The Meaning of a COVID-19 Second Wave

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I’ve been hearing the term “second wave” being used more and more frequently in connection with the COVID-19 crisis. For instance, in this article [1] about Singapore, Taiwan and Hong Kong facing a second wave of coronavirus cases from citizens returning from overseas. This seems faulty logic to me: it isn’t a second wave, it’s a continuation of the first wave relocating from a different geographical place. I don’t mean just to single out this article because numerous TV and radio newscasters, newspaper articles and websites worldwide are commonly using the same kind of wonky logic in connection with a so-called coronavirus second wave. When what they really mean is that the same source of the virus has either: (i)  lead to a continuation of cases from another location or (ii) made a reappearance after initial efforts for containment have only been partially successful.

Why do we describe resurgence in coronavirus cases in an inconsistent manner with the phrase “a second wave”? What has happened that we can’t agree on the meaning of a term that is so important to the coronavirus crisis?

My answer is after the page jump.

One answer is that for a true second wave we need an outbreak of coronavirus from a second source that is different (in some meaningful way) from the first source. All viruses mutate and show genetic drift. For the coronavirus, since the initial outbreak in Wuhan China, there is no suggestion that a new variant strain has become active. Therefore, my contention is that instead of saying, a “second wave,” rather we should be saying a “continuation” or a “resurgence” of coronavirus cases.

I might not be trained in virology or epidemiology but I’m trained to think scientifically and I make conscious efforts to ensure what I say is based upon factual research. Accordingly, my response to the question I raised above: the phrase “second wave” is indelibly written into our global emotional memory of the Spanish Flu pandemic of 1918-9 (as I’ll get to shortly). When a new crisis emerges, our emotional response outweighs a logical or scientific one. So we’ve stuck to using terminology which doesn’t convey a correct scientific meaning.

It’s my contention is that this needs to change: it’s time to settle upon a consistent meaning for what a “second wave” is. Journalists have an important role in setting a standard that the rest of the community can follow.

Q. Does it matter that “second wave” as a term is being scientifically misused?

For a full answer to this, I need to explain about the use of the term “second wave” during the Spanish Flu outbreak during 1918-9. This explanation will follow below.

The short answer is not much- at present. However, if at a future point there is a true second wave of coronavirus then the phrase “second wave” will have lost much of its meaning. Very likely we’ll fail to heed the warning or shake off our complacency. In that event, incorrect terminology will have had a major negative impact on our response to the threat.

Spanish Flu of 1918-9

The Spanish Flu started in March 1918, lasted two years, infected up to 500 million people worldwide (around ⅓-rd of the world population at the time), of which up to 50 million died, This was more than the total fatalities during the preceding 4 years of WWI [2]. The initial spread of the virus was thought to be brought about by soldiers returning after WWI. The first infections in the United States weren’t particularly deadly. but that changed, during a horrific 3-month period during the fall-autumn which become known as the “second wave.” The second wave spread around the world (affecting NSW Australia in two high-mortality waves during 19/3/1919–27/5/1919 and 28/5/1919–30/9/1919  [3]).

From the above paragraph, you can readily see how the severity of the second wave of the Spanish Flu has etched its way into the collective memory of succeeding generations. Naturally, when coronavirus outbreaks occurred in early 2020 it raised fears in the minds of many that an even more deadly second wave was looming a few months down the track.

There were third and successive waves as of infection as well. In America, the third wave [2] occurred during the summer of 1919 and was almost as severe as the second wave. Outbreaks after the third wave became progressively weaker and until the virus simply disappeared into the endemic background of seasonal influenza.

Replication of the Virus within Cells

A virus consists of a few proteins and some genetic material. Their apparent simplicity disguises a sophisticated strategy to subvert the molecular machinery of the host cells that they evade and turn them into nanoscale manufacturing centres for producing more virus. This process is known as viral replication.  If you’re looking the understand viruses in more depth I recommend “Molecular and Cellular Biology of Viruses” by Phoebe Lostroh, a rather technical but beautifully illustrated textbook on the subject [4].

The influenza virus is typically subject to high rates of mutation. For Influenza, each replication can result in one mutation per offspring genome. Resulting in a number of somewhere around 10,000 mutated offspring for each infected cell. This gives ample opportunity for natural selection and genetic drift to lead to a significant range of diversity in the virus over a time span of several months to a year or two. It’s this diversity, and the appearance of deadly new strains of the virus, behind the second and third waves in the Flu of 1918-9.

Mutations give rise to a relatively slow rate of viral diversity referred to as genetic drift. [As an important side note: genetic drift should be distinguished from genetic shift which can occur if two viruses infect the same cell. In this case, some of the offspring will have recombined genome sequences from each of the parent viruses. Genetic shift is of greater concern, because there is the potential for a pandemic, since the immune response for one or other of the parent viruses will not be effective against the offspring (see Ref 4, p430-1)].

By way of contrast, there are strong reasons to believe that coronaviruses have a molecular proofreading mechanism which corrects misincorporated genetic information from being passed on to the next generation (as is illustrated in Ref 4. pg 157).  hence genetic drift occurs at a significantly lower rate for coronaviruses than for influenza.

Because of a lower rate of mutation, it is unlikely that we’ll see the same kind of the second wave of the coronavirus infections in 2020 as occurred in the Spanish influenza of 1918-9. Any resurgence in infections will likely be the result of human error in failure to contain the virus or from allowing people to spread the virus by travelling across regions. This shouldn’t be called a “second wave” because that term implies that something unexpected has happened with the virus itself (i.e., that it has mutated).

Our fears that the worse of the coronavirus is just around the corner in a second wave is misplaced. On the other hand, the coronavirus is likely to remain for around for a long time. It’s unlikely to weaken in the way that the Spanish Flu did after 1919. The coronavirus of 2020 and the H1N1 Influenza of 1918-9 are distinctly different kinds of beasts,


[1] Liza Lin and Joyu Wang, The Wall Street Journal, “Singapore, Taiwan and Hong Kong Face Second Wave of Coronavirus Cases,” published: 17th March 2020, accessed: 23 March 2020, available online (subscription based):

[2] Dave Roos, History, “Why the Second Wave of the 1918 Spanish Flu Was So Deadly,” published: 03 March 2020, accessed: 23 March 2020, available online:

[3] NSW State Archives and Records, “Pneumonic Influenza (Spanish Flu), 1919,” accessed: 24 March 2020, available online:

[4] Phoebe Lostroh, “Molecular and Cellular Biology of Viruses” CRC Press, Taylor and Francis Group, Boca Raton, FL (2019).

Updated: 22nd August, 2020 because I thought that the article was important enough to receive wider circulation. So I submitted it to The Guardian for  publication.

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