My idea is that strict lockdowns put greater evolutionary pressure on the coronavirus by restricting oppurtunities to be transmitted, meaning that a faster-spreading variant had much less competition.

Is this at all plausible? Was it just as likely for a faster-spreading variant to become the predominant one without lockdowns?

  • $\begingroup$ It's actually a complicated trade-off between the total amount of time that the virus has time to mutate and number of hosts it can mutate in. You've basically selected the wrong answer. aliential's answer links to a paper that does this sort of (non-trivial) analysis. I'll also note there that it's much harder to quantify the chance that rare "human lab" events can occur, which are thought to be at the origin of the latest UK variant of concern. virological.org/t/… $\endgroup$ – Fizz Jan 10 at 18:46
  • $\begingroup$ Okay, I guess that I am not going to select an answer, as I am not really qualified to judge. That answer made sense to me at the time. $\endgroup$ – kCODINGeroo Jan 11 at 19:23
  • $\begingroup$ @kCODINGeroo Why do you ask a question if you aren't qualified to accept an answer? Only you as the original poster can accept an answer. $\endgroup$ – David Jonsson Feb 14 at 6:22

While I get your intuition, the hypothesis seems implausible

  • Emerge of new CoV variants should be considered proportional to the current spread of the virus. Each virus has a certain mutation rate that surely does not depend on lock-downs.
  • It seems implausible to interpret lock-downs as physical limitations to viral spread, that could potentially be overcome by any mutation.
  • Even if CoV magically learned to teleport to different households, such an ability would always represent immense advantages; an advantage that does not need lock-downs to be effective
  • Lastly, the differential viral competition is neglectable so far; we are at 6 of 100 thousand infected persons. So basically a 0% chance that a virus would infect a person who has acquired an immunity due to a previous CoV infection. In your model this person, who is immune, further would need to NOT be immune because quarantine prevented the (previous) infection.

This is more plausible (second point below) and less plausible (third point below).

  • Selective advantage The emergence of a new strain of a virus relates to the selective advantage (Gordo 2009). This selective advantage might be that the reproduction rate is relatively higher.

  • Reproduction rate The selective advantage (in terms of relative growth rate) is based on the relative growth rate of the virus. Because the growth rate for viruses is not directly proportional to the reproduction rate (Wallinga 2009), this means that better selective advantage is not exactly the same as better reproduction rate (and that is just the selective advantage due to reproduction rate). Instead, it is more like related to the reproduction rate minus one. The relative (initial) growth rate of the mutated virus (made dimensionless by multiplying with generation time) gives the relative growth factor $$\text{growthrate} \times \text{generation time} = \overbrace{s}^{\text{selective advantage}} = R_{mutant}- R_{other}$$ If you have some mutation that gives an improved effective reproduction factor $R_{mutant}/R_{other} = c$ then the difference $R_{mutant}- R_{other}$ will be larger for a larger $R_{other}$. This is not the case with a lockdown ($R$ will be typically lower) and in a situation with a specific ratio $R_{mutant}/R_{other} = c$ the relative growth of the mutant will be smaller if $R_{other}$ is lower

  • What makes reproduction rate higher? There is a small catch with this second point (from which you could conclude that growth of new strains is higher without lockdowns). Another non-linearity is that the reproduction rate is not scaling linearly with the infectivity of the virus.

    For instance Ferrari et.al. (2006) model the probability of infection as an exponential function of the rate of transmission

    The susceptible nodes become infected in the next time-step with binomial probability 1−exp(−βI), where β is the rate of transmission across an edge, and I is the number of infected nodes to which the individual is connected.

    The infections are a function of time and proximity (and also the susceptibility and infectiousness of people), and this is not homogeneously distributed. This makes that a simple reduction of 'infectivity' by half is not at the same time also making the effective reproduction rate become halved.

    You could see the reproduction number being buffered in some sense. There is an excess/overflow of transmission in some parts of the network. When you are sick, then most likely your family members are gonna get sick as well. When the virus becomes half less transmissible, then it is not like only half your family members are gonna get sick. Reducing the transmissibility might have an effect for short-term contacts (which are important pathways as well), but it is of less influence for intensive contacts.

    This buffering makes that the transmissibility of the virus (the reproduction rate) is not so much controlled by the changes in the properties of the virus. The transmission is more controlled by the human traffic and contact network (and the fluctuations occurring within this network/traffic). If an average person sees, on average, only 3 people within the infectious period, then the basic reproduction number will be at most 3 and it can't suddenly make a big jump. You can not infect more than 3 people if you do not see more than 3 people, so the virus can become more transmissible but it won't influence the reproduction rate 'as much' (unless there is an entirely different mode of transport). (I am putting stress on 'as much' because there will be some influence, just like adding acid to a buffer will not have zero effect, but it just won't be the same)

    Any growth of small mutations in new strains is (initially) more likely to be occurring randomly. Viruses mutate a lot, and there will a lot of probability that there is a lucky sample (many others will be unlucky) that might accidentally reach some area with a fast growth rate and with little competition (isolation from competition is a good, but also likely, route for a non-competitive mutation to grow in number). This randomness becomes larger when the total numbers are smaller. If a new strain hits a (relatively) clean area then it will spread out without any/much competition and it can become big (especially if it is an area without much control) and spread over a large area unnoticed.

    This isolation might be more likely in a scenario with strict lockdowns, which makes the spread of the virus more chaotic (it's like rolling a dice a few times, you'll be more likely to get the same number with a high frequency in comparison to rolling the dice often; the lockdowns make the spread dependent on fewer dice rolls and give more chances to some mutation to slip through, reach some prosperous less lock downed area, and become more dominant)

So, in general there is no clear influence from a lockdown. In general the emergence of new variants relates to Fisher's fundamental theorem of natural selection

  • "The rate of increase in fitness of any organism at any time is equal to its genetic variance in fitness at that time."

The second point above (lower fitness/growth-rate results in lower natural selection) relates to the fact that it we reduce the fitness with a factor $c<1$ by a lockdown, than the variance of the fitness changes by a factor $c^2$. The change of the fitness will scale with $c^2$ and the relative change of the fitness will change with $c$.

The third point above relates to a breaking of the assumptions (there's no homogeneous spread of the virus). Breakdowns can create relatively separate/isolated regions and the spread may not be via a Malthusian growth model but instead more chaotic (with random branches like a thunder bolt). This makes it not unthinkable that a variant emerges quickly by a random effect and without much difference in selective advantage.

Some references


Current Biology 30, R841–R870, August 3, 2020 R857, does support some of your theory.

The paper summarizes the scientific basis of their statements:

Even though the adaptive significance of genetic variants remains to be established, we can use evolutionary theory to gain insights about how natural selection might act on disease characteristics.

The mutation rate is related to the population size which has stayed nearly as high this winter as it was with dense crowds previously, regardless of distancing, so the following statement is all the more likely,

some mutations may become more strongly selected in the presence of social distancing if they allow for viral transmission despite the intervention (for example, mutations affecting aerosolization or persistence in the environment).

i.e. physical distancing will select for better breach of distancing, and quarantineing will select for higher transmission during the asymptomatic days prior to fever.

The transmission methods aren't very well know, i.e. asymptomatic transission, transmission by children, peak transmission before symptoms appear, rates of contact Vs airborn transmission.

So, you are right, distancing encourages mutants that reproduce and transmit despite distancing tactics.


Do lockdowns help new mutations emerge? - No.
Mutations appear at an approximately constant rate in every genome replucation event. In this sense, the lockdowns reduced the overall number of mutations, by reducing the number of infections and new replucation events.

Could lockdowns help new mutations become prevalent? - Possibly. Whether a new mutation survives and becomes widespread depends on its fitness, vis-à-vis the adverse environment in which the virus exists. The more contagious viral strain has a selective advantage over the other strains. The speed with which such a strain pushes out the other strains out of the existence, i.e., the time that it needs to fix in the population, depends on the effective population size. In this respect, lockdown resulted in reducing the effective population size, which could have resulted in faster fixation of the more contagious strain. (It is important to keep in mind that the lockdown wasn't waterproof - the virus was still spreading, although at a lower pace.)

In other words, the lockdown could have acted as an evolutionary bottleneck, reducing the viral diversity at the expense of the less fit strains.

Has this really happened? - No. We are not dealing with this situation, but rather with a viral strain that has emerged only recently, which is certainly far from having fixed in the population. One cannot even be sure that it has a selective advantage - it is more contagious, but may have other, yet unknown, shortcomings.

If the new strain does have selective advantage, the future lockdowns might "help" it to become the dominant strain. This shows that lockdowns are not sufficient to eradicate a virus - as opposed to completely quarantining/isolating whole groups of population, as was done in China or during the Ebola outbreaks. Eradicating the virus however never was the point of the lockdowns: they were implemented to slow down its spread, so that it does not overwhelm healthcare systems, so that effective testing procedures could be put in place, and to allow time for developing vaccines.


You are the victim of the "post hoc ergo propter hoc" fallacy: just because event B follows event A doesn't mean that B is caused by A. The probability of a mutation to occur depends on the number of virions out there multiplied with some constant that models the faithfulness of the virus reproduction machinery. The lock-down was instituted because the number of infected persons - and hence virions - was high. Thus, both the lock-down and the occurrence of mutations share the same cause, one of the possible reasons for nonsense correlations.

  • $\begingroup$ I don't think the question makes any claims (and thus commits a fallacy) - it is more an inquiry about a possible relation between two events. Also, emergence of a new strain depends not only on the availability of mutations, but also on the evolutionary pressures, the random drift, the population structure - all of which were affected by a lockdown. $\endgroup$ – Vadim Jan 15 at 11:00
  • $\begingroup$ The OP - whether formulated as question or as statement - contains a hypothesis. This hypothesis is based on a nonsense correlation. And the probability of a mutation arising depends on the factors I mentioned; the factors you named determine whether this mutation can spread. $\endgroup$ – Engelbert Buxbaum Jan 16 at 7:59
  • $\begingroup$ the OP is asking about the emergence and spread of the new strsin, not just about a mutation. In fact, they even do not mention mutations. $\endgroup$ – Vadim Jan 16 at 8:44

The question asks about some advantage of a "fast" spreading virus. By intuition a population of not infected individuals spared out by lock-downs seems like some "open field" a fast virus might run through unhindered, then impeding other strains by some kind of pre-established dominance.

However trivial that may appear, the allegory of a fast run through open fields is able to suggest


to be considered when answering the question, as in any case there are different strains of virus involved.

It is difficult to find any resources on how to infer from empirical findings of super-infection to selective advantages for "faster" spreading variants.

According to primary resource Wikipedia, however, there is a caveat to use of terminology:


"(...) In virology, the definition is slightly different. Superinfection is the process by which a cell that has previously been infected by one virus gets co-infected with a different strain of the virus (...)"

whereas with bacteria any co-infection does imply resistance of one species to the antibiotic that is efficient against the other one is ecluded from the definition of "super-infection".

The definition of the term super-infection thus leads to distinguishing the concept of super-infection (i.e being infected by two or several strains of the virus at the same time) from the concept of


(Let's say the faster variant did its spread, thus having induced immunity that is effective against the slower variant lagging behind). Understanding the logics of super-infectivity in respect of cross-immunity needs differentiating infectiousness of disease against symptomatic disease. i.e. understanding "spreading the disease while not getting sick", cp. Explain asymptomatic viral infection (ie covid) with no symptoms

However, there is proof that super-infection with multiple variants of CoV-19 exists, compare:

Sashittal, Characterization of SARS-CoV-2 viral diversity within and across hosts https://www.biorxiv.org/content/10.1101/2020.05.07.083410v1.full

CoV2 turned out to be able to mutate to a "superinfectant variant":


Assuming that a fast variant has some advantage in a still healthy, uninfected population after lockdown ended implicitly assumes that any existing infections and immunities that had been induced would impede and inhibit any "slower", less infectious strain.

This is debatable, in my opinion it isn't so. There does exist "super-infection" by different strains of CoV-19 in one and the same individuals. This was proved by empirical studies (see reference above), which showed antigen of different i.e. of potentially faster and slower strains in probes taken from one and the same individuals.

What does make a variant "faster"?

Of a "faster" variant may be known that it is more infectious, yet not more dangerous. It is not better enduring underneath the radiation of the sun (to be neglected), but some higher replication rate that results in higher viral loads which lead to "faster" infections as they spread among a population. "Faster" is to be seen in the time needed for more individuals to be infected. Speed thus becomes infectiousness.

Cross-immunity even if it existed thus may more easily be understood as "lagging behind" the infectivity of super-infection. In super-infection highly contagious variants and less replicating co-exist and are transmitted "in sum".

Even if a "faster" variant did induce effective cross-immunity that needs not to exclude super-infection in the sense of transmitting the disease as a multi-strain infection. One person being super-infected is able to transmit several strains that simultaneously replicate in the person infected.

Super-infection implies that the higher infectious (named "faster") variant induces symptomatic disease and is transmitte together wit w the slower variant which is only transmitted and does not become virulent in infected persons.

Even if there were cross-immunity of a faster against a slower variant a spread of a super-infection is possible, as according to basic knowlege immunity arises with time lag (and there exists symptomless transmittance). To put it simple: cross-immunity arises with the disease, however infection happens before symptoms of the diseasem hence cross-immunity, arise.

My argument in a nutshell:

  1. Super-infection has been proven, hence no cross-immunity or other mechanism that would hinder co-existance of variants

  2. "Fastness" translates to higher viral loads of the more infectious strain which, counterintuitively, does not exlude the simulataneous transfer of less infectious strains.

Thus, in my opinion lockdowns in their effect of sparing healthy individuals from infection do not cause and are not the reason for a selective advantage of "faster" spreading strains, as super-infection was proved, implying that a higher infectious strain does not out-compete the less infectious strain it is transmitted along with.

Further information on super-infection and inhibition of competing strains as the opposite scenario see:

Berngruber, Inhibition of Superinfection and the Evolution of Viral Latency "(...) when superinfection inhibition and resistance against it coevolve in an arms race (...)"

Some other referene: https://jvi.asm.org/content/84/19/10200


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