Into the SARS-CoV-2 playgrounds: investigating the origins of the Belgian second wave, from an Antwerp perspective (preprint)

BackgroundBelgium has been struggling with a second pandemic wave caused by SARS-CoV-2. AimThe goal of this study was to estimate rates of carriership and viral loads in the general population in order to evaluate the dynamics leading to the second wave. MethodsSince the major Antwerp hospitals implemented extensive (pre-)admission SARS-CoV-2 screening of patients (eg. prior to elective surgery), they have gathered valuable information regarding the viral prevalence, incidence, and viral loads in the general population throughout the pandemic period. Prevalences and incidences were calculated and compared with available governmental data (numbers of positively tested and contacted cases). Major government coronavirus responses were taken into account. ResultsThe overall positivity rate of (pre)admission screenings was 1.3% (35.4% of positive cases carrying high viral loads). The highest prevalence of carriership was found in the elderly (2.6% for +80 y). 0-18 year-olds tested positive in 0.9% of cases. We estimated that, by extrapolation of cohort data, 20.3 % of the Antwerp population contracted the virus, whereas only 3.0 % was tested positive. In September, restriction measures were eased at a time when increased incidences were being observed. ConclusionThe estimation that only a small proportion of the positive cases (including cases with high viral loads) was detected and traced, in combination with a country-wide easing of restriction measures within a period of increasing incidences (and within an overall high base-line prevalence of the virus), were, in our opinion, the major drivers in the origin of the second pandemic wave.

Symptomatic SARS-CoV-2 re-infection of a health care worker in a Belgian nosocomial outbreak despite primary neutralizing antibody response. (preprint)

Background. It is currently unclear whether SARS-CoV-2 re-infection will remain a rare event, only occurring in individuals who fail to mount an effective immune response, or whether it will occur more frequently when humoral immunity wanes following primary infection. Methods. A case of re-infection was observed in a Belgian nosocomial outbreak involving 3 patients and 2 health care workers. To distinguish re-infection from persistent infection and detect potential transmission clusters, whole genome sequencing was performed on nasopharyngeal swabs of all individuals including the re-infection case's first episode. IgA, IgM, and IgG and neutralizing antibody responses were quantified in serum of all individuals, and viral infectiousness was measured in the swabs of the reinfection case. Results. Re-infection was confirmed in a young, immunocompetent health care worker as viral genomes derived from the first and second episode belonged to different SARS-CoV-2 clades. The symptomatic re-infection occurred after an interval of 185 days, despite the development of an effective humoral immune response following symptomatic primary infection. The second episode, however, was milder and characterized by a fast rise in serum IgG and neutralizing antibodies. Although contact tracing and virus culture remained inconclusive, the health care worker formed a transmission cluster with 3 patients and showed evidence of virus replication but not of neutralizing antibodies in her nasopharyngeal swabs. Conclusion. If this case is representative of most Covid-19 patients, long-lived protective immunity against SARS-CoV-2 might not be likely.