TY - JOUR
T1 - Lockdowns exert selection pressure on overdispersion of SARS-CoV-2 variants
AU - Nielsen, Bjarke Frost
AU - Eilersen, Andreas
AU - Simonsen, Lone
AU - Sneppen, Kim
PY - 2022/9
Y1 - 2022/9
N2 - The SARS-CoV-2 ancestral strain has caused pronounced super-spreading events, reflecting a disease characterized by overdispersion, where about 10% of infected people causes 80% of infections. New variants of the disease have different person-to-person variations in viral load, suggesting for example that the Alpha (B.1.1.7) variant is more infectious but relatively less prone to superspreading. Meanwhile, mitigation of the pandemic has focused on limiting social contacts (lockdowns, regulations on gatherings) and decreasing transmission risk through mask wearing and social distancing. Using a mathematical model, we show that the competitive advantage of disease variants may heavily depend on the restrictions imposed. In particular, we find that lockdowns exert an evolutionary pressure which favours variants with lower levels of overdispersion. We find that overdispersion is an evolutionarily unstable trait, with a tendency for more homogeneously spreading variants to eventually dominate.Significance One of the most important and complex properties of viral pathogens is their ability to mutate. The SARS-CoV-2 pandemic has been characterized by overdispersion – a propensity for superspreading, which means that around 10% of those who become infected cause 80% of infections. However, evidence is mounting that this is not a stable property of the virus and that the Alpha variant spreads more homogeneously. We use a mathematical model to show that lockdowns exert a selection pressure, driving the pathogen towards more homogeneous transmission. In general, we highlight the importance of understanding how non-pharmaceutical interventions exert evolutionary pressure on pathogens. Our results imply that overdispersion should be taken into account when assessing the transmissibility of emerging variants.
AB - The SARS-CoV-2 ancestral strain has caused pronounced super-spreading events, reflecting a disease characterized by overdispersion, where about 10% of infected people causes 80% of infections. New variants of the disease have different person-to-person variations in viral load, suggesting for example that the Alpha (B.1.1.7) variant is more infectious but relatively less prone to superspreading. Meanwhile, mitigation of the pandemic has focused on limiting social contacts (lockdowns, regulations on gatherings) and decreasing transmission risk through mask wearing and social distancing. Using a mathematical model, we show that the competitive advantage of disease variants may heavily depend on the restrictions imposed. In particular, we find that lockdowns exert an evolutionary pressure which favours variants with lower levels of overdispersion. We find that overdispersion is an evolutionarily unstable trait, with a tendency for more homogeneously spreading variants to eventually dominate.Significance One of the most important and complex properties of viral pathogens is their ability to mutate. The SARS-CoV-2 pandemic has been characterized by overdispersion – a propensity for superspreading, which means that around 10% of those who become infected cause 80% of infections. However, evidence is mounting that this is not a stable property of the virus and that the Alpha variant spreads more homogeneously. We use a mathematical model to show that lockdowns exert a selection pressure, driving the pathogen towards more homogeneous transmission. In general, we highlight the importance of understanding how non-pharmaceutical interventions exert evolutionary pressure on pathogens. Our results imply that overdispersion should be taken into account when assessing the transmissibility of emerging variants.
KW - Overdispersion
KW - Evolution
KW - Superspreading
KW - Non-pharmaceutical interventions
KW - Overdispersion
KW - Evolution
KW - Superspreading
KW - Non-pharmaceutical interventions
U2 - 10.1101/2021.06.30.21259771
DO - 10.1101/2021.06.30.21259771
M3 - Journal article
SN - 1755-4365
VL - 40
JO - Epidemics
JF - Epidemics
M1 - 100613
ER -