How many people do you know who’ve contracted influenza in the last 12 months? Think carefully. Good old fashioned normal flu? According to the graphic below, there aren’t that many. In fact, in the space of 12 months, influenza has all but disappeared. Why? This extract from Science highlights the spectacular fall-off.
In March, as the Southern Hemisphere braced for winter flu season while fighting COVID-19, epidemiologist Cheryl Cohen and colleagues at South Africa’s National Institute for Communicable Diseases (NICD) set up a plan to learn from the double whammy. They hoped to study interactions between seasonal respiratory viruses and SARS-CoV-2, which causes COVID-19. Does infection with one change a person’s risk of catching the other? How do people fare when they have both?
But the flu season — and the answers — never came. NICD’s Centre for Respiratory Disease and Meningitis, which Cohen leads, has logged only a single flu case since the end of March. In previous years, the country’s surveillance platforms, which capture a sampling of flu cases from doctors offices, hospitals, and clinics, have documented, on average, about 700 cases during that period, Cohen says. “We’ve been doing flu surveillance since 1984, and it’s unprecedented.”
There are a number of factors that may have affected the 2020 influenza season. Masks, for one. More focus on hand hygiene and the disinfection of household surfaces, and then, social distancing. Add to that the closure of schools, children are the major engine for influenza transmission, and you can see possibly why the seasonal flu is having a hard time.
There is another reason though, and it has to do with viruses in general. They seem to prefer healthy hosts.
Viruses exhibit really strange behavior that we don’t as yet fully understand. When a new strain emerges, older viruses will often go into a phase of inactivity. It’s almost as though they are able to assess the landscape of potential hosts and realize they offer slim pickings. Scientists don’t fully understand this mechanism or what drives it.
Anecdotally, where I find myself currently ensconced in a remote village in the Philippines, Covid-19 is a rarity, almost no cases have presented. Here, the common flu virus is still alive and well, doing the rounds, and our rainy season brought with it all the usual flu encapsulated miseries.
So does this mean that traditional influenza will be back when the coronavirus runs its course? Possibly. We just don’t know enough about viruses to be sure. There is an alternative scenario though. One that becomes more likely with each passing day.
The possibility that this particular coronavirus, which is, don’t forget, a member of the family of influenza viruses, sticks around. Permanently. That our new term for flu becomes Covid. That we are already in the midst of a really terrible “flu” season that we’ve simply chosen to intentionally ‘mislabel’.
What supports this potential outcome?
The SARS-CoV-2 is an influenza virus with a twist. Its symptoms, when you first start feeling the effects of being infected, are initially indistinguishable from regular influenza. That’s why we need to rely on tests before we treat Covid-19 patients.
I take issue with articles like those issued by the WHO that seek to underline the differences between the regular influenza virus and SARS-CoV-2. This simply increases the public perception that we are dealing with something that’s not an influenza virus. Surely the time has come to admit that despite the severity and transmissibility of SARS-CoV-2, it is nothing more than a really aggressive influenza. A new breed of “flu”.
If your body fails to destroy the virus, that’s when things take a turn for the worse and when SARS-CoV-2 shows its true colors. It possesses an array of tools, a viral box of tricks, if you will, that regular “old school” influenza can only dream of.
Although it follows the conventional flu virus by using our nose and mouth to gain access to our bodies, that’s pretty much where the similarities end. Initial symptoms that appear flu-like are actually a precursor or warning for what can and does follow in some people. Unlike influenza, which pretty much limits itself to cardio and pulmonary attacks, the SARS-Cov-2 virus uses our bloodstream to transport itself to every organ and orifice of our bodies.
From your little toe to your brain, everything you own is fair game for this virus and there is emerging evidence that even those who don’t develop severe Covid-19, still sustain damage to their lungs and, perhaps, even other organs. We are only just starting to understand the long term impacts on survivors.
We use the term “influenza” to describe a whole range of viruses that cause respiratory like symptoms in their hosts. The coronavirus is part of this family, and while your organs, brain, and circulatory system are all at risk from it, it is still the lungs that are most likely to sustain serious damage from Covid-19, If it walks like a duck and quacks like a duck, even though it may have grown a few new feathers, it’s still a duck. Just a far more dangerous duck.
To have a context for the severity of influenza pandemics it might be helpful to know the death count of a typical flu season. Current estimates for the annual number of deaths from influenza are around 400,000 deaths per year. Paget et al (2019) suggest an average of 389,000 with an uncertainty range 294,000 from 518,000.
This means that in recent years (pre-Covid) the flu was responsible for the death of 0.0052% of the world population — one person out of 18,750. It is a number so negligible as to pay it no heed, which is exactly what flu became to us. A negligible concern. Unless you were old or suffered from a related condition that made contracting influenza potentially deadly, catching flu was simply an annoying part of life for most. Millions, possibly billions, were infected each year.
The interactive graph below shows our increase in life expectancy since the 1830s.
If the 1918 “Spanish Flu” pandemic estimates of 50 million deaths published by Johnson and Mueller are used, it implies that the Spanish flu killed 2.7% of the world population. If it was in fact higher, as the report suggests— 100 million— then the global death rate would have been 5.4% of the global population in 1918, estimated to have been around 1.8 billion.
In 2020, with over 140 million recorded births globally, you can see how even the 2 million deaths from Covid-19 cannot impact this curve. We have become too prolific and the old adage, “safety in numbers” may very well no longer count in our favor. Our proclivity for breeding and increased numbers merely offers viruses an untold wealth of opportunities.
Interestingly, as the graph shows, 1918 was the last time the world’s population experienced a contraction. In the last century, we’ve faced other influenza pandemics, but all have paled in comparison to the 1918 outbreak.
- The Russian Flu pandemic of 1977–78 was caused by the same H1N1 virus that caused the Spanish flu. According to Michaelis et al. (2009) around 700,000 died worldwide
- According to a WHO publication the “Hong Kong Flu” (1968–1969) killed between 1 and 4 million people
- Estimates for the death toll of the “Asian Flu” (1957–1958) vary between 1.5 and 4 million.
- Two decades before the Spanish flu the Russian flu pandemic (1889–1894) is believed to have killed 1 million people.
Viruses don’t just disappear. Take the H1N1 variant. Fifty years after the Spanish Flu pandemic, it was back. Reduced deaths can easily be attributed to our access to antibiotics, a relatively new medical tool to combat infections, and improved hygiene protocols. By the late seventies, we understood the nature of the enemy we were facing and how best to neutralize it.
So is the coronavirus flu, or isn’t it?
Yes, it is and no, it isn’t. In the strict sense of viral lineage, it is not an influenza virus. Both are enveloped, single-stranded RNA viruses, and both are encapsidated by nucleoprotein but there are fundamental differences between normal flu viruses and SARS-CoV2, notably the following;
- Polarity. The influenza virus is comprised of 8 single-stranded negative-sense, viral RNA segments. SARS-CoV-2 has single-stranded, non-segmented, positive-sense, viral RNA.
- Influenza viruses rely on the collaborative functions of 2 viral surface proteins, haemagglutinin (HA) and neuraminidase (NA) to enter and exit host cells. SARS-CoV-2 is covered in spike (S) proteins that facilitate invasion of host cells. S proteins bind to the host cell receptor, angiotensin-converting enzyme 2 (ACE2)
- Scientists also point to the different strains of Influenza viruses and the single strain of SARS-CoV-2. It is, however, early days and the mutations of the virus are now in evidence.
There is a very real possibility that SARS-CoV-2 will replace older influenza strains by establishing dominance in the host population (us). Failure to acknowledge this may be one of the reasons we’ve mishandled the pandemic so badly in terms of information and disseminating “need to know” details to the public. Trying to classify it as anything other than a new deadly strain of influenza may very well have hurt our efforts to contain it.
Rather than reclassifying it as its own deadly disease, we need to consider expanding our classification of influenza viruses to include it.
Yes, it is far more deadly than conventional strains of influenza, but as we’ve discussed, that doesn’t change its origins and nature and at some point, we may have to face the one glaring and unpleasant fact we’ve been avoiding.
The SARS-CoV-2 virus has supplanted influenza strains, replacing H1N1 and other common strains. and is now, officially, here to stay.
We need to deal with this unpleasant reality, adjust the public perception of the virus, and call a spade a spade. The virus will not magically disappear at some point in the near future. Everything we know about it suggests otherwise. It is mutating, frequently and rapidly and we are not going to simply wake up one morning to a world that is free of SARS-CoV-2. That is a pipedream and needs to be removed from the publics’ mindset.
SARS-CoV-2 is here to stay and we have to start working with that knowledge as the basis for our plans for the future. Medically, scientifically, economically, and as societies. We need to open up our world again and at the same time implement enforceable mandates for effective (not the current tea strainers we use) masks and social distancing.
Vaccines make up an integral part of our limited arsenal, but it is critical that they do not cause us to become complacent, that would be a false currency, given the nature of the virus and protection can be transient.
We need to start learning to co-exist with the new enemy, as we can no longer afford to try and “sit it out”. The virus doesn’t need to pay a mortgage our feed its children. We do and there are workable solutions we can implement to achieve this. We need to be addressing these now and with urgency.
SARS-CoV-2 has established itself as the top dog, and other common influenza strains will now take a back seat, waiting for it to show weakness. Perhaps in ten years, perhaps in fifty. When the opportunity presents, these “old familiars” will return, possibly exhibiting new tricks their years of isolation may have enabled. H1N1 is proof of their longevity, patience, and resilience.
We are directly responsible for many of these changes in viral behavior and viral evolution. Our drugs are not without impact on the viruses and we should never lose sight of the fact that for each countermeasure we deploy, viruses possess the ability to evolve and respond in kind. We need to be hyper-vigilant as our use of new technologies simply amplifies this risk.
Viruses have evolved and co-existed alongside us and our fates are, like it or not, inseparably intertwined.
We may also be dependant on viruses in ways we don’t yet fully understand. Our genetic code is in part comprised of bits of viral DNA amassed over generations, some of which are beneficial to our survival. This symbiotic relationship shouldn’t be ignored in our efforts to eradicate them. We need to examine ways of controlling and negating their impact on us as a species, rather than seeking to destroy them.
In our haste to counter, we may unleash a new strain that is far less tolerant of human life. To date, we’ve simply been lucky. We need to responsibly engineer our way to more good fortune and find ways to sustain this incredibly complex relationship in relative safety till we fully understand it. Only then can we seek to alter it.
So to re-examine our opening question again, you do know someone who contracted influenza this season, only it’s Covid-19, not the “normal flu” virus we would far rather have bumped into. It’s fair to say, considering this, that globally, the outlook for the 2021 “flu season” just became really bleak. It’s going to be a killer unless we act now to negate the impact of the SARS-CoV-2 virus. That means all of us, on the same page, acting cohesively and responsibly.
Spread the word. Killer flu on the loose! Get your flu (covid vaccine)shot, mask up and mind the gap.