Passage IV

NATURAL SCIENCE: The following passage is adapted from an article titled “Flu Pandemic" by Robin Mrantz Henig (©1992 by The New York Times).

The existence of the influenza vaccine may give us a sense of false security when it comes to the possibility of a pandemic outbreak of influenza, (A pandemic is an international epidemic, with disease occurring at a higher-than-expected rate on several continents at once.)

More stable viruses, like smallpox and polio, are relatively easy to control with an effective one-time vaccine. Not influenza. Because the virus mutates so frequently, the flu vaccine must be concocted anew each year, based on scientists' best guess of what surface proteins will determine the nature of the next season's outbreak. Once they forecast the probable composition of the virus, scientists choose the appropriate antigens (substances that stimulate an immune response) to make their vaccine. They must know by mid-February of any year which antigens to include in the following winter's formulations, if they hope to insure production of adequate amounts of vaccine for delivery by the start of the flu season in December.

But the scientists who must determine what virus will cause the next year's illness run a high chance of being wrong. Some observers have put the odds of success at no better than 50-50. Even when they are right, the vaccine lasts only as long as that year's strain.

Any discussion of influenza must include a discussion of how the virus itself changes from one strain to the next. The mutations that lead to major changes in viral surface antigens—changes that create the pandemic strains of influenza—are quite rare. Pandemic strains have occurred just three times in this century: in 1918, the year of the so-called Spanish flu; in 1957 when a new strain called the Asian flu emerged; and in 1968, when a third strain was introduced, known as the Hong Kong flu.

Compared with the Spanish flu pandemic, the more recent outbreaks were extraordinarily mild. When the Asian flu first emerged, the attack rate was the expected 25 percent, but the mortality rate was relatively low; about 70,000 Americans died. With the Hong Kong flu, there were just 28,000 deaths. This lower mortality rate could be traced to the fact that of the two major antigens on the virus's surface, the Asian flu and Hong Kong flu differed in only one. This meant that most people had at least partial immunity to the new 1968 virus, which might have tempered its effects.

The explanation for the influenza virus's mutability lies in the arrangement of its genes. Because its genetic material is packaged in the form of ribonucleic acid (RNA), random mutations during replication are relatively common and are passed on intact to the virus's offspring. It takes just 12 to 15 weeks to change a flu virus's genetic arrangement by a significant degree.

The new form of the virus differs in ways that may be minor, but it nevertheless renders ineffective the antibodies formed in response to an old influenza infection. This change is known as antigenic drift.

More significant is another kind of antigenic change that also occurs as a result of the virus's genetic structure. The flu virus has what is known asa segmented genome, a weakly bound string of genes with clefts between each of eight segments. Each viralgene is responsible for the manufacture of one or two distinct viral proteins. The segments are physically connected, but only loosely so; they easily come apart and rearrange with other viral segments if different influenza viruses are nearby. The insertion of new segments from different viruses, especially from viruses of animal (rather than human) origin, leads to the process of genetic “reassortment.”

The resulting “reassortants,” if they involve genes that code for proteins in the virus's surface antigens, can lead to major changes in the influenza virus's configuration—a process that is known as antigenic shift.

For genetic reassortment to occur, a cell must be simultaneously infected with more than one influenza virus of more than one animal strain. Such co-infection does not readily occur in human beings, but it happens often in what are known as the reservoir animals. These animals, primarily ducks and other birds and swine, can be infected with influenza from any source—human, avian, or mammalian—without getting sick.

Fortunately for us, though genetic reassortment itself happens frequently, the creation of a.new reassortant capable of infecting human beings is quite rare. But when such a human-infecting reassortant does emerge—part human, part bird, or pig—the potential for a new influenza pandemic has arrived.