I would like to move on to other subjects, away from SARS-COV-2, but I feel obliged to explain a number of important issues I haven’t really seen other people discuss before. The reason so many people have now died from SARS-COV-2, with 900,000 deaths in the United States alone so far, is almost entirely down to how we have treated this virus. Millions of people have died, who didn’t have to die. Additionally, the reason this virus has had the opportunity to behave so differently from any other virus, is because we ourselves paved the way for this virus.
SARS-COV-2 became far more dangerous than I originally anticipated, because I did not anticipate that humans would genuinely be so stupid as to continue with their lockdown experiment. To help you understand how SARS-COV-2 became so dangerous, I want to offer you a metaphor. Imagine you own a forest. The forest has a problem with rats. You don’t particularly like rats, they cause you and your neighbors problems, so you decide to deploy rat poison in the forest. It’s not the best rat poison you could use, in fact you were warned that the rats may be resistant to it, but you figured that something is better than nothing, so you strew it onto the forest floor.
Initially after you deployed your poison the number of rats declined, but quite rapidly you were left with more rats than ever before. What had happened was that after you deployed your poison, the other small mammals in the forest, hamsters, mice, rabbits, hares, hedgehogs andsoforth began to eat from the poison too. These animals died out. Eventually the rats that survived had developed complete resistance to your poison and so now they were not just unaffected by it, they benefited from the fact that you had gotten rid of all the other animals with which they live in competition, as they moved to take over their nests and holes.
Now I want you to take this idea and see for yourself if it could apply to the novel coronavirus. When this coronavirus came into existence, it had an advantage over all the other respiratory viruses, in that nobody had ever encountered it before. Some people had some useful cross-immunity from other coronaviruses, but most people had no real preparation for a virus of this nature.
In contrast, whenever influenza, adenoviruses, human corona viruses, rhinoviruses, respiratory synctial viruses, metapneumoviruses and other respiratory viruses try to spread themselves, they run into a problem that almost all adults have already had an encounter with them, or their close relatives. The immune system comes prepared for the battle. This is a big part of the reason the novel corona virus had such a high rate of transmission: Most of its potential hosts had no relevant pre-existing immunity.
Generally speaking, whenever we try to stop the coronavirus from spreading through social distancing measures, those measures also prevent other viruses from spreading to the same degree. If staying at home prevents you from getting infected with one respiratory virus, we would also expect it to work for another respiratory virus. Imagine we implemented measures, that reduce the number of opportunities for respiratory viruses to infect another person by 25%. As an example, perhaps we moved from spending five days working at the office to just one day at the office.
Imagine two different viruses, an adenovirus and the novel coronavirus. The novel coronavirus at a certain point in time was able to spread from one infected host to another 1.5 infected hosts on average. In contrast, a competing adenovirus that sought to infect as many people as possible had to deal with people’s pre-existing immunity and could only jump in another 1.2 people on average.
With 25% of the opportunities to jump over lost due to government mandated social distancing policies, the adenovirus now gets to infect 0.9 new people per host. On the other hand, the novel corona virus has now gone from 1.5 infected hosts, to 1.125 hosts. One of these viruses is now on the path to extinction. The other virus continues to spread, but its now forced to spread at a slower pace. The life cycle of these type of respiratory viruses is not very long, it could be around five days on average.
Let’s say both viruses start out with 1000 hosts that they infected. After one hundred days, they have both gone through twenty cycles. How many people will get infected after one hundred days? For the Adenovirus, we’re looking at just 121 hosts who get infected now. On the other hand, for the coronavirus, we’re looking at 8433 people. What if we had no social distancing policies whatsoever and still had the 1.5 hosts infected? You would theoretically have 3.3 million people infected with the new coronavirus and 38337 people for the adenovirus. This is the sort of number that frightens epidemiologists, but you can’t just naively model exponential growth. As more people are infected, the chances that an infected person is surrounded by other infected people increases, meaning that high rates of infection eventually force the R number to come down on its own.
However, this is the eventual outcome we would see after a number of generations that is important to understand: Whereas the adenovirus has nearly gone extinct, infecting just a fraction of the people it would normally infect, the coronavirus has managed to spread itself unimpeded. Most people don’t understand this simple principle, even prominent scientists fail to understand it. This simple theoretical exercise we carried out here explains things that are otherwise difficult to understand, like the sudden mysterious absence of influenza during the pandemic: The measures that we used to discourage coronavirus infections made the corona virus spread slower, but they forced other viruses to gradually go (locally) extinct. How could measures that don’t get rid of SARS-COV-2 somehow force influenza to disappear? Now you hopefully understand how this could happen.
So, you might think to yourself “well this is actually great, imagine if we also had to deal with influenza, metapneumovirus and other viruses during the pandemic”. But that’s the wrong way of looking at this. These viruses are competing with each other for hosts. The very mild benign viruses are our friends. Whenever they infect us, we have to raise our defenses. Those defenses then also work when another virus shows up next and tries to enter our bodies. In the case of a relative deadly respiratory virus like SARS-COV-2, this is very useful.
So, take the five day cycle model that I showed you earlier. We go crazy in march and shut everyone inside their homes. A hundred days have passed, it’s now summer and we have forced the mild respiratory viruses into nigh extinction, whereas SARS-COV-2 continued to spread. Summer passes, we enter fall and the temperature, lack of sun and humidity levels begin to favor the spread of respiratory viruses again.
Whereas normally vast swathes of us would now start getting infected with the common respiratory viruses, these respiratory viruses now have to begin spreading again from a much lower baseline. Remember our earlier theoretical example, you can quite easily end up with 99% fewer hosts as the baseline from which the mild viruses start spreading again.
For influenza in particular, we know that this is roughly the number we’re looking at:
Many people look at graphs like this and think “oh we simply call the flu corona now”, not comprehending what really happened: The same measures that were meant to “flatten the curve” for SARS-COV-2 forced our mild friend influenza into near extinction. The near extinction of respiratory viruses like influenza then made it easier for SARS-COV-2 to spread.
Take a look with me at this study, that looks at the interference between different respiratory viruses:
The authors write:
We conducted an observational, cross-sectional study using samples collected by the Seattle Flu Study between 11 November 2018 and 20 August 2021. Samples that tested positive via RT-qPCR for at least one of 17 potential respiratory pathogens were included in this study. Semi-quantitative cycle threshold (Ct) values were used to measure pathogen load. Differences in pathogen load between monoinfected and coinfected samples were assessed using linear regression adjusting for age, season, and recruitment channel.
21,686 samples were positive for at least one potential pathogen. Most prevalent were rhinovirus (33·5%), Streptococcus pneumoniae (SPn, 29·0%), SARS-CoV-2 (13.8%) and influenza A/H1N1 (9·6%). 140 potential pathogen pairs were included for analysis, and 56 (40%) pairs yielded significant Ct differences (p < 0.01) between monoinfected and co-infected samples. We observed no virus-virus pairs showing evidence of significant facilitating interactions, and found significant viral load decrease among 37 of 108 (34%) assessed pairs. Samples positive with SPn and a virus were consistently associated with increased SPn load.
Here you see what I mean. Whereas we see 37 examples of cases where infection with one virus inhibits the spread of another virus, we see NO examples where the viruses make it easier for each other to infect us. When the pigeons and the raccoons in your neighborhood consume your garbage, the rats die of hunger. Similarly, when the influenza virus goes around infecting human beings, other viruses find themselves lacking susceptible hosts.
Let’s look at another study.
Virus-virus interactions influence the epidemiology of respiratory infections. However, the impact of viruses causing upper respiratory infections on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication and transmission is currently unknown. Human rhinoviruses cause the common cold and are the most prevalent respiratory viruses of humans. Interactions between rhinoviruses and cocirculating respiratory viruses have been shown to shape virus epidemiology at the individual host and population level. Here, we examined the replication kinetics of SARS-CoV-2 in the human respiratory epithelium in the presence or absence of rhinovirus. We show that human rhinovirus triggers an interferon response that blocks SARS-CoV-2 replication. Mathematical simulations show that this virus-virus interaction is likely to have a population-wide effect as an increasing prevalence of rhinovirus will reduce the number of new coronavirus disease 2019 cases.
Our good friend the rhinovirus infects our respiratory tract. The infected cells reacts with an interferon response, alerting neighboring cells and our white blood cells that something is wrong. It’s now very hard for SARS-COV-2 to infect us, because our immune system realizes: It’s time to be on the lookout for respiratory viruses here!
This is significant, because the rhinovirus is normally the most widespread respiratory virus. Just as with influenza, the social distancing policies forced our friend into near extinction.
Another study confirms these findings:
In summary, coinfection assays showed that SARS-CoV-2 replication is strongly or moderately impaired by a concurrent pre-existing RV/IAV infection or IBV infection, respectively, but that SARS-CoV-2 does not impair subsequent replication of RV or influenza viruses.