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1.
Preprint em Inglês | medRxiv | ID: ppmedrxiv-22270494

RESUMO

BackgroundDuring the first two years of the COVID-19 pandemic, the circulation of seasonal influenza viruses was unprecedentedly low. This led to concerns that the lack of immune stimulation to influenza viruses combined with waning antibody titres could lead to increased susceptibility to influenza in subsequent seasons, resulting in larger and more severe epidemics. MethodsWe analyzed historical influenza virus epidemiological data from 2003-2019 to assess the historical frequency of near-absence of seasonal influenza virus circulation and its impact on the size and severity of subsequent epidemics. Additionally, we measured haemagglutination inhibition-based antibody titres against seasonal influenza viruses using longitudinal serum samples from 165 healthy adults, collected before and during the COVID-19 pandemic, and estimated how antibody titres against seasonal influenza waned during the first two years of the pandemic. FindingsLow country-level prevalence of influenza virus (sub)types over one or more years occurred frequently before the COVID-19 pandemic and had relatively small impacts on subsequent epidemic size and severity. Additionally, antibody titres against seasonal influenza viruses waned negligibly during the first two years of the pandemic. InterpretationThe commonly held notion that lulls in influenza virus circulation, as observed during the COVID-19 pandemic, will lead to larger and/or more severe subsequent epidemics might not be fully warranted, and it is likely that post-lull seasons will be similar in size and severity to pre-lull seasons. FundingEuropean Research Council, Netherlands Organization for Scientific Research, Royal Dutch Academy of Sciences, Public Health Service of Amsterdam. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSDuring the first years of the COVID-19 pandemic, the incidence of seasonal influenza was unusually low, leading to widespread concerns of exceptionally large and/or severe influenza epidemics in the coming years. We searched PubMed and Google Scholar using a combination of search terms (i.e., "seasonal influenza", "SARS-CoV-2", "COVID-19", "low incidence", "waning rates", "immune protection") and critically considered published articles and preprints that studied or reviewed the low incidence of seasonal influenza viruses since the start of the COVID-19 pandemic and its potential impact on future seasonal influenza epidemics. We found a substantial body of work describing how influenza virus circulation was reduced during the COVID-19 pandemic, and a number of studies projecting the size of future epidemics, each positing that post-pandemic epidemics are likely to be larger than those observed pre-pandemic. However, it remains unclear to what extent the assumed relationship between accumulated susceptibility and subsequent epidemic size holds, and it remains unknown to what extent antibody levels have waned during the COVID-19 pandemic. Both are potentially crucial for accurate prediction of post-pandemic epidemic sizes. Added value of this studyWe find that the relationship between epidemic size and severity and the magnitude of circulation in the preceding season(s) is decidedly more complex than assumed, with the magnitude of influenza circulation in preceding seasons having only limited effects on subsequent epidemic size and severity. Rather, epidemic size and severity are dominated by season-specific effects unrelated to the magnitude of circulation in the preceding season(s). Similarly, we find that antibody levels waned only modestly during the COVID-19 pandemic. Implications of all the available evidenceThe lack of changes observed in the patterns of measured antibody titres against seasonal influenza viruses in adults and nearly two decades of epidemiological data suggest that post-pandemic epidemic sizes will likely be similar to those observed pre-pandemic, and challenge the commonly held notion that the widespread concern that the near-absence of seasonal influenza virus circulation during the COVID-19 pandemic, or potential future lulls, are likely to result in larger influenza epidemics in subsequent years.

2.
Preprint em Inglês | medRxiv | ID: ppmedrxiv-20155572

RESUMO

Transmission of SARS-CoV-2 leading to COVID-19 occurs through exhaled respiratory droplets from infected humans. Currently, however, there is much controversy over whether respiratory aerosol microdroplets play an important role as a route of transmission. By measuring and modeling the dynamics of exhaled respiratory droplets we can assess the relative contribution of aerosols in the spreading of SARS-CoV-2. We measure size distribution, total numbers and volumes of respiratory droplets, including aerosols, by speaking and coughing from healthy subjects. Dynamic modelling of exhaled respiratory droplets allows to account for aerosol persistence times in confined public spaces. The probability of infection by inhalation of aerosols when breathing in the same space can then be estimated using current estimates of viral load and infectivity of SARS-CoV-2. In line with the current known reproduction numbers, our study of transmission of SARS-CoV-2 suggests that aerosol transmission is an inefficient route, in particular from non or mildly symptomatic individuals.

3.
Preprint em Inglês | medRxiv | ID: ppmedrxiv-20086439

RESUMO

In the current COVID-19 pandemic a key unsolved question is the duration of acquired immunity in recovered individuals. The recent emergence of SARS-CoV-2 precludes a direct study on this virus, but the four seasonal human coronaviruses may reveal common characteristics applicable to all human coronaviruses. We monitored healthy subjects over a time span of 35 years (1985-2020), providing a total of 2473 follow up person-months, and determined a) the time to reinfection by the same seasonal coronavirus and b) the dynamics of coronavirus antibody depletion post-infection. An alarmingly short duration of protective immunity to coronaviruses was found. Reinfections occurred frequently at 12 months post-infection and there was for each virus a substantial reduction in antibody levels as soon as 6 months post-infection.

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