By William A. Haseltine
CAMBRIDGE – Like surfers looking out for the next big breaker before the first one has passed, epidemiologists and public-health officials in the United States are bracing themselves for a fresh surge of COVID-19 infections later this year. The fear is that this second wave will coincide with the peak of the 2020-21 US influenza season, triggering a new flood of hospital patients in dire need of respiratory support.
The fear is justified, based on what we know about coronaviruses and influenza. For both, infections begin rising in November and peak at some point in December, January, or February, before subsiding by April.
What is less certain is how high the waves for each infection will be. Although we understand influenza infection patterns much better than that of the SARS-CoV-2 virus that causes COVID-19, influenza remains a known unknown. Its strains vary from year to year in terms of both transmissibility and severity. In some years, the number of lives lost to influenza in the US can be as low as 12,000. But during the 2017-18 winter, a particularly lethal strain led to the death of an estimated 80,000 Americans – the highest such toll in at least 40 years.
The annual variation in influenza strains means that we need to create a new vaccine each year. But there’s a catch: the vaccine needs to be prepared well in advance of peak flu season – and often before the new influenza strain even appears. If the vaccine matches fairly accurately, it limits both the severity of an illness due to infection and the number of deaths due to complications from the disease.
But our 2017-18 vaccine was not a good match. By January 2018, hospitals were overwhelmed, emergency rooms were turning away ambulances, and medical centers were implementing now-familiar measures such as setting up triage tents in parking lots, restricting visits by friends and family, and canceling elective surgeries.
The severity of the 2020-21 influenza season will therefore depend on how well our vaccine matches the strain of the virus, and on the particular strain itself. But it will also depend on our own behavior and how readily we spread the infection to others.
Compared to influenza viruses, the behavior of SARS-CoV-2 is a much greater unknown. What we infer is mostly based on the behavior of the four cold-causing coronaviruses that have been circulating in the US since at least the 1960s, when they were first discovered.
The seasonal appearance of these viruses closely resembles that of influenza, except that infections do not disappear in the summer months; instead, they continue at a reduced frequency. Indeed, the notion that heat and humidity will eliminate SARS-CoV-2 is belied by ongoing infections in Singapore and coastal West Africa.
In fact, the seasonality of viral infections overall remains a mystery. Some think that viruses like influenza and coronavirus peak in winter because cold, dry weather dries our mucous membranes, rendering us more susceptible to viral infections. Others observe that, in winter, we gather more closely together indoors, facilitating transmission.
These theories seem plausible until one considers other viruses, like polio and cold-causing rhinoviruses, which peak in summer. And the mystery only deepens when we come to viruses that are seasonal in temperate climates and maintain a near-constant (albeit lower) infection rate in the tropics.
With SARS-CoV-2 unlikely to disappear on its own, and absent an effective vaccine or prophylactic drug, the main factor influencing the magnitude of a second wave of infections is how well we control the epidemic between now and then. The number of people actively infected by the virus in October – the so-called human reservoir – will determine the size and speed of the expected second wave. Limiting the number of infections now will reduce the number of infections later.
Unfortunately, the US is not limiting COVID-19 infections enough to avoid a severe second wave. Our current control measures – limited testing and largely voluntary self-isolation for those known to be infected or exposed – are unlikely to eliminate the virus from the population. Countries that so far have tackled the disease successfully have much broader testing regimes and have implemented exhaustive contact-tracing programs that identify all those potentially infected and move them to supervised facilities, often at a local hotel, where they are monitored for symptoms.
As US communities reopen and behavior patterns loosen still further, we will be forced to face the consequences of our insufficient action. Come October, I expect that we will be on the brink of another deadly round of COVID-19 infections. And if a significant wave of influenza infections crashes down upon us at the same time, even more people will die.
Having the medical means to prevent SARS-CoV-2 transmission will diminish the size and impact of a second COVID-19 wave. Indeed, with strong support by governments, the pharmaceutical and biotechnology industries, and non-profit foundations, efforts to develop a vaccine and drugs that may block the virus’s transmission have shifted into high gear in laboratories around the world. With seven vaccines and at least one drug with prophylactic potential currently in clinical trials, I am confident that we will be able to limit SARS-CoV-2 transmission in the near future.
But the question is when. To have an impact on a second wave of US infections this autumn, a vaccine or prophylactic drug must be widely available by the very beginning of the season. That will require maximum coordinated efforts by researchers, manufacturers, and regulators.
Although such a scenario is possible, we will need to be both smart and lucky to avoid what nature has in store for us come winter. And without a medical breakthrough, we will have to prepare for the worst.
Haseltine, a scientist, biotech entrepreneur, and infectious disease expert, is Chair and President of the global health think tank ACCESS Health International.
Frontpage December 4, 2018