The first results of Moderna’s Covid-19 vaccine trials were officially published Tuesday and the news was good—patients injected with the mRNA-based vaccine produced antibodies that fight the Covid-19 virus.
Just how good is this good news? That depends on whether or not you accept the fundamental assumption underlying this generation of Covid-19 vaccines as fact.
To proclaim these trials a success is to take for granted that exposing people to viral proteins will trigger a vigorous, long-lasting immune response. But studies of the molecular biology of SARS-CoV-2, along with the natural history of the coronavirus family, may offer evidence to the contrary.
Vaccines don’t act as shields, protecting you from a disease. Instead they act more as alarms. Just like a fire alarm won’t put out the fire, a vaccine won’t prevent you from infection. They’re just a means to alert your immune system early on that a danger exists. In the end, it’s your immune system—including those antibodies—that does all the work.
Several recent studies have found that antibodies to SARS-CoV-2 decline in strength and number in the weeks and months following infection. One study describes a decline in even neutralizing antibodies, which are thought to be protective against reinfection and disease.
While this decline is not without precedent and is in fact typical of human coronavirus infections, the question is what it portends for the pandemic and for the success of Covid-19 vaccines.
SARS-CoV-2 is broadly similar to the four coronaviruses that cause about one third of all common colds. Each year, the same four viruses infect us the world over, sweeping the Northern Hemisphere from December to February; south of the Equator from May to July; and in the tropics, year-round. These waves of infection, which with rare exceptions cause minor symptoms only, have repeated year in and year out since the discovery of the virus in the 1960s.
In the 1970s two independent teams of medical researchers conducted experiments to determine whether or not the same coronavirus strain might reinfect and give a cold to the same person. Volunteers who were deliberately exposed to the virus contracted colds and recovered. A year later, they were again exposed to the same virus—and again were infected and developed cold symptoms. These experiments established that protective immunity to the cold-causing coronavirus is short-lived.
I call this phenomenon “get it and forget it,” and it describes the interaction between these viruses and our immune systems that is so unique. Confronted with a cold-causing coronavirus, our bodies evidently forget that we were infected at all.
For us, this leaves us susceptible to annual colds, which are generally harmless but a nuisance besides. For the viruses, this is a winning strategy, as it rids them of the need to change to survive. At present, we don’t understand coronaviruses in sufficient detail to know why our immunity to them so short-lived.* What we do know is that if SARS-CoV-2 behaves as its coronavirus cousins do, Covid-19 is sure to become a seasonally recurring pandemic.