TO HUMAN. BUT THAT’S OF COURSE WHERE IT GETS PROBLEMATIC, BECAUSE NOTHING IS BLACK AND WHITE, AS I SAID, WHEN YOU GET INTO THAT SETTING WHERE YOU HAVE PEOPLE WITH THESE CO-MORBIDITIES OR IMMUNE SUPPRESSION, THEN THE TRANSMISSION SEEMS TO BE ACTUALLY VERY EE PISHT. EFFICIENT. SO IT’S NOT A BLACK AND WHITE STORY, THERE’S ALL THESE KIND OF DIFFERENT LAYERS. I PUT THIS SLIDE IN JUST BECAUSE IT’S PRETTY AND ALSO IT MARKS FROM LIKE MERS TO EBOLA. THE THING WITH EBOLA IS — WHEN I STARTED WORKING IN EBOLA, I KIND OF CONSIDERED THAT A NICHE VIRUS. AS IT WAS ALREADY SAID, WE HAVE AROUND 23 OUTBREAKS OVER THE LAST FOUR DECADES. BUT THEY’RE VERY SMALL. THE LARGEST ONE BEFORE THIS WAS AROUND 500 PEOPLE. SO WE DIDN’T REALLY KNOW, WE NEVER EXPECTED THAT IT WOULD, LIKE, EXPLODE AS IT DID IN WEST AFRICA. SO MY LONG TERM PROGRAM WAS ABOUT PROVIDING FUNDAMENTAL KNOWLEDGE ON THE DRIVER OF EBOLA OUTBREAK. THEN OF COURSE WHEN SOMETHING LIKE THIS HAPPENED, IT’S ACTUALLY ASTONISHING FOR A VIRUS WHICH WAS DISCOVERED IN 1976, HOW LITTLE WE KNOW OF VERY, VERY BASIC INFORMATION M SO WE RECEIVE THIS BEFORE THERE’S A LITTLE BIT DIFFERENT RENDITION FROM THE ONE DR. FAUCI SHOWED, BUT BASICALLY EACH AND EVERY ARROW, YOU CAN PUT A QUESTION MARK. WE JUST DON’T REALLY KNOW. WE JUST DON’T KNOW HOW IT CIRCULATES, WE DON’T REALLY KNOW HOW TO TRANSMIT IT, EITHER TO NON-HUMAN PRIMATES, OR THERE’S BEEN — THE REPUBLIC OF CO
CONGO, YOU SEE — THIS KIND OF NICELY SHOWS THAT THERE IS AN OPPORTUNITY FOR RELATIVELY EASY TRANSMISSION, AND SOME OF THESE OUTBREAKS HAVE BEEN REALLY TIED BACK TO EATING BUSH MEAT AND THE FINDING OF DEAD GORILLAS SUCCUMB TO EBOLA VIRUS. SO THIS IS REPUBLIC OF CONGO WHERE WE CATCH REALLY BIG BATS, WE TAKE SAMPLES AND WE FOLLOW THIS POPULATION, WE HAVEN’T FOUND A VIRUS BUT WE FIND SERO PREVALENCE OF EBOLA VIRUS IN THESE BATS TO THIS, WHERE WE ACTUALLY PROVIDE DIAGNOSTIC SUPPORT, WHICH IS OF COURSE SOMETHING YOU NEVER HOPE TO DO. AND THIS IS IN MONROVIA, AND THIS IS THE SETTING WE HAD. THIS IS BOB FISHER WHO’S IN MY LAB. I THINK THE INTERESTING THING IS THAT EVERYBODY KIND OF HAS AN OPINION AND IF YOU DON’T DO YOUR SCIENCE TOO WELL, THESE OPINIONS CAN CAN BE VERY PROBLEMATIC. SO THIS IS THE FIRST GENOME PAPER OF — DERIVED SEQUENCES OF EBOLA, PUBLISHED IN “SCIENCE,” AND THEY OBSERVE AN AMINO ACID AND SUBSTITUTION RATE ROUGHLY TWICE AS HIGH IN 2014. SO EVERYBODY IS TRAINED TO THINK FLU, EVERYBODY IS TRAINED TO THINK, OH, IF YOU HAVE MUTATIONS, IT ADAPTS TO HUMANS, IT BECOMES MORE TRANSMISCIBLE, IT BECOMES MORE PATHOGENIC, IT’S ALREADY KIND OF INTERESTING FOR SOMETHING — BETWEEN 50 AND 90% HAVE BECOME MORE PATHOGENIC, MORE PEOPLE WITH OPINIONS, BUT MICHAEL OTEROME REALLY PUTTING SOME OIL ON THE DISCUSSION OF POTENTIAL AIRBORNE TRANSMISSION OF THIS VIRUS. SO WHY IS IT PROBLEMATIC? FIRST BECAUSE THERE’S NO SOME ID EVIDENCE FOR THE CASE BUT IT WOULD PUT A REALLY, REALLY BIG DENT IN THE EFFORTS OF PEOPLE TRYING TO STOP THE OUTBREAK IF THAT WOULD BE PICKED UP, NOBODY WOULD HAVE BEEN ALLOWED TO COME BACK THROUGH THE U.S., PUT IN QUARANTINE, THEY ACTUALLY PUT ALL THE MILITARY PEOPLE IN QUARANTINE, FORTUNATELY WE WERE NOT PUT IN QUARANTINE. BUT THEN WHICH I THINK IT’S ANOTHER SUCCESS STORY OF THE NIH, NIAID N THIS OUTBREAK, IS THAT WE ACTUALLY HAVE VERY GOOD COLLABORATION. MO WEE BORDERS NICELY TO GUINEA, AND THEY HAD INTRODUCTION OF CASES INT INTO — THEY PICKED UP THESE IMPORTED CASES FROM GUINEA REALLY FAST AND THEY WERE ABLE TO CLEANSE THAT INTRODUCTION SO IT COULDN’T BECOME AN OUTBREAK. SO WHEN WE GOT THOSE ISOLETTES IN OR WE GOT THOSE VIRAL SAMPLES FROM THESE PEOPLE IN WE SEQUENCED THEM, WE ACTUALLY SHOWED UPON ANALYSIS THAT THIS KIND OF — THAT IT ACTUALLY, IF YOU GO BACK AND DO YOUR ANALYSIS, IT ACTUALLY HAS — NUCLEOTIDE SUBSTITUTION RATE AS WAS RECORDED WITH ANY PREVIOUS OUTBREAK AND THIS WAS THE ONE FROM THE GUYER OUTBREAK, THERE’S NO SUBSTITUTION RATE AND THEY’RE WORRIED ABOUT THE DOOMSDAY SITUATION BY BECOMING MORE TRANSMISCIBLE BY AIR IS NOT REALLY THE CASE HERE. OF COURSE WE DON’T REALLY KNOW, BUT THERE’S NO INDICATION OF ENHANCED SUBSTITUTION RATE, AND THEN OF COURSE YOU NEED TO UNDERSTAND TRANSMISSION, SO THIS VIRUS IS KIND OF — IT’S KIND OF NICE, BECAUSE AGAIN, IT’S NOT BLACK AND WHITE. IT HAS ALL THESE DIFFERENT LAYERS. SO IT’S VERY INFECTIOUS, SO YOU NEED VERY LITTLE VIRUS TO BECOME INFECTED. AND IT’S VERY TRANSMISCIBLE. HOWEVER, BECAUSE YOU HAVE A RELATIVELY LONG INCUBATION TIME, YOU CAN ACTUALLY STOP IT QUITE EASILY TOO. BECAUSE IT NOT ONLY HAS A LONG INTUBATION TIME, BUT THE MOMENT YOU GET YOUR FEBRILE ILLNESS, AND WE ACTUALLY GET DAY IT ON THAT, YOU DON’T SHED THAT MUCH VIRUS UNTIL THE END OF YOUR DISEASE STATE, SO THAT’S WHEN YOU’RE ACTUALLY INFECTIOUS. AND THESE ARE THE KIND OF COMMON KNOWN TRANSMISSION ROUTES. DROPLET TRANSMISSION, AND PREDOMINANTLY BODY FLUID COMPACT. AND I THINK THIS KIND OF SHOWS THAT THIS IS THE — FACILITY WHERE WE PROVIDED IT DIAGNOSIS, THIS IS RUN BY MSF, AND YOU CAN SEE THERE’S ONLY A VERY — BARRIER BETWEEN THE SIDE WHERE THE PATIENTS ARE AND WHERE WE WOULD BE, AND THAI THAT’S
BASICALLY A 3-FOOT AREA, 3-FOOT FENCE. SO IT WOULD BE TRULY AIRBORNE TRANSMISCIBLE, AND OF COURSE NOW WE KNOW THAT ALL THE STANDARD MEASUREMENTS OF STOPPING AN OUT ITBREAK LIKE QUARANTINE, WERE FUELLY VERACTUALLY VERY
EFFICACIOUS IN STOPPING THIS OUTBREAK. SO GETTING BACK TO THAT DATA WHICH WASN’T PRESENT AT THE START, ONE OF THE EXPERIMENTS I ALWAYS WANTED TO DO WAS BASICALLY IF AN ANIMAL DICE OF EBOLA VIRUS, WHICH WE DO IN THE LAB, SO I TOOK NON-HUMAN PRIMATES FROM VACCINE STUDY OF,
AND I PUT THEM IN AN ENVIRONMENTAL CHAMBER AT CONDITIONS WE OBSERVE IN LIBERIA, AND I WOULD JUST SAMPLE THEM OVER TIME. SO WHY IS THAT RELEVANT? ONE, OF COURSE, HA YOU WANT TO KNOW HOW LONG IS THIS VIRUS INFECTIOUS AFTER THAT, AND SECOND IS, WE DO A LOT OF BODY TRACING, SO IF SOMEBODY DIES, THEY PICK UP THE BODY AND THEY TAKE A SAMPLE, AND YOU NEED TO KNOW HOW WELL THIS PROCEDURE IS. BECAUSE IF THAT VIRUS — IF THIS PERSON IS EBOLA-VIRUS-POSITIVE, THEN OF COURSE ALL THE CONTACT TRACING NEEDS TO START. AND WHAT WE ACTUALLY NICELY SHOW IS TWO THINGS, EBOLA VIRUS STAYS VIABLE FOR AROUND SEVEN DAYS IN SOMETHING WHICH IS DECOMPOSING, AND SECONDLY, IF YOU TAKE ORAL SWABS UP TO 10 WEEKS AFTER THAT, YOU CAN STILL DETECT EBOLA VIRUS RNA. WHICH I THOUGHT WAS KIND OF SURPRISING. SO ANOTHER THING WHICH ALSO POINTS OUT ON THE PUBLIC HEALTH INFRASTRUCTURE IN THOSE KIND OF COUNTRIES, SO WE HAVE AN EBOLA OUTBREAK AT HAND, SO THIS IS DATA FROM MONROVIA, WHERE WE BOTH TEST FOR EBOLA AND MALARIA, AND IN YELLOW, WE SEE EBOLA, IN GREEN A COMBINATION BETWEEN EBOLA AND MALARIA POSITIVE, AND IN BLUE, MALARIA POSITIVE. SO ONE THING IS CLEAR, WE GET — A LOT OF PEOPLE WHO JUST HAVE MALARIA, SO YOU CANNOT DISTINGUISH WHERE A PATIENT HAS EBOLA OR MALARIA. NOT THAT SURPRISING FOR ME. BUT THAT MEANS THAT YOU NEED TO HAVE VERY GOOD DIAGNOSTIC SERVICES BECAUSE — AND WE WERE ABLE TO PROVIDE — OVER TIME FOR UNDER THREE HOURS FROM ENTRY OF A SAMPLE IN OUR DIAGNOSTIC FACILITY TO THE RESULTS, BECAUSE OF COURSE THESE PEOPLE RUN THE RISK, THEY ARE IN A PREPHASE WHERE THEY’RE STILL IN CONTACT WITH POTENTIAL PEOPLE WITH EBOLA BUT YOU WANT TO TAKE THEM OUT. AND SECONDLY, YOU SEE THAT THE BURDEN OF MALARIA IS IT CONTINUOUSLY HIGH IN LIBERIA THROUGHOUT THE YEAR. I WOULD EXPECT SOME KIND OF PEAKS THERE BUT IT JUST SEEMS TO BE CONTINUOUSLY HIGH. ANOTHER INTERESTING STORY IS THAT WE SURFACE OF EBOLA IN LIBERIA, WHERE WE HAD A CASE HERE ON MARCH 14, AND MARCH 13 THE WOMAN ENTERS THE EBOLA TREATMENT UNIT AND EVENTUALLY SUCCUMBS, AND THERE WAS NO EVIDENCE OF CONTACT WITH ANYONE FROM EITHER SIERRA LEONE OR GUINEA, NO AT110 DANCE TO FUNERAL, SO IT WAS KIND OF UNCLEAR HOW THIS PERSON BECAME INFECTED. ALTHOUGH WE KIND OF FIGURED OUT THAT THIS PERSON HAD SEX WITH SOMEBODY WHO WAS A SURVIVOR AND WHO WAS ACTUALLY SURVIVED EBOLA IN SEPTEMBER 2013, AND WE MAN AND TO GET A SEMEN SAMPLE OF THIS PERSON WHO TURNED OUT TO BE POSITIVE. SO NOW WE HAVE A NICE KIND OF EPIDEMIOLOGICAL KIND OF SCHEME TOGETHER WHERE THIS SUGGESTS THAT THIS PERSON BECAME INFECTED BY A SEXUAL TRANSMISSION, WHICH HAS BEEN DOCUMENTED BEFORE WITH MARBURG VIRUS WHICH IS KIND OF RELATED, BUT FOR THIS OUTBREAK, WAS NEW. THIS IS GREAT WORK BY COLLEAGUES, IT WAS A LOT OF GOVERNMENT, CDC WAS THERE, AND — U.S. EMIRATES WAS THERE, ABLE TO PUT A DEEP SEQUENCER IN LIBERIA, ENORMOUS EFFORT, IT TOOK THEM THREE MONTHS TO GET IT RUNNING, BUT THEY GOT IT RUNNING AND WE GOT THOSE SAMPLES AND WE COULD NICELY SHOW THAT YES, THIS PERSON HAS A VERY HIGH CHANCE OF BEING INFECTED BY THE SAMPLE OF THAT MALE SURVIVOR BECAUSE IT HAD THE SAME SIGNATURE. SO BASED ON NOT ONLY JUST CLASSIC EPIDEMIOLOGY BUT COLLECTING IT — IT KIND OF NICELY PROVED THIS CASE. THEN WE FOLLOWED IT UP WITH CLASSIC EXPERIMENTS LIKE HOW STABLE WOULD EBOLA BE IN SEMEN. THIS IS DONE IN ROCKY MOUNTAIN LABS, AND IT ACTUALLY STAYS OUT VIABLE IN SEMEN FOR AROUND 20 DAYS. IF YOU SPIKE IT WITH A RELATIVELY HIGH DOSE. IF YOU GO INTO MORE REALISTIC DOSE, WHICH IS AROUND — IT STAYS VIABLE FOR AROUND FOUR DAYS, BUT MORE IMPORTANTLY, WE KIND OF SHOW THAT THE DIAGNOSTIC PROCEDURES WE USE — IT’S KIND OF INTERESTING, RIGHT? BECAUSE IT’S ALL KIND OF AMATEUR WORK, WE’RE ALL KIND OF ACADEMICS, BUT NONE OF THESE ASSAYS WE RUN ARE NORMALLY APPROVED FOR THE THINGS WE’RE RUNNING THEM FOR, IN THIS CASE, SEMEN, SO IT WORKS REALLY WELL BUT BECAUSE IT’S NON-HOMOGENEOUS FLUID, IT’S SOMETIMES THE STANDARD DEVIATION IN WHAT YOU GET IS A LITTLE BIT HIGHER. I THINK THIS WAS MENTIONED BY TONY, HOW DO WE PREPARE FOR THIS KINTHESE KIND OF FUTURE
OUTBREAKS. WHO HAS THESE NICE GRAPHS WITH RANKING, IF YOU’RE IN THIS PART OF THE RANKING, IT’S OBVIOUSLY NOT GOOD AND I THINK THIS TELLS IT EVERYTHING, 10 DOCTORS PER 100,000 PEOPLE, WITH ONE OR LESS THAN INIT, THAT’S OBVIOUSLY A HUGE PROBLEM. NOT ONLY FOR EBOLA, BIGGER KILLER, BY FAR BIGGER KILLER THAN EBOLA. THIS REALLY NEEDS TO BE HELPED. SO PART OF IT — SO I’M NOT TRADING PHYSICIANS BUT I’M TRADING THE NEXT GENERATION OF AR CAN — TRAINING SCIENTISTS, THESE RESEARCH QUESTIONS I BRING TO THEM, AND HOPEFULLY WE HAVE A GOOD NEXT GENERATION OF AFRICAN SCIENTISTS. THIS WAS ACTUALLY DURING THE CHIKUNGUNYA OUTBREAK IN 2011, THEY DIDN’T HAVE ANY — VIRUS DIAGNOSTICS RUNNING, THIS IS THE REPUBLIC OF CONGO, WE SHOW THAT THE OUTBREAK THEY HAD WAS ACTUALLY CAUSED BY CHIKUNGUNYA. HERE WE’RE TRAINING INTO THE PROPER USE OF FLEXIBLE FILM ISOLATORS FOR DEALING WITH EBOLA SAMPLES, AND I THINK THIS IS SOMETHING WE SHOULD BE FOCUSING ON MORE AT THE RESEARCH COMMUNITY TRYING TO REACH OUT TO THOSE KIND OF COUNTRIES TRYING TO TRAIN THE NEXT GENERATION OF SCIENTISTS IN THOSE KIND OF COUNTRIES. THIS IS MY GROUP IN ROCKY MOUNTAIN LAB. YOU CAN SEE I DRESSED DOWN FOR THE OCCASION A BIT. WITH MY STUDENTS. I HAVE A LOT OF COLLABORATORS FROM JORDAN TO REPUBLIC OF CONGO CONGO, COLORADO STATE, WITHOUT WHOM I WASN’T ABLE TO DO THE DROMEDARY CAMEL WORK, AND THEN OF COURSE ALL THE GUYS AND GIRLS WHO ROTATED THROUGH MONROVIA. I’LL BE RE IT DI TO ADDRES READY
TO ADDRES
S SOME QUESTIONS. [APPLAUSE]>>I HAVE A QUESTION. SO WHEN YOU WERE TALKING ABOUT THE TRANSMISSION FROM ACROSS SPECIES, WHEN YOU GUYS VACCINATED THE CAMELS, WAS THE GOAL TO MAKE SURE THAT CAMELS DIDN’T SPREAD AMONGST CAMELS OR WOULD IT BE THOSE CAMELS THAT HAD THAT INIT FEKTION SPREADING TO HUMANS, WOULD IT BE THE GOAL TO MAKE SURE THAT THOSE CAMELS DIDN’T TRANSMIT TO HUMANS?>>ONE OF COURSE WOULD BE EITHER COMPLETE STERILE PROTECTION OF REDUCTION OF SHEDDING SO YOU DON’T GET THE ZOONOTIC TRANSMISSION, SO FROM DROMEDARY CAMEL O TO IT HUMAN, BUT EVENTUALLY IF YOU REALLY WANT TO BE SUCCESSFUL, YOU NEED TO STOP THE CIRCULATION OF THE VIRUS AMONG DROMEDARY CAMELS, WHETHER SPECIFIC FARMS, SPECIFIC COUNTRIES OR AN EVEN WIDER GEOGRAPHICAL RANGE THAT REMAINS TO BE SEEN BUT IT’S BOTH OF THOSE TWO GOALS.>>VINCENT, CAN YOU TELL US, WHAT IS THE DIFFERENCE IN THE MOLECULAR STRUCTURE OF EBOLA RESTIN IN THE MONKEYS HERE AND RESTIN VERSUS EBOLA ZAIRE, WHICH WAS THE HUMAN –>>SO EBOLA HAS FIVE DIFFERENT SPECIES. RESTIN IS THE ONLY ONE WHICH IS NOT PATHOGENICALLY HUMAN, BUT IT IS HIGHLY PATHOGENIC IN NON-HUMAN PRIMATES. SO THERE ARE SUFFICIENT DIFFERENCES TO CLASSIFY THEM AT DIFFERENT SPECIES. BASED ON PATHOGENESIS, WE KNOW WHAT’S VERY IMPORTANT THAT’S THE SAME WITH MERS AND SARS, THAT ONE OF THE WAY THESE VIRUSES ARE SO PATHOGENIC FOR HUMANS IS THAT THEY BLOCK THE HUMAN INNATE RESPONSE VERY STRONGLY. SO IF YOU HAVE THE MOLECULAR CLONES OF EBOLA AND RESTIN AND YOU SWAP OUT — ONE OF THE PROTEINS WHICH REALLY STRONGLY BLOCKS — THEN THE RESTIN BECOMES PATHOGENIC AND THE AIR BECOMES LEATHER PATHOGENIC, LESS
PATHOGENI
C, TO CAUSE OR EITHER NOT CAUSE DISEASE INTO THE NEXT HOST.>>HOW MANY NUCLEOTIDES IS THE SEQUENCE IT ARE WE TALKING ABOUT ONE OR TWO OR –>>I THINK THAT WOULD BE IN THE 30, 40% RANGE. OTHERWISE IT WOULDN’T CLASSIFY AS A DISTINCT SPECIES. SO THEY’RE BOTH — AND THEY’RE ALSO –GENIC DIFFERENCES. SO NORMALLY THE IDEA IS IF YOU WOULD HAVE A GP VACCINE BASIC — IN ZAIRE, IT DOESN’T PROPERLY PROTECT AGAINST SUDAN.>>SO VINCENT, THANK YOU, IT WAS A GREAT TALK. I’D LIKE TO ASK YOU, IN THIS REGION, THERE’S ALSO A LOT OF LASA, AND YOU KNOW, YOU LOOKED AT MALARIA AND CO-INFECTIONS. WILL YOU OR HAVE YOU HAD AN OPPORTUNITY TO LOOK AT LASA AND ALSO WITH THE INCIDENCE OF LASA IN THIS REGION, ARE THE STAFF NOW CAPABLE OF MAYBE LOOKING AT A DIAGNOSTIC FOR LASA?>>THE INCIDENTS IN THAT PARTICULAR REGION — SO ONE OF THE REASONS WHY WE DIDN’T IMPLEMENT IT DURING THE OUTBREAK IS BECAUSE THERE WAS NO WAY YOU COULD ACTUALLY DO SOMETHING ABOUT IT, WHICH IS KIND OF PROBLEMATIC. SO IF I TEST SOMETHING POSITIVE FOR LASA, LIKE MSF OR SOMEBODY ELSE TAKING CARE OF THOSE PATIENTS NEED TO DO SOMETHING ABOUT IT, WE HAVEN’T DONE THAT. BUT WE’RE DEFINITELY GOING TO GO — SO IF YOU GO BACK TO THOSE NON-MALARIA, NON-EBOLA SAMPLES, YOU PROBABLY CAN EXPECT A WHOLE RANGE OF DIFFERENT — INCLUDING — I WOULD EXPECT PREDOMINANTLY ARBO VIRUSES BUT WE’RE GOING TO GO — WE HAVE LIKE HALF OF THOSE SAMPLES AND PROBABLY GOING TO REACH OUT TO CDC FOR THE OTHER HALF TO SEE IF WE CAN COME UP WITH SOME DEEM SEQUENCING IT — OTHER THAN EBOLA DURING THAT OUTBREAK.>>HI. I WAS WONDERING HOW THE GAIN OF FUNCTION AND SELECT AGENT MANDATES HAVE AFFECTED YOUR RESEARCH IN RECENT YEARS.>>SO I STOPPED DOING SOME STUFF. SO I WAS VERY — I’M VERY INTERESTED IN SOME MOLECULAR MECHANISMS IN HOW CERTAIN VIRUSES WOULD ACQUIRE PATHOGENICITY. AND FOR INSTANCE, SWAPPING OUT DIFFERENT GENES WOULD — IT’S NOT IMPOSSIBLE BUT IT’S JUST TOO MUCH HASSLE SO I KIND OF FOR NOW STOPPED DOING IT. AND MERS IS NOT A SELECT AGENT, BUT IT’S ALSO — IT’S NOT REALLY CLEAR WHERE IT’S AT. BUT YES, IT’S A MAJOR POTENTIAL HURDLE.>>WHAT’S THE EFFECT OF GLOBAL WARMING ON THE DISTRIBUTION OF ANY OF THESE VIRUSES? NOT SO MUCH THE ONES YOU’VE BEEN TALKING ABOUT, BUT –>>I THINK REALLY — IF YOU LOOK AT THE BIGGEST IMPACT WOULD BE — DISEASES, WHICH WE ALREADY SAW WITH THE — EE GYP TIE CROSS BRED OF CHIKUNGUNYA, CHIKUNGUNYA IS A NICE CASE EXAMPLE — IS A NICE EXAMPLE. PIG BORN ENCEPHALITIS SEEMS TO BE CROPPING UP, AS TSV WOULD BE AAN IMPORTANT ONE. SO THE AREA, IF YOU LOOK AT CENTRAL AFRICA, DOESN’T SEEM TO BE TOO MUCH AFFECTED BY GLOBAL WARMING, SO I WOULD MORE LOOK AT FRINGES WHERE YOU WOULD HAVE TEMPERATURE RISING, LIKE UP AND DOWN, SO YOU WOULD SEE DIFFERENT DISTRIBUTION OF VECTORS. I THINK THAT’S GOING TO HAVE — LIKE WE ALREADY SEE IT HAS A BIG IMPACT, THINKING ABOUT DENGUE, EVEN YELLOW FEVER, CHIKUNGUNYA, I THINK IT’S GOING TO HAVE A HUGE IMPACT.>>SO IF YOU COMBINE THAT WITH OUR WATER POLICIES IN THIS COUNTRY OF DRAINING — OF NOT DRAINING AND LODZIN LOSING
WATER, SO YOU MIGHT ANTICIPATE WE’RE GOING TO SEE LOTS AND LOTS OF MOSQUITO AND — EVEN –>>LIKE YOU WOULD EXPECT DID — ALREADY EXPECT — MOSQUITOES ARE ALREADY HERE, RIGHT, AS FAR NORTH AS LIKE NEW YORK. I DON’T KNOW IF THERE ARE ANY RECORDED CASES OF CHIKUNGUNYA, BUT I THINK THAT’S SOMETHING YOU CAN EXPECT.>>ARE THERE ANY OTHER QUESTIONS? IF NOT, THANK YOU VERY, VERY MUCH. [APPLAUSE]

2 Comments

  • Reply offmeds2nite February 6, 2016 at 8:05 am

    Anthony Fauci is the best!

  • Reply Venkatesh Talikota October 12, 2017 at 7:05 am

    Tony is the best!

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