A Preceding Low-virulence Strain Pandemic Inducing Immunity Against COVID-19 (preprint)

Abstract The COVID-19 pandemic is thought to began in Wuhan, China in December 2019. Mobility analysis identified East-Asia and Oceania countries to be highly-exposed to COVID-19 spread, consistent with the earliest spread occurring in these regions. However, here we show that while a strong positive correlation between case-numbers and exposure level could be seen early-on as expected, at later times the infection-level is found to be negatively correlated with exposure-level. Moreover, the infection level is positively correlated with the population size, which is puzzling since it has not reached the level necessary for population-size to affect infection-level through herd immunity. These issues are resolved if a low-virulence Corona-strain (LVS) began spreading earlier in China outside of Wuhan, and later globally, providing immunity from the later appearing high-virulence strain (HVS). Following its spread into Wuhan, cumulative mutations gave rise to the emergence of an HVS, known as SARS-CoV-2, starting the COVID-19 pandemic. We model the co-infection by an LVS and an HVS, and show that it can explain the evolution of the COVID-19 pandemic and the non-trivial dependence on the exposure level to China and the population-size in each country. We find that the LVS began its spread a few months before the onset of the HVS, and that its spread doubling-time is ∼ 1.59 ± 0.17 times slower than the HVS. Although more slowly spreading, its earlier onset allowed the LVS to spread globally before the emergence of the HVS. In particular, in countries exposed earlier to the LVS and/or having smaller population-size, the LVS could achieve herd-immunity earlier, and quench the later-spread HVS at earlier stages. We find our two-parameter (the spread-rate and the initial onset time of the LVS) can accurately explain the current infection levels (R^2=0.74; correlation p-value (p) of 5x10^-13 ). Furthermore, countries exposed early should have already achieved herd-immunity. We predict that in those countries cumulative infection levels could rise by no more than 2-3 times the current level through local-outbreaks, even in the absence of any containment measures. We suggest several tests and predictions to further verify the double-strain co-infection model and discuss the implications of identifying the LVS.

A preceding low-virulence strain pandemic inducing immunity against COVID-19 (preprint)

Countries highly exposed to incoming traffic from China were expected to be at the highest risk of COVID-19 spread. However, COVID-19 case numbers (infection levels) are negatively correlated with incoming traffic-level. Moreover, infection levels are positively correlated with population-size, while the latter should only affect infection-level once herd immunity is reached. These could be explained if a low-virulence strain (LVS) began spreading a few months earlier from China, providing immunity from the later emerging known SARS-CoV-2 high-virulence strain (HVS). We find that the dynamics of the COVID-19 pandemic depend on the LVS and HVS spread doubling-times and the delay between their initial onsets. We find that LVS doubling-time to be $T_L\sim1.59\pm0.17$ times slower than the HVS ($T_H$), but its earlier onset allowed its global wide-spread to the levels required for herd-immunity. In countries exposed earlier to the LVS and/or having smaller population-size, the LVS achieved herd-immunity earlier, allowing less time for the spread of the HVS, and giving rise to lower HVS-infection levels. Such model accurately predicts a country's infection-level ({\rm R^{2}=0.74}; p-value of {\rm 5.2\times10^{-13}}), given only its population-size and incoming-traffic from China. It explains the negative correlation with incoming-traffic ($c_{exp}$), the positive correlation with the population size (n_{pop}) and their specific relations (${\rm N}_{{\rm cases}}\propto n_{pop}^{{\rm T_{L}/{\rm T_{H}}}}\times c_{exp}^{{\rm T_{L}/{\rm T_{H}-1}}}$). We find that most countries should have already achieved herd-immunity. Further COVID-19-spread in these countries is limited and is not expected to rise by more than a factor of 2-3. We suggest tests/predictions to further verify the model and biologically identify the LVS, and discuss the implications.

A preceding low-virulence strain pandemic inducing immunity against COVID-19 (preprint)

The COVID-19 pandemic is thought to began in Wuhan, China in December 2019. Mobility analysis identified East-Asia and Oceania countries to be highly-exposed to COVID-19 spread, consistent with the earliest spread occurring in these regions. However, here we show that while a strong positive correlation between case-numbers and exposure level could be seen early-on as expected, at later times the infection-level is found to be negatively correlated with exposure-level. Moreover, the infection level is positively correlated with the population size, which is puzzling since it has not reached the level necessary for population-size to affect infection-level through herd immunity. These issues are resolved if a low-virulence Corona-strain (LVS) began spreading earlier in China outside of Wuhan, and later globally, providing immunity from the later appearing high-virulence strain (HVS). Following its spread into Wuhan, cumulative mutations gave rise to the emergence of an HVS, known as SARS-CoV-2, starting the COVID-19 pandemic. We model the co-infection by an LVS and an HVS and show that it can explain the evolution of the COVID-19 pandemic and the non-trivial dependence on the exposure level to China and the population-size in each country. We find that the LVS began its spread a few months before the onset of the HVS and that its spread doubling-time is \sim1.59\pm0.17 times slower than the HVS. Although more slowly spreading, its earlier onset allowed the LVS to spread globally before the emergence of the HVS. In particular, in countries exposed earlier to the LVS and/or having smaller population-size, the LVS could achieve herd-immunity earlier, and quench the later-spread HVS at earlier stages. We find our two-parameter (the spread-rate and the initial onset time of the LVS) can accurately explain the current infection levels (R^2=0.74); p-value (p) of 5.2x10^-13). Furthermore, countries exposed early should have already achieved herd-immunity. We predict that in those countries cumulative infection levels could rise by no more than 2-3 times the current level through local-outbreaks, even in the absence of any containment measures. We suggest several tests and predictions to further verify the double-strain co-infection model and discuss the implications of identifying the LVS.