Ignoring Deadly Viruses (

By Donald S. Burke

In the past few weeks, three suspect SARS cases have been detected in China's Guangdong province, and there have been six confirmed deaths from bird flu in Vietnam, and one suspected fatality in Thailand. Will a new global pandemic -- either of SARS or the avian influenza -- erupt any time soon? No one knows for sure, but the signs are worrisome. Public health agencies in Asia, supported by the World Health Organization, are on high alert. 

A better understanding of how such viruses evolve and spread is crucial for preventing another epidemic. Take influenza. Most vertebrates have their own influenza viruses that circulate regularly and widely within their species. This is the case with the H5N1 avian virus now rampant among poultry in Southeast Asia. Such viruses can occasionally jump from their animal hosts to humans. Indeed flu infections occur surprisingly often in humans who have close contact with birds or animals. But usually it is not then transmitted on to other humans, because the virus is poorly adapted to the species. Only rarely does a new virus become sufficiently human-adapted that it can spread from person to person.

But some viruses have developed evolutionary tricks that make them exceptions to this rule. And influenza viruses are especially adept at swapping genes between viruses and adapting into a form that can spread among humans. That is highly significant, as all known major global influenza pandemics emerged in this way, when a bird or animal virus swapped genes with a human virus to create a new virus capable of spreading from person to person.

This kind of intimate knowledge of how influenza viruses evolve and spread has allowed us to come up with a strategy to reduce the risk of the recent cases spiraling into a pandemic in East Asia. Culling infected flocks, reducing human contact with infected birds, and administering human influenza vaccines to those who have frequent contact with birds -- to minimize the opportunity for gene swapping -- are all sound strategies to prevent the emergence of a new human-adapted strain that could spread rapidly around the world.

Computer simulations suggest that knowing how viruses evolve is crucial to understanding how they cause epidemics. Unfortunately, most viruses are much more poorly understood than influenza. Take the AIDS virus. The origins of this dreadful pandemic virus are only dimly understood. Genetic sequence data of viruses taken from humans and from chimpanzees suggests that the human virus probably evolved from a chimp AIDS-like virus. My own preliminary studies in the Congo basin suggest that there is an ongoing "viral chatter" of cross-species transmissions from monkeys and apes into humans who hunt them for bush meat. AIDS viruses are also adept at gene swapping, so it is tempting to speculate this viral adaptation technique led to the emergence of AIDS, although the details as to how this happened -- namely what viruses originally swapped genes with other viruses -- remain unclear.

A similar lack of understanding about how the SARS coronavirus evolved hampers our ability to fight that disease. Although civets may be the animal reservoir from which the SARS coronavirus emerged last year, this is by no means proven. Even more problematic is our inability to differentiate between coronavirus strains that are human-adapted and those that are civet-adapted. For instance, we don't know if the three recent cases in Guangdong involve infections with a human-adapted form of the coronavirus that can spread from person to person. If so, another SARS pandemic may be imminent. Or are they simply examples of the occasional cross-species transmission of the coronavirus from animals to humans? In this case, there is little danger of another naturally occurring pandemic and the priority should instead be tighter safety standards at the laboratories where the more dangerous strain of the coronavirus is still stored.

Unintentional release of extinct human-adapted viruses -- "biobungling" -- arguably poses as serious a threat to global health as bioterrorism or a natural outbreak. Again an example from influenza is instructive: Genetic sequencing of the global pandemic 1977 H1N1 influenza virus has shown it to be identical to an H1N1 strain that became extinct outside laboratories in the 1950's. The most plausible scenario is that the 1977 virus was one stored for decades in a laboratory freezer and thawed for experimental study during the 1976 swine influenza scare: a "self-fulfilling prophecy" epidemic. Two research workers -- one in Singapore and one in Taiwan -- have already experienced laboratory acquired infections with human-adapted SARS coronavirus strains; luckily no epidemic ensued from either.

While massive new biodefense budgets in the U.S. are pouring billions into test-tube studies and techno gadgetry, support for studies into how viruses evolve and spread lags far behind. Our understanding of viral biodiversity in animals in agricultural settings and in the jungled regions of our planet is sketchy at best. Data on cross-species infections with viruses other than influenza is essentially absent. And studies on how viruses adapt to new hosts are simply not being done. Medical research agencies like the National Institutes of Health dismiss such field research as nonscientific fishing expeditions, while ecology oriented agencies like the National Science Foundation view them as belonging in the health domain. If we ever hope to interpret "viral chatter" such as we now hear from Asia, we must role up our sleeves, muddy our boots, and study real viruses where they occur in natural settings.

Dr. Burke is professor of international health and epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland.

Op-ed article originally published in the January 26, 2004, edition of The Asian Wall Street Journal.

"Reprinted from The Asian Wall Street Journal © 2004 Dow Jones & Company, Inc.  All rights reserved.”