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Unformatted text preview: Emerging Viruses
Hemorrhagic fever viruses are among the most dangerous biological agents known. New ones are discovered every year, and artiﬁcial as well as natural environmental changes are favoring their spread
by Bernard Le Guenno n May 1993 a young couple in New Mexico died just a few days apart from acute respiratory distress. Both had suddenly developed a high fever, muscular cramps, headaches and a violent cough. Researchers promptly started looking into whether similar cases had been recorded elsewhere. Soon 24 were identiÞed, occurring between December 1, 1992, and June 7, 1993, in New Mexico, Colorado and Nevada. Eleven of these patients had died. Bacteriological, parasitological and virological tests conducted in the aÝected states were all negative. Samples were then sent to the Centers for Disease Control and Prevention ( CDC ) in Atlanta. Tests for all known viruses were I conducted, and researchers eventually detected in the serum of several patients antibodies against a class known as hantaviruses. Studies using the techniques of molecular biology showed that the patients had been infected with a previously unknown type of hantavirus, now called Sin Nombre ( Spanish for Òno nameÓ). New and more eÝective analytical techniques are identifying a growing number of infective agents. Most are viruses that 10 years ago would probably have passed unnoticed or been mistaken for other, known types. The Sin Nombre infections were not a unique occurrence. Last year a researcher at the Yale University School of Medicine was accidentally infected with Sabiˆ, a virus Þrst isolated in 1990 from an agricultural engineer who died from a sudden illness in the state of S‹o Paulo, Brazil. Sabiˆ and Sin Nombre both cause illnesses classiÞed as hemorrhagic fevers. Patients initially develop a fever, followed by a general deterioration in health during which bleeding often occurs. SuperÞcial bleeding reveals itself through skin signs, such as petechiae (tiny releases of blood from vessels under the skin surface), bruises or purpura (characteristic purplish discolorations). Other cardiovascular, digestive, renal and neurological complications can follow. In the most serious cases, the patient dies of massive hemorrhag- Copyright 1995 Scientific American, Inc. PATRICK ROBERT SYGMA Improvements in Diagnosis T he seeming emergence of new viruses is also helped along by rapid advances in the techniques for virological identiÞcation. The Þrst person diagnosed with Sabiˆ in S‹o Paulo (called the index case) was originally thought to be suÝering from yellow fever. The agent actually responsible was identi- SCIENCE SOURCE/PHOTO RESEARCHERS, INC. es or sometimes multiple organ failure. Hemorrhagic fever viruses are divided into several families. The ßaviviruses have been known for the longest. They include the Amaril virus that causes yellow fever and is transmitted by mosquitoes, as well as other viruses responsible for mosquito- and tick-borne diseases, such as dengue. Viruses that have come to light more recently belong to three other families: arenaviruses, bunyaviruses (a group that includes the hantaviruses) and Þloviruses. They have names like Puumala, Guanarito and Ebola, taken from places where they Þrst caused recognized outbreaks of disease. All the arenaviruses and the bunyaviruses responsible for hemorrhagic fevers circulate naturally in various populations of animals. It is actually uncommon for them to spread directly from person to person. Epidemics are, rather, linked to the presence of animals that serve as reservoirs for the virus and sometimes as vectors that help to transfer it to people. Various species of rodent are excellent homes for these viruses, because the rodents show no signs when infected. Nevertheless, they shed viral particles throughout their lives in feces and, particularly, in urine. The Þloviruses, for their part, are still a mystery : we do not know how they are transmitted. Hemorrhagic fever viruses are among the most threatening examples of what are commonly termed emerging pathogens. They are not really new. Mutations or genetic recombinations between existing viruses can increase virulence, but what appear to be novel viruses are generally viruses that have existed for millions of years and merely come to light when environmental conditions change. The changes allow the virus to multiply and spread in host organisms. New illnesses may then sometimes become apparent. ZAIREAN RED CROSS members bury victims of the Ebola virus in Kikwit earlier this year. At least 190 died in the epidemic. Poor medical hygiene and unsafe funeral practices helped to propagate the infection. Þed only because a sample was sent to a laboratory equipped for the isolation of viruses. That rarely happens, because most hemorrhagic fever viruses circulate in tropical regions, where hospitals generally have inadequate diagnostic equipment and where many sick people are not hospitalized. Even so, the rapid identiÞcation of Sin Nombre was possible only because of several years of work previously accumulated on hantaviruses. Hantaviruses typically cause an illness known as hemorrhagic fever with renal syndrome; it was described in a Chinese medical text 1,000 years ago. The West Þrst became interested in this illness during the Korean War, when more than 2,000 United Nations troops suffered from it between 1951 and 1953. Despite the eÝorts of virologists, it was not until 1976 that the agent was identiÞed in the lungs of its principal reservoir in Korea, a Þeld mouse. It took more than four years to isolate the virus, to adapt it to a cell culture and to prepare a reagent that permitted a diagnostic serological test, essential steps in the study of a virus. It was named Hantaan, for a river in Korea. The virus also circulates in Japan and Russia, and a similar virus that produces an illness just as serious is found in the Balkans. A nonfatal form exists in Europe. It was described in Sweden in 1934 as the Ònephritic epidemic,Ó but its agent was not identiÞed until 1980, when it was detected in the lungs of the bank vole. Isolated in 1983 in Finland, the virus was named Puumala for a lake in that country. Outbreaks occur regularly in northwestern Europe. Since 1977, 505 cases have been recorded in northeastern France alone. The number of cases seems to be increasing, but this is probably because doctors are using more biological tests than formerly, and because the tests in recent years have become more sensitive. Thus, it is only for about a decade that we have had the reagents necessary to identify hantaviruses. Thanks to these reagents and a research technique that spots antibodies marking recent infections, scientists at the CDC in 1993 were quickly on the track of the disease. The presence of speciÞc antibodies is not always deÞnite proof of an infection by the corresponding pathogen, however. False positive reactions and cross-reactions caused by the presence of antibodies shared by diÝerent viruses are possible. A more recent technology, based on the polymerase chain reaction, permits fragments of genes to be ampliÞed (or duplicated ) and sequenced. It provided conÞrmation that a
A. B. DOWSETT SPL/Photo Researchers, Inc. b
SCOTT CAMAZINE Photo Researchers, Inc. c
A. B. DOWSETT SPL/Photo Researchers, Inc. d HEMORRHAGIC FEVER VIRUSES vary greatly in appearance under the electron microscope. Lassa ( a ), found in Africa, is an arenavirus, a kind that is typically spherical. Hantaviruses ( b ) cause diseases of different varieties in many regions of the world. Tick-borne encephalitis virus ( c ) is an example of a flavivirus, a group that includes yellow fever and dengue. Ebola ( d ) is one of the filoviruses, so called because of their filamentous appearance. The images have been color-enhanced. Copyright 1995 Scientific American, Inc. SCIENTIFIC AMERICAN October 1995 57 the patients were indeed infected with hantaviruses. The identiÞcation of Sin Nombre took no more than eight days. The Infective Agents he primary cause of most outbreaks of hemorrhagic fever viruses is ecological disruption resulting from human activities. The expansion of the world population perturbs ecosystems that were stable a few decades ago and facilitates contacts with animals carrying viruses pathogenic to humans. This was true of the arenavirus Guanarito, discovered in 1989 in an epidemic in Venezuela. The Þrst 15 cases were found in a rural community that had started to clear a forested region in the center of the country. The animal reservoir is a species of cotton rat; workers had stirred up dust that had been contaminated with dried rat urine or excrementÑone of the most frequent modes of transmission. Subsequently, more than 100 additional cases were diagnosed in the same area. Other arenaviruses responsible for hemorrhagic fevers have been known for a long timeÑfor example, Machupo, which appeared in Bolivia in 1952, and Jun’n, identiÞed in Argentina in 1958. Both those viruses can reside in species of rodents called vesper mice; the Bolivian species enters human dwellings. Until recently, an extermination campaign against the animals had prevented any human infections with Machupo since 1974. After a lull of 20 years, however, this virus has reappeared, in the same place: seven people, all from one family, were infected during the summer of 1994. Jun’n causes Argentinian hemorrhagic fever, which appeared at the end of the 1940s in the pampas west of Buenos Aires. The cultivation of large areas of maize supported huge populations of the species of vesper mice that carry this virus and multiplied contacts between these rodents and agricultural workers. Today mechanization has put the operators of agricultural machinery on the front line: combine harvesters not only suspend clouds of infective dust, they also create an aerosol of infective blood when they accidentally crush the animals. The arenavirus Sabiˆ has, so far as is known, claimed only one life, but other cases have in all probability occurred in Brazil without being diagnosed. There is a real risk of an epidemic if agricultural practices bring the inhabitants of S‹o Paulo into contact with rodent vectors. In Europe, the main reservoirs of the hantavirus PuumalaÑthe bank vole and yellow-necked Þeld mouseÑare 58 Global Reach of Hemorrhagic Fever Viruses T Hantavirus Sin Nombre strikes 114 and kills 58 in New Mexico, Colorado and Nevada in 1993, after a rodent population grows rapidly. In 1994 a researcher at Yale University is accidentally infected with Sabià but survives. Federal officials are put into a panic in 1989 when monkeys housed in a quarantine facility in Reston, Va., start dying from an Ebola-type filovirus. Rift Valley fever outbreak in 1987 follows damming of the Senegal River in Mauritania. More than 100 cases of illness are caused by Guanarito in 1989. The epidemic started in a rural community that had begun to clear a forest. Machupo causes dozens of deaths in San Joaquín, Bolivia, during the 1950s; seven are infected in 1994. Junín kills many agricultural workers in the Argentinian pampas in the1940s.
JOHNNY JOHNSON In 1990 an agricultural engineer dies and a laboratory worker falls ill with the arenavirus Sabià in the state of São Paulo, Brazil. woodland animals. The most frequent route of contamination there is inhalation of contaminated dust while handling wood gathered in the forest or while working in sheds and barns. Humans are not always the cause of dangerous environmental changes. The emergence of Sin Nombre in the U.S. resulted from heavier than usual rain and snow during spring 1993 in the mountains and deserts of New Mexico, Nevada and Colorado. The principal animal host of Sin Nombre is the deer mouse, which lives on pine kernels: the excep- tional humidity favored a particularly abundant crop, and so the mice proliferated. The density of the animals multiplied 10-fold between 1992 and 1993. Transmission by Mosquitoes S ome bunyaviruses are carried by mosquitoes rather than by rodents. Consequently, ecological perturbations such as the building of dams and the expansion of irrigation can encourage these agents. Dams raise the water table, which favors the multiplication of SCIENTIFIC AMERICAN October 1995 Copyright 1995 Scientific American, Inc. Hantavirus Puumala causes frequent illness in northwest Europe; the infection is believed to result from inhalation of contaminated dust when handling wood. Seven laboratory workers preparing cell cultures from the blood of vervet monkeys die from Marburg virus in 1967. Hantaviruses have caused illness with renal syndrome for more than 1,000 years. Between 1951 and 1953, 2,000 United Nations troops are infected with Hantaan. Dengue fever, caused by a flavivirus, is spreading from its home territory in Southeast Asia. Rift Valley fever infects 200,000 following construction of the Aswan Dam in 1970 and causes 600 deaths. A further outbreak occurs during the 1990s. A researcher handling samples from wild chimpanzees being decimated by an epidemic in Ivory Coast is infected with a type of Ebola. In 1976 and again in 1979, Ebola spreads wildly through N’zara and Maridi in Sudan’s southern grasslands. In 1970, 25 hospital workers and patients suffer from Lassa fever, caused by an arenavirus, in Lassa, Nigeria. Ebola, a filovirus, kills about 300 around a hospital in Yambuku, Zaire, in 1976. More than 190 die from an Ebola outbreak in Kikwit, Zaire, in the spring of 1995. ARENAVIRUS FILOVIRUS ANIMAL FILOVIRUS OUTBREAK FLAVIVIRUS HANTAVIRUS RIFT VALLEY FEVER (BUNYAVIRUS) the insects and also brings humans and animals together in new population centers. These two factors probably explain two epidemics of Rift Valley fever in Africa : one in 1977 in Egypt and the other in 1987 in Mauritania. The virus responsible was recognized as long ago as 1931 as the cause of several epizootics, or animal epidemics, among sheep in western and South Africa. Some breeders in contact with sick or dead animals became infected, but at the time the infection was not serious in humans. The situation became more grim in 1970. After the construction of the Aswan Dam, there were major losses of cattle; of the 200,000 people infected, 600 died. In 1987 a minor epidemic followed the damming of the Senegal River in Mauritania. Rift Valley fever virus is found in several species of mosquitoes, notably those of the genus Aedes. The females transmit the virus to their eggs. Under dry conditions the mosquitoesÕ numbers are limited, but abundant rain or irrigation allows them to multiply rapidly. In the course of feeding on blood, they then transmit the virus to humans, with cattle acting as incubators. Contamination by Accident A lthough important, ecological disturbances are not the only causes of the emergence of novel viruses. Poor medical hygiene can foster epidemics. In January 1969 in Lassa, Nigeria, a nun who worked as a nurse fell ill at work. She infected, before dying, two other nuns, one of whom died. A year later an epidemic broke out in the same hos59 Copyright 1995 Scientific American, Inc. SCIENTIFIC AMERICAN October 1995 pital. An inquiry found that 17 of the 25 persons infected had probably been in the room where the Þrst victim had been hospitalized. Lassa is classed as an arenavirus. Biological industries also present risks. Many vaccines are prepared from animal cells. If the cells are contaminated, there is a danger that an unidentiÞed virus may be transmitted to those vaccinated. It was in this way that in 1967 a culture of contaminated blood cells allowed the discovery of a new hemorrhagic fever and a new family of viruses, the Þloviruses. The place was Marburg, Germany, where 25 people fell ill after preparing cell cultures from the blood of vervet monkeys. Seven died. Other cases were reported simultaneously in Frankfurt and in Yugoslavia, all in laboratories that had received monkeys from Uganda. The monkeys themselves also died, suggesting that they are not the natural reservoir of Marburg virus. Four cases died. Eighty-Þve of them had received an injection in this hospital. The epidemic led to the identiÞcation of a new virus, Ebola. The Marburg and Ebola viruses are classiÞed as Þloviruses, so called because under the electron microscope they can be seen as Þlamentous structures as much as 1,500 nanometers in length (the spherical particle of an arenavirus, for comparison, is about 300 nanometers in diameter ). These two representatives of the Þlovirus family are exceedingly dangerous. In 1989 specialists at the CDC were put in a panic when they learned that crab-eating macaques from the Philippines housed in an animal quarantine facility in Reston, Va., were dying from an infection caused AGRICULTURAL WORKERS in some parts of the world are at risk of infection by arenaviruses, which are often carried by rodents. Machinery stirs up dried rodent urine containing the viruses and can create an aerosol of infective blood if the animals are accidentally crushed. of natural infection with Marburg have been reported in Africa, but neither the reservoir nor the natural modes of transmission have been discovered. What is clear is that Marburg can propagate in hospitals: secondary cases have occurred among medical personnel. In 1976 two epidemics of fever caused by a diÝerent virus occurred two months apart in the south of Sudan and in northern Zaire. In Zaire, around Yambuku Hospital, by the Ebola River, 318 cases were counted, and 280 persons 60 by an Ebola-type Þlovirus. The virus was also isolated from other animal facilities that had received monkeys from the Philippines. No human illnesses were recorded in the wake of this epizootic, however, which demonstrates that even closely related viruses can vary widely in their eÝects. In January of this year we isolated a previously unknown type of Ebola from a patient who had infected herself handling samples from wild chimpanzees that were being decimated by a strange epidemic. That the chimpanzees, from Ivory Coast, succumbed is further evidence that primates are not ÞlovirusesÕ natural reservoir, which has not yet been identiÞed. Although Marburg has infect- ed few people, Ebola surfaced again to cause a human epidemic in Zaire this past May [ see box on pages 62 and 64 ]. A Shifting, Hazy Target T he extreme variability and speed of evolution found among hemorrhagic fever viruses are rooted in the nature of their genetic material. Hemorrhagic fever viruses, like many other types, generally have genes consisting of ribonucleic acid, or RNA, rather than the DNA employed by most living things. The RNA of these viruses is Ònegative strandedÓÑbefore it can be used to make viral proteins in an infected cell, it must be converted into a positive SCIENTIFIC AMERICAN October 1995 Copyright 1995 Scientific American, Inc. RIFT VALLEY FEVER VIRUS, a bunyavirus, is transmitted by mosquitoes from cattle and sheep to humans. Dams allow multiplication of the insects by raising the water table and bring people and animals together in new locations, causing epidemics. strand by an enzyme called RNA polymerase. RNA polymerases cause fairly frequent errors during this process. Because the errors are not corrected, an infected cell gives rise to a heterogeneous population of viruses resulting from the accumulating mutations. The existence of such ÒquasispeciesÓ explains the rapid adaptation of these viruses to environmental changes. Some adapt to invertebrates and others to vertebrates, and they confound the immune systems of their hosts. Pathogenic variants can easily arise. There is another source of heterogeneity, too. A characteristic common to arenaviruses and bunyaviruses is that they have segmented genomes. ( The bunyaviruses have three segments of RNA, arenaviruses two.) When a cell is infected by two viruses of the same general class, they can then recombine so that segments from one become linked to segments from the other, giving rise to new viral types called reassortants. Although we have a basic appreciation of the composition of these entities, we have only a poor understanding of how they cause disease. Far beyond the limited means of investigation in local tropical hospitals, many of these viruses are so hazardous they cannot be handled except in laboratories that conform to very strict safety requirements. There are only a few such facilities in the world, and not all of them have the required equipment. Although it is relatively straightforward to handle the agents safely in culture ßasks, it is far more dangerous to handle infected monkeys: researchers risk infection from being scratched or bitten by sick animals. Yet the viruses cannot be studied in more common laboratory animals such as rats, because these creatures do not become ill when infected. We do know that hemorrhagic fever viruses have characteristic eÝects on the body. They cause a diminution in the number of platelets, the principal cells of the blood-clotting system. But this diminution, called thrombocytopenia, is not suÛcient to explain the hemorrhagic symptoms. Some hemorrhagic fever viruses destroy infected cells directly; others perturb the immune system and aÝect cellsÕ functioning. Among the Þrst group, the cytolytic viruses, are the bunyaviruses that cause a disease called Crimean-Congo fever and Rift Valley fever; the Þloviruses Marburg and Ebola; and the prototype of hemorrhagic fever viruses, the ßavivirus Amaril. Their period of incubation is generally short, often less than a week. Serious cases are the result of an attack on several organs, notably the liver. When a large proportion of liver cells are destroyed, the body cannot produce enough coagulation factors, which partly explains the hemorrhagic symptoms. The viruses also modify the inner surfaces of blood vessels in such a way that platelets stick to them. This clotting inside vessels consumes additional coagulation factors. Moreover, the cells lining the vessels are forced apart, which can lead to the escape of plasma or to uncontrolled bleeding, causing edema, an accumulation of ßuid in the tissue, or severely lowered blood pressure. The arenaviruses fall into the noncytolytic group. Their period of incubation is longer, and although they invade most of the tissues in the body, they do not usually cause gross lesions. Rather the viruses inhibit the immune system, which delays the production of antibodies until perhaps a month after the Þrst clinical signs of infection. Arenaviruses 61 Copyright 1995 Scientific American, Inc. SCIENTIFIC AMERICAN October 1995 BARRY ROSS EbolaÕs Unanswered Questions
by Laurie Garrett ast spring in Kikwit, Zaire, Ebola proved once again that despite the agonizing and usually fatal illness it provokes, the microbe cannot in its present incarnation spread far—unless humans help it to do so. The virus is too swiftly lethal to propagate by itself. In the early waves of an epidemic, it kills more than 92 percent of those it infects, usually within a couple of weeks. Such rapidity affords the microbe little opportunity to spread unaided, given the severity of the illness that it causes. In each of the four known Ebola epidemics during the past 19 years, people have helped launch the virus from its obscure rain forest or savanna host into human populations. In 1976 in Yambuku, an area of villages in Zaire’s northern rain forest, the virus’s appearance was multiplied dozens of times over by Belgian nuns at a missionary clinic who repeatedly used unsterilized syringes in some 300 patients every day. One day someone arrived suffering from the then unknown Ebola fever and was treated with injections for malaria. The syringes efficiently amplified the viral threat. In both 1976 and 1979, humans helped the virus spread wildly in N’zara and Maridi, in the Sudan’s remote southern grasslands. Improper hospital hygiene again played a key role, and local burial practices, which required the manual removal of viscera from cadavers, compounded the disaster. Medical and funeral settings were likewise crucial in Kikwit earlier this year. Infections spread via bodily fluids among those who tended the dying and washed and dressed the cadavers. The major amplification event that seems to have started the epidemic, early in the new year, was an open casket funeral. The deceased, Gaspard Menga, probably acquired his infection gathering firewood in a nearby rain forest. The virus spread rapidly to 13 members of the Menga L family who had cared for the ailing man or touched his body in farewell, a common practice in the region, or cared for those who got Ebola from Menga. A second amplification event occurred in March inside Kikwit General Hospital. Overrun by cases of incurable bloody diarrhea, hospital officials thought they were facing a new strain of bacteria. The doctors ordered a laboratory technician to draw blood samples from patients and analyze them for drug resistance. When he took ill, the hospital staff thought that his enormously distended stomach and high fever were the results of typhus infection and performed surgery to stave off damage. The first procedure was an appendectomy. The second was a horror. When the physicians and nurses opened the technician’s abdomen again for what they expected to be repair work, they were immediately drenched in blood. Their colleague died on the operating table from uncontrolled bleeding. The contaminated surgical team became the second wave of the epidemic. he virus’s reliance on unintended help from humans forces attention to the common thread that runs through the known Ebola epidemics: poverty. All the outbreaks have been associated with abysmal medical facilities in which poorly paid (or, in the case of Kikwit, unpaid) medical personnel had to make do with a handful of syringes, minimal surgical equipment and intermittent or nonexistent running water and electricity. It seems quite possible that Ebola (and other hemorrhagic fever viruses) might successfully exploit similar conditions occurring anywhere in the world. As air transportation be( continued on page 64 ) T suppress the number of platelets only slightly, but they do inactivate them. Neurological complications are common. Hantaviruses are like arenaviruses in that they do not destroy cells directly and also have a long period of incubation, from 12 to 21 days. They target cells lining capillary walls. Hantaan and Puumala viruses invade the cells of the capillary walls in the kidney, which results in edema and an inßammatory reaction caused by the organÕs failure to work properly. Sin Nombre, in contrast, invades pulmonary capillaries and caus- es death by a diÝerent means: it leads to acute edema of the lung. Prospects for Control S everal research groups are trying to establish international surveillance networks that will track all emerging infectious agents. The World Health Organization has established a network for tracking hemorrhagic fever viruses and other insect-borne viruses that is particularly vigilant. Once a virus is detected, technology holds some promise for combating it. An antiviral medication, ribavirin, proved eÝective during an epidemic of hantavirus in China. A huge eÝort is under way in Argentina to develop a vaccine to protect people against Jun’n. KAREN KASMANSKI Matrix PORTABLE ISOLATOR UNITS equipped with air filters have been maintained by the U.S. Army since 1980 for evacuating personnel carrying suspected dangerous pathogens. The equipment would be used to bring patients needing specialized care to an isolation facility at Fort Detrick, Md., but has never been called on for this mission. 62 SCIENTIFIC AMERICAN October 1995 Copyright 1995 Scientific American, Inc. ( continued from page 62) comes more readily available and affordable, viruses can be more easily moved around the planet. The rapid deterioration in public health and medical facilities in the former Soviet Union and other regions should therefore be cause for concern. The exact nature of the risk, of course, depends on the Ebola virus’s biology, much of which remains mysterious. Throughout the summer, researchers from the University of Kinshasa, the U.S. Centers for Disease Control and Prevention, the Pasteur Institute in Paris, the National Institute of Virology in Johannesburg and the World Health Organization combed Kikwit for answers to questions that have puzzled scientists since the first Yambuku epidemic: What are the precise constraints on Ebola’s transmission? And where does it hide between epidemics? The two Sudanese epidemics started among cotton factory workers. At the time scientists scoured the N’zara complex for infected insects or bats, but although the animals were plentiful, none carried the virus. In Yambuku, suspicions fell on a range of rain-forest animals, including monkeys. Again, however, no trapped animals tested positive for infection. Surveys conducted during the late 1970s in conjunction with a WHO effort to control monkeypox found no infected primates or large animals in central Africa. The rain forest frequented by Gaspard Menga contained abundant rats, bats, mice and snakes. Trapping efforts in the region may eventually reveal Ebola’s hideout. For the present, though, the virus’s reservoir remains unknown. Also unknown is whether shared drinking water, foods and washing facilities can transmit infection. ecause all outbreaks to date have involved transmission by fluids, control has consisted of fairly straightforward, low-cost efforts. Patients were isolated, and the citizenry instructed to turn over their unwashed dead to authorities. MASKED AND GLOVED health worker disinfects a bed used by a patient stricken by the Ebola virus in Kikwit, Zaire. Once residents appreciated the links between tending the sick, washing a cadaver and dying of Ebola, epidemics quickly ground to a halt. One way that Ebola could escape such controls would be through a major mutational event that made it more easily transmissible. Were Ebola, or any hemorrhagic fever virus, to acquire genetic characteristics suitable for airborne transmission, an outbreak of disease anywhere would pose a threat to all humanity. As far as is known, nobody has ever acquired the microbe from inhaled droplets coughed into the air (although it can certainly be passed in saliva during a kiss). There are usually many genetic differences between fluid-borne microbes and airborne ones, so it seems unlikely that the jump could be made easily. But the question has never been specifically studied in the case of Ebola, because research on microbes that are found primarily in developing countries has for many years been poorly funded. LAURIE GARRETT is a reporter for Newsday and the author of The Coming Plague: Newly Emerging Diseases in a World Out of Balance ( Penguin USA, 1995 ). B Indeed, vaccines against the Rift Valley fever in animals, and against yellow fever in humans, are already approved for use. Yet despite the existence of yellow fever vaccine, that disease is now raging in Africa, where few are vaccinated. Other approaches are constrained because it is diÛcult or impossible to control animals that are natural reservoirs and vectors for the viruses or to predict ecological modiÞcations that favor outbreaks of disease. There was an eÝective campaign against rodent vectors during the Lassa and Machupo arenavirus outbreaks, but it is not usually possible to sustain such programs in rural regions for long periods. Precautions can be taken in laboratories and hospitals, which have ironically served as ampliÞers in several epidemics. In the laboratory, viruses responsible for hemorrhagic fevers must be handled in maximum conÞnement conditions (known in the jargon as biosafety level 4). The laboratory must be kept at lowered pressure, so that no potentially infectious particle can escape; the viruses themselves should be conÞned in sealed systems at still lower pressure. In hospitals, the risk of infection from a patient is high for some viruses, so strict safety measures must be followed: hospital personnel must wear masks, gloves and protective clothing; wastes must be decontaminated. A room with lowered pressure is an additional precaution. Since penicillin has been in widespread use, many people had started to believe that epidemics were no longer a threat. The global pandemic of HIV, the virus that causes AIDS, has shown that view to be complacent. Hemorrhagic fever viruses are indeed a cause for worry, and the avenues to reduce their toll are still limited. The Author
BERNARD LE GUENNO leads the national reference center for hemorrhagic fever viruses at the Pasteur Institute in Paris. He graduated with a degree in pharmacology from Bordeaux University in 1972 and has been a virologist at Pasteur since 1983. This article was adapted from one by Le Guenno in the June issue of Pour la Science, the French edition of ScientiÞc American. Further Reading
GENETIC IDENTIFICATION OF A HANTAVIRUS ASSOCIATED WITH AN OUTBREAK OF ACUTE RESPIRATORY ILLNESS. Stuart T. Nichol et al. in Science, Vol. 262, pages 914Ð917; November 5, 1993. HANTAVIRUS EPIDEMIC IN EUROPE, 1993. B. Le Guenno, M. A. Camprasse, J. C. Guilbaut, Pascale Lanoux and Bruno Hoen in Lancet, Vol. 343, No. 8889, pages 114Ð115; January 8, 1994. NEW ARENAVIRUS ISOLATED IN BRAZIL. Terezinha Lisieux M. Coimbra et al. in Lancet, Vol. 343, No. 8894, pages 391Ð392; February 12, 1994. FILOVIRUSES AS EMERGING PATHOGENS. C. J. Peters et al. in Seminars in Virology, Vol. 5, No. 2, pages 147Ð154; April 1994. ISOLATION AND PARTIAL CHARACTERISATION OF A NEW STRAIN OF EBOLA VIRUS. Bernard Le Guenno, Pierre Formentry, Monique Wyers, Pierre Gounon, Francine Walker and Christophe Boesch in Lancet, Vol. 345, No. 8960, pages 1271Ð1274; May 20, 1995. 64 SCIENTIFIC AMERICAN October 1995 Copyright 1995 Scientific American, Inc. PATRICK ROBERT SYGMA ...
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