The ongoing pandemic of SARS-CoV-2 presents novel challenges and opportunities for the use of phylogenetics to understand and control its spread. Here, we analyze the emergence of SARS-CoV-2 in Russia in March and April 2020. Combining phylogeographic analysis with travel history data, we estimate that the sampled viral diversity has originated from at least 67 closely timed introductions into Russia, mostly in late February to early March. All but one of these introductions were not from China, suggesting that border closure with China has helped delay establishment of SARS-CoV-2 in Russia. These introductions resulted in at least 9 distinct Russian lineages corresponding to domestic transmission. A notable transmission cluster corresponded to a nosocomial outbreak at the Vreden hospital in Saint Petersburg; phylodynamic analysis of this cluster reveals multiple (2-3) introductions each giving rise to a large number of cases, with a high initial effective reproduction number of 3.0 [1.9, 4.3].

The ongoing pandemic of SARS-CoV-2 presents novel challenges and opportunities for the use of phylogenetics to understand and control its spread. Here, we analyze the emergence of SARS-CoV-2 in Russia in March and April 2020. Combining phylogeographic analysis with travel history data, we estimate that the sampled viral diversity has originated from 67 closely timed introductions into Russia, mostly in late February to early March. All but one of these introductions came from non-Chinese sources, suggesting that border closure with China has helped delay establishment of SARS-CoV-2 in Russia. These introductions resulted in at least 9 distinct Russian lineages corresponding to domestic transmission. A notable transmission cluster corresponded to a nosocomial outbreak at the Vreden hospital in Saint Petersburg; phylodynamic analysis of this cluster reveals multiple (2-4) introductions each giving rise to a large number of cases, with a high initial effective reproduction number of 3.7 (2.5-5.0).

Geographical variation in severe acute respiratory syndrome coronavirus 2 (SARS­‐CoV­‐2) spread requires seroprevalence studies based on local tests, but robust validation is needed. We summarize an evaluation of antibody tests used in a serological study of SARS‐­CoV­‐2 in Saint Petersburg, Russia. We validated three different antibody assays: chemiluminescent microparticle immunoassay (CMIA) Abbott Architect SARS‐­CoV­‐2 immunoglobulin G (IgG), enzyme­ linked immunosorbent assay (ELISA) CoronaPass total antibodies test, and ELISA SARS­‐CoV‐­2‐­IgG‐­EIA‐­BEST. Clinical sensitivity was estimated with the SARS­‐CoV­‐2 polymerase chain reaction (PCR) test as the gold standard using manufacturer recommended cutoff. Specificity was estimated using pre­pandemic sera samples. The median time between positive PCR test results and antibody tests was 21 weeks. Measures of concordance were calculated against the microneutralization test (MNA).Sensitivity was equal to 91.1% (95% confidence intervbal [CI]: 78.8–97.5), 90% (95% CI: 76.4–96.4), and 63.1% (95% CI [50.2–74.7]) for ELISA Coronapass, ELISA Vector­Best, and CMIA Abbott, respectively. Specificity was equal to 100% for all the tests. Comparison of receiver operating characteristics has shown lower AUC for CMIA Abbott. The cut­off SC/O ratio of 0.28 for CMIA Abbott resulted in a sensitivity of 80% at the same level of specificity. Less than 33% of the participants with positive antibody test results had neutralizing antibodies in titers 1:80 and above. Antibody assays results and MNA correlated moderately. This study encourages the use of local antibody tests and sets the reference for seroprevalence correction. Available tests' sensitivity allows detecting antibodies within the majority of PCR­ positive individuals. The Abbott assay sensitivity can be improved by incorporating a new cut­off. Manufacturers' test characteristics may introduce bias into the study results.

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