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a true reckoning of its genetic diversity. By the end of the twentieth century, scientists had identified dozens of strains, which belonged to two great lineages, known as HRV-A and HRV-B. In 2006, Ian Lipkin and Thomas Briese of Columbia University were searching for the cause of flu-like symptoms in New Yorkers who did not carry the influenza virus. They discovered that a third of them carried a strain of human rhinovirus that was not closely related to either HRV-A or HRV-B. Lipkin and Briese dubbed it HRV-C, and since then, researchers have found that this third lineage is common around the world. From one region to another, the variations in HRV-C’s genes are few, which suggests that the virus wasted no time spreading through our species. In fact, the common ancestor of all HRV-C may be just a few centuries old.

The more strains of rhinoviruses scientists discover, the better they come to understand their evolution. All human rhinoviruses share a core of genes that have changed very little as the viruses have spread around the world. Meanwhile, a few parts of the rhinovirus genome are evolving very quickly. These regions appear to help the virus avoid being killed by our immune systems. When our bodies build antibodies that can stop one strain of human rhinovirus, other strains can still infect us because our antibodies don’t fit on their surface proteins. Consistent with this hypothesis is the fact that people are typically infected by several different human rhinovirus strains each year.

The diversity of human rhinoviruses makes them a very difficult target to hit. A drug or a vaccine that attacks one protein on the surface of one strain may prove to be useless against others that have a version of that protein with a different structure. If another strain of human rhinovirus is even a little resistant to such treatments, natural selection can foster the spread of new mutations, leading to much stronger resistance.

Despite the diversity of rhinoviruses, some scientists are optimistic that they can develop a cure for the common cold. The fact that all strains of human rhinoviruses share a common core of genes suggests that the core can’t withstand mutations. In other words, viruses with mutations in the core die. If scientists can figure out ways to attack the rhinovirus core, they may be able to stop the disease. One promising target is a stretch of genetic material in rhinoviruses that folds into a loop shaped like a clover leaf. Every rhinovirus scientists have studied carries the same clover-leaf structure, which appears to be essential for speeding up the rate at which a host cell copies rhinovirus genes. If scientists can find a way to disable the clover leaf, they may be able to stop every cold virus on Earth.

But should they? Human rhinoviruses certainly impose a burden on public health, not just by causing colds but by opening the way for more harmful pathogens. But the human rhinovirus itself is relatively mild. Most colds are over in a week, and 40 percent of people who test positive for rhinoviruses suffer no symptoms at all. In fact, human rhinoviruses may offer some benefits to their human hosts. Scientists have gathered a great deal of evidence that children who get sick with relatively harmless viruses and bacteria may be protected from immune disorders when they get older, such as allergies and Crohn disease. Human rhinoviruses may help train our immune systems not to overreact to minor triggers, instead directing their assaults to real threats. Perhaps we should not think of colds as ancient enemies but as wise old tutors.

Looking Down from the Stars

Influenza Virus

Influenza. If you close your eyes and say the word aloud, it sounds lovely. It would make a good name for a pleasant, ancient Italian village. Influenza is, in fact, Italian (it means influence). It is also, in fact, an ancient name, dating back to the Middle Ages. But the charming connotations stop there. Medieval physicians believed that stars influenced the health of their patients, sometimes causing a mysterious