Once upon a time there was a little flu virus. It was probably born in Kansas in late 1917 or 1918, although nobody is really sure. Its name was H1N1. It grew up to be very wicked.
The story of the new strain of swine influenza now circling the world actually starts a lot farther back than the 20th century, but the year the “Spanish influenza” appeared is a good place to start.
From the second week in March 1918, when soldiers at an Army camp in Kansas began to get ill, until the final mini-waves of 1920, the Spanish flu infected about 97 percent of the people on Earth and killed at least 50 million of them.
The virus probably came from waterfowl, which carry dozens of different flu viruses. At some point, either before or after it got into human beings, the virus got into pigs, a species that can be infected by avian and human strains. It has stayed in swines ever since, and in people for almost as long.
The swine-origin influenza A (H1N1) virus circulating in Mexico, the United States and Canada, and present in two dozen other countries, is a descendant of the Spanish flu H1N1 virus. In the past 90 years, though, a lot of new blood — metaphorically speaking — has entered its lineage. It does not look or act much like its notorious ancestor.
This might be a good place to address this A and H and N business.
Influenza virus is part of a family called Orthomyxoviridae. There are four sub-classifications — influenza virus A, influenza virus B, influenza virus C and thogotoviruses. It’s like citrus fruit, which encompass oranges, lemons, limes, grapefruit, etc.
Influenza A and B cause illness in people; the others almost never do. There are many, many types of influenza A but only one influenza B.
The diversity of influenza A arises from variations in the two proteins on its surface, called hemagglutinin (abbreviated H or HA) and neuraminidase (N or NA). Together, the proteins make up the face that a flu virus presents to the immune system of a bird, a pig or a human being.
In this setting, the face’s appearance is no small matter. The immune system’s ability to recognize a virus is one of the first steps in stopping it.
One strategy involves antibodies. They attack only if they are tailor-made for the virus, which requires the immune system to get a good look at the surface proteins. The immune system can offer the best protection if it has seen the pathogen before and has the right antibodies ready.
Think of H as hair and N as nose, two features for learning and remembering the identity of a virus. In the world of influenza A, there are 15 subtypes of H (straight blond, wavy red, short black, kinky black, etc.) and nine subtypes of N (Roman, ski jump, flared, long, etc.). Each subtype is numbered — H1N1, H3N2, H9N2 and so forth.
H1N1 is simply one combination of two of these subtypes that give the virus an appearance recognizable to the immune system — say, short black hair and a long nose. Within these subtypes, however, there are subtle — and sometimes not so subtle — variations. They arise from mutations in the genes governing the H and N proteins.
Over time, an H1N1 influenza A virus can change its appearance significantly through random mutation. It can streak its short black hair and put a gold stud in its long nose one year, and shave its hair into a Mohawk and add a diamond stud in the other nostril the next. Pile up enough of these, and pretty soon the immune system no longer recognizes it as the virus with the short black hair and the long nose it once knew — even though it still fits that description.
That is why the Spanish flu virus, the new swine flu virus and some of the human flu viruses circulating in recent winters can all be H1N1 viruses and yet look and behave so differently.
Research in the past few years on the Spanish flu virus — which has been reconstructed from fragments extracted from lung-tissue samples from people who died in 1918 — has revealed that much but not all of its killing potential resided in the H protein. One of the reassuring things about the new swine flu strain is that it does not have those same “virulence factors,” even though it shares the same broad H1N1 features.
Studies done in the past two weeks suggest that people who have received flu shots in the past few years — shots that protect against the most common human H1N1 strain in circulation — are not protected against this swine flu strain, even though it also is H1N1. Why? Because it looks so different to the immune system that the virus-killing antibodies do not react.
Such is the importance of looks, immunologically speaking.
The human H1N1 flu virus — and it’s “human” only because it is in us — that circulates each winter changes a little bit year to year in a phenomenon called “antigenic drift” as mutations creep into the H and N genes. But it can also change much more rapidly through something called “antigenic shift,” which happens when entire H or N proteins (or both) are swapped out wholesale for new versions.
This is possible because influenza’s genes are on eight separate strands, or “gene segments.” One or two or more can be replaced, like cards in draw poker.
That’s a rare event, however, and requires that two flu strains invade a single cell, replicate and then get their products mixed up in the packaging. The result is a virus dramatically different in immunological appearance, and sometimes in disease-causing capability, from either parent.
One way or another, a new influenza virus with the identity of H2N2 appeared in 1957. Because it was a new combination, nobody had immunity. It was called “Asian flu,” and it spread everywhere, outcompeting H1N1 strains, which disappeared in people but remained in pigs.
In 1968, another strain, an H3N2 combination, appeared on the scene. Nobody had immunity to it either. It had a world’s worth of susceptible victims and caused the “Hong Kong flu” pandemic that year and the next.
In 1977, a strange thing happened. The H1N1 virus, absent for years in people, reappeared. Curiously, it was almost exactly like the last strains in the 1950s. It was so close, in fact, that many people suspect it was released into the world by mistake from 1950s samples kept in a lab freezer.
Whatever the source, it spread widely as the “Russian flu,” infecting lots of people born after the disappearance of H1N1 two decades earlier.
Since then, H1N1 and H3N2 strains have been circulating, mutating in small ways, and infecting new victims year to year. At the moment, the dominant H1N1 strain is one called A/Brisbane/59/2007. By chance, the dominant H3N2 strain was also found in Brisbane, Australia, in 2007 and is named A/Brisbane/10/2007. Influenza B, which has caused about one-third of infections in the United States this flu season, is dominated by a strain called B/Florida/04/2006.
But now comes a whole new H1N1 virus. It is formally labeled A/California/04/2009, and it was taken from a 10-year-old boy in San Diego who came down with the flu on March 30. It has an H from an H1N2 virus circulating in American pigs and an N from an H1N1 virus found mostly in Eurasian ones.
Our immune systems, familiar with other H’s and N’s, do not know what to make of it. We have no antibodies against the combination, so we have no protection against it. And we will generate antibodies only if we get infected by the virus or vaccinated with a killed version of it; either way will teach the immune system what it looks like.
This is the swine flu or, as the federal government likes to call it, confusingly but inoffensively, the H1N1 strain.
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