THE GLOBALIZATION OFINFLUENZAInfluenza, better known as the "flu," is familiartomost of us. We havegrown upWIthIt,and the familiar flu season comes around everyyearwitha new variation of the flu bug. It does not matter whether you had the flu theyear before, you can still catch the new flu bug since it differs slightly fromthe previous year's version. Andifyou don't catch this year's version of £lu,then you might getityears later. Some peopletrytohedge their bets againstcatching the flu with a vaccination prepared ahead of time each yearandtai-~ d .J"re to combat the predicted seasonal variant. Despiteannuavaccmauonsin the United States, between thirty and forty thousand people die frominfluenza.each year.Ittakes at least six months to prepare vaccine.Bythe rimethe vaccine is ready for the flu season, the targeted virus may have changedenough to thwart the vaccine or another variant may have taken over.,__ ._~_~~~3J7What Is Influenza?Influenza picked up the nickname"flu"during the early twentieth century.Sincethen"flu"has become a catchall termformany unidentifiedand unre-latedh I'd"stmach flu" andSOrt-term illnesses The term has been app Ie to5 0other.' rher viral infectionsgastromtestinal disturbances, as well astomany aoftheu .pperrespiratorytract.Ifl .~~~~11uenza, like cold viruses, attacks the upper respuathroat d h I Th infection stems froman t e major airways leading into the ungs. e338 CHAPTER 20a closely related group of viruses carried through the air from an infected indi-vidual on a sneeze or cough, or transmitted by direct contact with infectednasal or oral secretions.The respiratory illness causedbyinfluenza generally ends within tendays. The virus targets the hair-like cells (ciliated epithelia) lining the upperrespiratory tract. These cells act as the first line of defense against invadersentering the airways. The targeted cells are infected and destroyed, leavingintact the underlying basal cell layer. New transitional epithelial cells gen-erate from the basal layer within five days} and new ciliated cells reappearwithin two weeks following the infection (Kilbourne 1975).Most influenza infections generally do not threaten life, with less thanaIpercent mortality rate among highly susceptible individuals (Kilbourne1975)·Symptoms of illness can vary from mild to severe, with rapid onsetfollowing an incubation period of one to three days. Common symptomsgrowing out of the immune reaction to the virus infection include fever,throbbing frontal headache, aching muscles, backache, general discomfort,exhaustion, loss of appetite, stuffy runny nose, and sore throat with drycough. Frequent sweating, dizziness, aching eyes, or light sensitivity can alsobe present. The fever drops within two to five days, and most of the generalsymptoms fade, leaving the respiratory symptoms to linger for a few moredays. Some adults complain of soreness in the center of the upper chest areafrom viral irritation of the underlying trachea, and some develop hoarseness.Children usually have more vague symptoms than adults. Some childrensuffer nausea, vomiting, and diarrhea along with the respiratory symptoms(Benenson 1995; Stuart-Harris 1965).Complications rarely occur from most types of influenza, but they canpose problems, either directly or indirectly, for highly susceptible individuals,particularly with the introduction of a new strain of the virus. Individualsmost likely to suffer from complications have immune systems unabletoreact adequately to the infection. This includes individuals under high stress,malnourished people, and those with preexisting health problems such asemphysema and heart disease. Pregnant women and heavy smokers have highsusceptibility to complications. Influenza infection can pave the way for othermicrobes to enter areas of the upper respiratory system damaged by the virusand spread into the lungs or occasionally other parts of the body. Sometimesthe influenza virus itself can reach into the lower branches of the bronchialairways and attack the lungs. Bronchitis and pneumonia are the mostTHE GLOBALIZATION OF INFLUENZA339common complications associated with influenza. Existing heart problemscan be amplified by the illness, and evidence has been found that the virusmay trigger encephalitis (Benenson 1995; Kilbourne 197511987;McCullersetal. '999; Sugaya et al.2002).Pneumonia directly caused by influenza virus can be deadly.Symp-toms of severe viral pneumonia usually develop quickly, within twentyhours of the onset of the flu. The fever goes up, bloody sputum is coughedup with difficult breathing, the individual suffers anxiety, and begins to turnblue. Death usually follows within five to ten days (Kilbourne 19751.The Agents of InfectionThree types of related influenza viruses exist, referredtoas types A, B,andC. They operate independently of one another, and infection with one typedoes not confer resistance to the other types. All three viruses have the samebasic RNA genome enclosed and protected by a lipid coat derived from theouter membrane of host cells. They acquire this coat when the newlyformed virus buds from the infected cell. Hundreds ofspike-like projectionsof two types of proteins protrude from the lipid membrane. One of thesehelps the viruses attach to and enter host cells, while the other one letsfledgling viruses out of host cells.Most of the spikes consist of a protein known as hemagglutinin(HI·The tip of each hemagglutinin spike holds the key binding activity that fitsinto the landing lock, the dimpled receptor site, on the surface of theIdh. . in stuk ist of neuraminidasese ecte ost cell. The remainmg protem spt es consiINI .fdvi bleak out of infectedactmg as an enzyme to help newly orme viruseshII . keanti enie-antibodyreac-est ce s (RUigrok 1998). Both prot ems provo e an ig. I . .holds by farthetlOns from the host immune system, but hernagg utmmmajor attraction while neuraminidase plays a lesser role., h lis without thehemag-Influenza viruses cannot gain accesstoost ceI. . .. iklocate and bindtotheg uttnin spikes Even when the hemagglutinin SpI esdI .et through the "door"Imped receptor sites on the target cell, they cannot g dfh . . The depressionformeate Outer membrane until they splitintotwo parts. .b h . ..f]id that facilitates this act,yt e receptor site contains a specific aCIdICuibII . t te the cell mern ranea OWlllgthe two parts of the hemagglutinintopene ra .bind. the process. Witan enter the cell while shedding the protective coatillal'