Citat:
Ja?Vi behöver andra markörer bara:
Neutralizing antibody response in non-hospitalized SARS-CoV-2 patients
214 A phenomenon that is critically discussed is the potential enhancement of infection by
215 non-neutralizing antibodies (ADE) (12). For our VNT-assays, we are using human cells
216 expressing a diverse set of Fc-receptors, and directly assess the rate of infected cells by
217 immunofluorescence or reporter-gene expression. Hence, we should be able to detect
218 enhancement of infection by serum that is not or only poorly neutralizing and in higher
219 dilution ranges. However, in none of our 49 sera we observed ADE at any of the dilutions
220 tested, indicating that at least antibodies generated in the natural context of SCoV2
221 infection do not contribute to severity of infection. This is in line with the absence of a
correlation between the number of symptoms and VNT50
222 in our patients (Fig. 2d). On the
223 other hand, our cohort is biased due to the fact that none of the patients was
224 hospitalized. Therefore, it will be important to analyze if ADE plays a potential role in
225 severe cases of COVID-19.
https://www.medrxiv.org/content/10.1101/2020.08.07.20169961v1.full.pdf
Neutralizing antibody response in non-hospitalized SARS-CoV-2 patients
/.../40 Altogether, we show that there is a wide breadth of antibody responses against SCoV2Intressant studie som faktiskt tar upp det där med förhastade slutsatser. Här att man kollar immunitet hos gruppen icke-hospitaliserade vilket begränsar studien enl. dem själva:
41 in patients that differentially correlate with virus neutralization. This highlights the
42 difficulty to define reliable surrogate markers for immunity against SCoV2.
214 A phenomenon that is critically discussed is the potential enhancement of infection by
215 non-neutralizing antibodies (ADE) (12). For our VNT-assays, we are using human cells
216 expressing a diverse set of Fc-receptors, and directly assess the rate of infected cells by
217 immunofluorescence or reporter-gene expression. Hence, we should be able to detect
218 enhancement of infection by serum that is not or only poorly neutralizing and in higher
219 dilution ranges. However, in none of our 49 sera we observed ADE at any of the dilutions
220 tested, indicating that at least antibodies generated in the natural context of SCoV2
221 infection do not contribute to severity of infection. This is in line with the absence of a
correlation between the number of symptoms and VNT50
222 in our patients (Fig. 2d). On the
223 other hand, our cohort is biased due to the fact that none of the patients was
224 hospitalized. Therefore, it will be important to analyze if ADE plays a potential role in
225 severe cases of COVID-19.
https://www.medrxiv.org/content/10.1101/2020.08.07.20169961v1.full.pdf
Men inga kliniska erfarenheter tyder ju på att ADE är någon kardinalkomplikation for COVID-19.