The Basics

Despite our best efforts to control SARS-CoV-2, the primary determinant of when and where the virus spreads is seasonality1,2,3,4. Seasonality is the rhythmic variability of a virus’s reproductive rate. When the reproductive rate is high, during peak season, then the virus spreads readily. When the reproductive rate is low, during the off season, the virus is still present in the environment but has a reduced ability to spread. The factors associated with viral seasonality are not well understood by modern science. So far, we think that the preeminent factors are changes in host behavior and environmental effects on host resistance1.

The seasonality of SARS-CoV-2 is something that lay-people like you and me had no way of knowing back in Spring of 2020, but the “experts” sure did. There are four Human Coronaviruses (colloquially known as HCoV): OC43, HKU1, 229E, and NL63. They contribute to the common cold and have been known to be seasonal for decades5, 6. In temperate climates, they surge in the late Fall / early Winter and remain at lower levels the rest of the year.

 

 

In addition to the four HCoV’s, there are two much more lethal coronaviruses, SARS-CoV-1 and MERS-CoV. Fortunately, neither of these have become endemic because they are not as contagious as the HCoV’s. That being said, they still provide strong evidence of coronavirus seasonality7, 8, 9. With SARS, MERS, and the four HCoVs all having well-known seasonality, it stands to reason that public health “experts” should have predicted a high degree of seasonality with SARS-CoV-2. Instead, the “experts” seemed to want to keep this obvious truth from the general population. They never talked about it. In some cases they even wrote papers trying to obfuscate or trivialize it.

The following systematic review10 was completed in April, but was withheld from publication until September:

“Furthermore, the spread of types of diseases caused by betacoronavirus, such as SARS-CoV-1 [11] and MERS-CoV [36], have already been shown to suffer the impact of climatic conditions. In both these coronoviruses, hot and humid climates demonstrated the ability to decrease the viability of these viruses, while in places with low temperature and humidity there was greater viral stability. The favorable cold and dry weather conditions facilitates the spread of the coronaviruses and seems to be the same for SARS-CoV-2 virus, as it was observed homogeneously in the included papers.

Why isn’t coronavirus seasonality, well known for decades, talked about more? When hard-lockdown states such as California, Illinois, Michigan, Pennsylvania, and New York experience dramatic surges during the late Fall (exactly when one would expect a seasonal surge), why are the people in those states blamed for their bad behavior?

Why is it always “we didn’t lock down enough” or “not enough people wore masks“?

Where are the public health “experts” who are humble and strong enough to simply say “we’re in coronavirus season and, while we expect people to heed our warnings, we understand that at least a little bit of this is unstoppable” ?


Let’s Dig a Little Deeper…

There are seven coronaviruses that are known to infect humans, and they are divided into two genera:

Alpha-coronavirus

HCoV-NL63
HCoV-229E

Beta-coronavirus

HCoV-OC43
HCoV-HKU1
SARS-CoV-1
MERS-CoV
SARS-CoV-2

Note: There are other genera of coronaviruses, but only the alpha- and beta-coronaviruses above are currently known to infect humans.

SARS-CoV-2 belongs to the betacoronavirus classification, which includes HCoVs OC43 and HKU1. What’s interesting about these two is that they always take turns being dominant each year11, 12. In Figure 1 (above) and Figure 2 (below), you can see this as OC43 and HKU1 occupying alternating peaks each year.

 

Immunologically speaking, we think this alternating-year phenomenon happens because antibodies against HCoVs tend to last about 6-12 months13, 14. At the start of each new seasonal wave, some of the population still has lingering protection against last year’s preeminent HCoV. This means the HCoV that dominated last year has way more herd immunity to fight through than the HCoVs that were more dormant. The net effect is that no HCoV becomes the champion in back-to-back seasons.

Notice in Figure 2 how HCoVs have disappeared from circulation just like Influenza. Last year, the peak of HKU1 season was January 4. At the time of this writing we are a week away from that date and no HCoV’s are being detected. Something is going on that is causing SARS-CoV-2 to eliminate both Influenza and its sibling HCoVs.


Why Is Coronavirus Immunity Short-Lived?

On an organism level, the body responds to viral infection by deploying a wide variety of defense mechanisms15. Chief among these is the antibody response16, whereby the immune system creates proteins that target and neutralize foreign pathogens. A successful antibody response will help prevent future infection, but somewhat strangely the human body only maintains coronavirus antibodies for about a year13, 14. This is in stark contrast to other viruses like Mumps and Measles, for which the human body will maintain antibodies for life17. Why does the body decide that some viral infections can be quickly forgotten, but others must be remembered forever?

It seems logical to assume that severity of the disease should be directly proportional to the level of immunological response. If a virus doesn’t really bother us, why waste precious humoral resources dealing with it? Just leave it alone. On the other hand, if a virus knocks us on our ass, we ought to take note and be better prepared next time.

Indeed, the immune system has the ability to moderate serum antibody levels based on a multitude of factors, including frequency of exposure to similar pathogens18. In the specific case of SARS-CoV-2, we’ve already established that production of neutralizing antibodies is very highly correlated with the severity of symptoms19, 20, 21, 22.

In Figure 3 (above), the green line indicates a more robust antibody response amongst patients who developed severe symptoms. Notice that the non-critical patients begin to reduce antibodies at ~21 days, whereas the critical patients continue to increase antibody levels throughout the study.

In Figure 4 (below), antibody response is almost perfectly associated with disease severity.

 

Unfortunately, even when the body produces a copious amount of coronavirus antibodies, it seems to discard those antibodies relatively quickly. While we don’t yet know exactly how long SARS-CoV-2 neutralizing antibodies will last, it seems reasonable to expect that serological decline will be comparable to or greater than that of SARS-CoV-1 and MERS-CoV. That would mean that even severe cases could experience reinfection after just a few years23. This is somewhat strange and unexpected, given that childhood exposure to harmless viruses like Mumps, Measles, and Varicella (Chickenpox) will result in lifelong antibodies. So again we have to ask, why does the body decide that some viral infections can be quickly forgotten, but others must be remembered forever?

When it comes to coronaviruses, we really don’t know. Reinfection is relatively common with HCoVs, so we’d expect the occasional re-challenge to result in antibody sustainment. SARS-CoV-1 and MERS-CoV are both impactful enough that we’d expect severe cases to result in more profound antibody durability. For whatever reason, the human immune system just doesn’t seem as concerned with maintaining coronavirus antibodies as it should be. It seems very likely that the body prefers to utilize other components of the immune system. T-cells, in particular, are believed to play a key role in pathogenic prevention of COVID-1924, 25, 26. While it is a blessing that the body has such mechanisms to fall back on, antibodies are necessary to prevent reinfection. Without antibodies, it doesn’t matter how robust the immunological response is–infection can occur.

 

Since the overwhelming majority of SARS-CoV-2 infections lead to mild or moderate symptoms, it is safe to assume that antibody seroprevalence will follow seasonal cycles. This will cause the virus to eventually settle into the same seasonal rhythm that the HCoVs exhibit. The vaccines will further accentuate seasonality because they have been designed to reduce symptoms, not prevent infection.


The Proof Is in the Pudding

At the end of the day, whatever we know or don’t know about the SARS-CoV-2 immunological response pales in comparison to what we see in the real world data. All the theory and logic can make perfect sense, but if the empirical evidence says that you’ve got things wrong, then you’ve got things wrong.

So how does seasonality hold up when we look at the data? Really well, it turns out.

Let’s shoot through some real-world data that I believe will convince you that seasonality is the primary determinant of when and where SARS-CoV-2 spreads. We’ll look at a few of the major geographical regions of the USA. All of these charts plot the number of daily COVID cases per capita over time.

 


The Midwest

Figure 5: COVID-19 Per-Capita Case Curves for:
Illinois, Iowa, Michigan, Minnesota, Montana, Nebraska,
North Dakota, South Dakota, Wisconsin, Wyoming

The most recent major seasonal surge took place in the Midwest and came to an end in early November. What’s interesting about the Midwest region is that it includes several “lockdown” states run by Democrat governors, and several relatively free states run by Republican governors. Despite the states’ wide disparities in mitigation efforts, they all rose and fell according to the same seasonal clock, as you can see in the figure above. All the heavy-handed restrictions in hard-blue Illinois, Minnesota, and Michigan did not prevent them from surging. Similarly, the lack of restrictions in South Dakota, Wyoming, and Nebraska did not prevent them from coming down once the season passed.

Even more interesting is the direct comparison between South Dakota and North Dakota. While South Dakota Governor Kristi Noem refused to restrict business or implement a mask mandate at any point in the surge, North Dakota Governor Doug Burgum panicked and implemented heavy business restrictions and a state-wide mask mandate in early November, right as cases were just reaching their peak. Despite lacking any business restrictions or mask mandate, South Dakota cases came down exactly the same way that North Dakota cases came down. The season simply ended. It ended the same way for wide open states as it did for locked down states.

 


The Southeast

Figure 6: COVID-19 Per-Capita Case Curves for:
Alabama, Florida, Georgia, Mississippi, South Carolina

The Southeast is made up of Republican governors who have been relatively relaxed compared to the rest of the USA. Their cases rose and fell in unison during the “Sunbelt Surge” of the Summer, then they proceeded to stay at lower levels for a couple months before entering another surge in the late Fall. Notice that their case climb didn’t really kick in until November, as compared to the Midwest states, who began to climb in September and October.

Now, granted, these states all have Republican governors, so we might expect their public policies to be roughly similar. They’ve each implemented different mitigation efforts at different times, but the net results are pretty much identical. Is it possible that all the people in all of these states decided to get serious about stopping COVID at the same time in July, then they all proceeded to stop caring about COVID at the same time in November? It seems more likely to me that they they just share betacoronavirus season.

 


The Northeast

Figure 7: COVID-19 Per-Capita Case Curves for:
Delaware, Connecticut, Massachusetts, New Jersey,
New York, Pennsylvania, Rhode Island

Ah, home, sweet home. Who remembers Dr. Fauci heaping praise on New York in July because they “did it correctly” ? Can anyone follow-up with him to ask what the heck went wrong?

These states are all run by Democrat governors, with the exception of Massachusetts Republican Governor Charlie Baker who is essentially a Democrat. They all have extremely robust mask mandates and economic restrictions. What went wrong? Why did all of those mitigation efforts work so well from May to October–a full six months–and then they completely failed in November? Hopefully by now you know the answer: it was their turn. They all went up together, and they all are coming down together, regardless of which state implemented whatever policy at any time.

 


The Southwest

Figure 8: COVID-19 Per-Capita Case Curves for:
Arizona, California

I chose to include these two states as a “mini-region” because I find their direct comparison to be particularly poignant. It’s hard to argue with the fact that these states are governed pretty differently.

Arizona Republican Governor Doug Ducey implemented some restrictions during the early summer, but the state has been mostly wide open since then and he has resisted public lamentations to implement restrictions as cases have surged.

California Democrat Governor Gavin Newsom has literally restricted just about everything that a governor can restrict. California’s mitigation efforts have been so robust and complete that even Politico exclaimed “Locked-down California runs out of reasons for surprising surge“.

Yet despite their differences, Arizona and California have experienced shockingly similar seasonal spread. Let me ask you: given that their per-capita case rates have been identical, would you rather live in the free and open state or the locked down state?

 


By now you should have a good appreciation of the seasonality of SARS-CoV-2. In addition to the USA regions described above, you can see the same seasonal effect all over the world: European regions, the Pacific Rim, South America, etc. It’s simply not possible that all of these global seasonal surges happened because some undisclosed percentage of the population all decided to stop wearing masks at the same time. The truth is that your region gets the virus when it’s time to get the virus, and it sweeps through until it’s done or the season ends.

So try not to feel so guilty next time the “experts” blame the sins of nature on you. It’s not your fault.

 

References

  1. Seasonality of viral infections: mechanisms and unknowns
  2. Misconceptions about weather and seasonality must not misguide COVID-19 response
  3. Spread of SARS-CoV-2 Coronavirus likely constrained by climate
  4. Global Seasonality of Human Seasonal Coronaviruses: A Clue for Postpandemic Circulating Season of Severe Acute Respiratory Syndrome Coronavirus 2?
  5. Global Seasonality of Human Coronaviruses: A Systematic Review
  6. Epidemiology and Clinical Presentations of the Four Human Coronaviruses 229E, HKU1, NL63, and OC43 Detected over 3 Years Using a Novel Multiplex Real-Time PCR Method
  7. Seasonality of Respiratory Viral Infections: Will COVID-19 Follow Suit?
  8. The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus
  9. Global seasonal occurrence of middle east respiratory syndrome coronavirus (MERS-CoV) infection
  10. Effects of temperature and humidity on the spread of COVID-19: A systematic review
  11. Human coronavirus circulation in the United States 2014-2017
  12. Interactions between seasonal human coronaviruses and implications for the SARS-CoV-2 pandemic: A retrospective study in Stockholm, Sweden, 2009–2020
  13. The time course of the immune response to experimental coronavirus infection of man
  14. Seasonal coronavirus protective immunity is short-lasting
  15. Immune responses to viruses
  16. A systematic review of antibody mediated immunity to coronaviruses: kinetics, correlates of protection, and association with severity
  17. Duration of humoral immunity to common viral and vaccine antigens
  18. Maintenance of Serum Antibody Levels
  19. Antibody Responses to SARS-CoV-2 in Patients With Novel Coronavirus Disease 2019
  20. Disease severity dictates SARS-CoV-2-specific neutralizing antibody responses in COVID-19
  21. Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections
  22. Rapid Decay of Anti–SARS-CoV-2 Antibodies in Persons with Mild Covid-19
  23. The dynamics of humoral immune responses following SARS-CoV-2 infection and the potential for reinfection
  24. What is the role of T cells in COVID-19 infection? Why immunity is about more than antibodies
  25. SARS-CoV-2 T cell immunity: Specificity, function, durability, and role in protection
  26. Pre-existing immunity to SARS-CoV-2: the knowns and unknowns