John M. Barry is the author of “The Great Influenza: The Story of the Deadliest Pandemic in History”, and Distinguished Scholar at the Tulane University School of Public Health and Tropical Medicine.

Making vaccines is hard. Making vaccines that keep up with mutations is even harder. The race is now on to keep up with the mutating coronavirus.

Mutations occur when the genetic code of an organism is not copied accurately during cell replication. This is true in humans and viruses, but viruses make orders of magnitude more copying mistakes than humans do. These mutations are random, and the vast majority have no impact on or damage the virus.

For example, influenza mutates so rapidly that approximately 99 percent of virus particles produced by an infected cell are defective — so defective that they cannot infect another cell and replicate. Unfortunately, the part of the influenza virus most easily recognized by our immune systems — which the influenza vaccine mimics to stimulate an immune response — can mutate without destroying the virus’s ability to infect. Vaccine makers are constantly playing catch-up.

That's why making a flu vaccine is so difficult. Each year scientists change the vaccine to try to match changes in the virus, but vaccine production and distribution takes months. By the time people get inoculated, a precise match is impossible.

Because of this, the best influenza vaccine ever produced was only 60 percent effective in preventing illness. In most flu seasons, the success rate is usually considerably less; and in the 2004-2005 season, the vaccine was only 10 percent effective.

By contrast, the measles virus also mutates rapidly, but the part of the virus that the immune system recognizes — and that the vaccine mimics — cannot change. That’s why, despite billions of measles vaccinations over a period of decades, the virus has been unable to escape the vaccine.

We have already seen mutations in the spike protein of SARS-Cov-2 that allows the virus to enter cells more easily. That advantage is causing one variant to spread more rapidly; within a few months, it has become the dominant virus in the United Kingdom, and it has already spread to other countries.

Countries with robust systems to identify those infected with the variant, isolate them and trace contacts may have a chance to prevent the variant from becoming dominant or slow its spread until their populations are vaccinated. Unfortunately, the United States never built that infrastructure and the Centers for Disease Control and Prevention has predicted this variant could become the dominant virus here by March.

Increased transmissibility is a serious problem, but the Moderna and Pfizer vaccines work well against the variant first identified in the United Kingdom. If nothing else changed and if people comply with social distancing and masking, a wide distribution of the vaccine would eventually contain it.

More worrisome are two new strains: one in South Africa and one in Brazil. Lab studies indicate that the antibodies generated by the Moderna and Pfizer vaccines are less effective against the South African strain than against the previously dominant strain. It remains unclear how much difference this will make in people because the studies indicate that antibodies still work well enough to provide significant protection, and also because antibodies comprise only one part of the immune response; the variant might still be just as vulnerable to T-cells, memory B cells and the rest of our bodies’ immune response.

But it’s still troubling, and scientists are now preparing a booster shot designed specifically for the mutated spike protein of this strain.

More troubling may be the strain which has surfaced in Manaus, a Brazilian city of 2.2 million where an estimated 76 percent of the population has been infected and therefore should have enough naturally acquired immunity to constrain, if not suffocate, the spread of covid-19. That was the case for a while. But a new strain similar to the one in South Africa emerged, and infections caused by it are surging again in Manaus. This strongly suggests the virus has acquired the ability to evade naturally acquired immunity.

Both the Brazilian and South African strains have spread to other countries. On Monday, the strain from Manaus was identified in Minnesota.

Even if these new strains remain highly susceptible to the vaccines we already have, their emergence suggests that SARS-Cov-2 has the ability to mutate enough that it could, over time, evade a vaccine.

That means several things. First, the virus is never going away. Even if it could be eliminated from the human population, it can infect other mammals, mutate in them and then jump back to humans.

Second, the more people infected, the more opportunity the virus has to mutate in a direction that creates problems. So, it is in the self-interest of wealthy countries to get vaccines distributed worldwide to limit those opportunities.

Third, covid-19 will become much like influenza, requiring year-round, worldwide, surveillance of new strains and regular updating and administration of vaccines. We may not need a new vaccine every year, but we will need new vaccines, nonetheless.

There is one other answer. Scientists must search for parts of the virus that remain stable amid mutations and still generate an immune response. With influenza, scientists have made progress toward this. For both viruses, that’s the vaccine we need. That is now the holy grail.

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