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This is a PDF file of a peer-reviewed paper that has been accepted for publication. Although unedited, the content has been subjected to preliminary formatting. Nature is providing this early version of the typeset paper as a service to our authors and readers. The text and figures will undergo copyediting and a proof review before the paper is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers apply.
The SARS-CoV-2 Omicron variant was first identified in November 2021 in Botswana and South Africa1,2. It has in the meantime spread to many countries and is expected to rapidly become dominant worldwide. The lineage is characterized by the presence of about 32 mutations in the Spike, located mostly in the N-terminal domain (NTD) and the receptor binding domain (RBD), which may enhance viral fitness and allow antibody evasion. Here, we isolated an infectious Omicron virus in Belgium, from a traveller returning from Egypt. We examined its sensitivity to 9 monoclonal antibodies (mAbs) clinically approved or in development3, and to antibodies present in 90 sera from COVID-19 vaccine recipients or convalescent individuals. Omicron was totally or partially resistant to neutralization by all mAbs tested. Sera from Pfizer or AstraZeneca vaccine recipients, sampled 5 months after complete vaccination, barely inhibited Omicron. Sera from COVID-19 convalescent patients collected 6 or 12 months post symptoms displayed low or no neutralizing activity against Omicron. Administration of a booster Pfizer dose as well as vaccination of previously infected individuals generated an anti-Omicron neutralizing response, with titers 5 to 31 fold lower against Omicron than against Delta. Thus, Omicron escapes most therapeutic monoclonal antibodies and to a large extent vaccine-elicited antibodies.
We report the complete genome sequence of a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant (lineage B.1.1.529) from a Belgian patient with a history of recent travel to Egypt. At the time of writing, this genome constituted the first confirmed case of an infection with the Omicron variant in Europe.
Standard contact tracing practice for COVID-19 is to identify persons exposed to an infected person during the contagious period, assumed to start two days before symptom onset or diagnosis. In the first large cohort study on backward contact tracing for COVID-19, we extended the contact tracing window by 5 days, aiming to identify the source of the infection and persons infected by the same source. The risk of infection amongst these additional contacts was similar to contacts exposed during the standard tracing window and significantly higher than symptomatic individuals in a control group, leading to 42% more cases identified as direct contacts of an index case. Compared to standard practice, backward traced contacts required fewer tests and shorter quarantine. However, they were identified later in their infectious cycle if infected. Our results support implementing backward contact tracing when rigorous suppression of viral transmission is warranted.
Testing and contact tracing are standard tools for controlling the spread of COVID-191. Their effectiveness hinges on a sequence of processes encompassing testing coverage and timeliness, testing quality and speed of reporting, contact tracing speed and comprehensiveness and compliance with advice given2–6. We optimized this sequence of processes in the context of a public health program targeting around 33,000 higher education students through a combination of low barrier PCR testing with rapid turn-around-time, close integration of testing and tracing teams and IT infrastructure, community engagement and the implementation of bidirectional contact tracing by extending the contact tracing window from 2 to 7 days before symptom onset or test of the index case. We anticipate this combined intervention to help improve epidemic control.
Despite ubiquitous rollout of contact tracing to counteract the spread of COVID-19, few countries have been spared from widespread community transmission, highlighting the need for more effective tracing strategies1,2. Standard contact tracing practice identifies, quarantines and tests persons exposed to an infected person during the contagious period, assumed to start two days before symptom onset or diagnosis3,4. Backward contact tracing intends to identify the source of the infection and persons infected by the same source, either by extending the contact tracing window or investigating suspected source events. These approaches have shown promise in modelling studies, but lack empirical data supporting their efficiency5–7. In the first large cohort study on backward contact tracing for COVID-19, we found that extending the contact tracing window backward by 5 days increased the number of identified contacts by 49.2%. The risk of infection amongst these additional contacts was similar to contacts exposed during the standard tracing window and significantly higher than symptomatic individuals in a control group, leading to an increase of 42.0% in cases identified through contact tracing. The risk was not limited to attendees of suspected source events. Our results imply an urgent need to implement backward contact tracing globally.
Currently, the real-life impact of indoor climate, human behaviour, ventilation and air filtration on respiratory pathogen detection and concentration are poorly understood. This hinders the interpretability of bioaerosol quantification in indoor air to surveil respiratory pathogens and transmission risk. We tested 341 indoor air samples from 21 community settings in Belgium for 29 respiratory pathogens using qPCR. On average, 3.9 pathogens were positive per sample and 85.3% of samples tested positive for at least one. Pathogen detection and concentration varied significantly by pathogen, month, and age group in generalised linear (mixed) models and generalised estimating equations. High CO2 and low natural ventilation were independent risk factors for detection. The odds ratio for detection was 1.09 (95% CI 1.03–1.15) per 100 parts per million (ppm) increase in CO2, and 0.88 (95% CI 0.80–0.97) per stepwise increase in natural ventilation (on a Likert scale). CO2 concentration and portable air filtration were independently associated with pathogen concentration. Each 100ppm increase in CO2 was associated with a qPCR Ct value decrease of 0.08 (95% CI −0.12 to −0.04), and portable air filtration with a 0.58 (95% CI 0.25–0.91) increase. The effects of occupancy, sampling duration, mask wearing, vocalisation, temperature, humidity and mechanical ventilation were not significant. Our results support the importance of ventilation and air filtration to reduce transmission.
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