Supplementary data == The following is the Supplementary data to this article: == Recommendations == == Associated Data == This section collects any data citations, data availability statements, or supplementary materials included in this article

Supplementary data == The following is the Supplementary data to this article: == Recommendations == == Associated Data == This section collects any data citations, data availability statements, or supplementary materials included in this article. == Supplementary Materials ==. different SARS-CoV-2 genomes both belonging to clade 20A, with only one nonsynonymous mutation in the spike protein and clustered with viruses circulating in Geneva (Switzerland) at the time of each of the corresponding episodes. Seroconversion was documented with low levels of total Ig antiS RBD and anti-N antibodies at 1 month after the first contamination, whereas neutralizing antibodies quickly declined after the first episode and then were boosted by the reinfection, with high titres detectable 4 days after symptom onset. A strong memory B-cell response was detected at day 12 after onset of symptoms during reinfection, indicating that the first episode elicited cellular memory responses. == Conclusions == Rapid decline of neutralizing antibodies may put medical personnel at risk of reinfection, as shown in this case. However, reinfection prospects to a significant boosting of previous immune responses. Larger cohorts of reinfected subjects with detailed descriptions of their immune responses are needed to define correlates of protection and their duration after contamination. Keywords:COVID-19, Immunity, Reinfection, SARS-CoV-2, Sequencing == Introduction == Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfection has been described as soon as 2 months after an initial coronavirus disease 2019 (COVID-19) episode [1]. Reinfection events in immunocompetent [2,3] or immunosuppressed [4] patients have been observed in a limited numbers of individuals so far and are often incompletely documented. Such cases can provide information around the determinants of the quality and duration of the protective immune response elicited after SARS-CoV-2 main contamination and the risks associated with the emergence of new mutations. Here we statement a case of SARS-CoV-2 reinfection in a young healthy physician, leading to a second episode of moderate COVID-19. == Methods == Samples taken via nasopharyngeal swabs (NPSs) were collected using 3 mL universal transport medium tubes and tested for SARS-CoV-2 by real-time reverse transcriptase PCR (RT-PCR) using the Cobas 6800 SARS-CoV-2 RT-PCR assay (Roche, Basel, Switzerland). Computer virus loads were estimated from your cycle threshold (Ct) values retrieved for theEgene, as previously described [5]. Respiratory viruses were tested using an in-house RT-PCR panel during reinfection. Viral genome sequences of the first and the subsequent infections were recovered using a whole-genome sequencing approach (Microsynth, Balgach, Switzerland). In addition, Sanger sequencing was performed on both specimens to total uncovered regions in theSgene. Immunoglobulins were measured using commercially available packages (Elecsys Anti-SARS-CoV-2 anti-N and Elecsys Anti-SARS-CoV-2 anti-S, Roche, Rotkreuz, Switzerland; and ELISA IgG S1, Euroimmun AG, Lbeck, Germany). Neutralizing antibody titres were assessed by a plaque reduction neutralization assay using serially diluted sera. Memory B cell (MBC) responses were assessed in peripheral blood mononuclear cells. Supplementary Methods are available in the online version of the article. Written informed consent was obtained from the patient. == Results == On 10 April 2020, a 36-year-old asymptomatic female physician tested positive for SARS-CoV-2 (viral weight of DBPR112 1 1.26E+05 copies/mL) on a NPS collected during an active nosocomial DBPR112 outbreak investigation (Fig. 1(A)). Two days later, she developed asthenia and headache lasting for 2 weeks, and experienced slight memory loss and difficulties concentrating upon resuming work. Independent of this episode, she was enrolled into a longitudinal cohort study assessing the seroprevalence of COVID-19 in healthcare workers (HCWs) at our institution, for which sequential serum sampling was performed starting 1 week before the first episode. Anti-S1 IgG was unfavorable 7 days before the first contamination; seroconversion was confirmed at day DBPR112 14 and 1 month after contamination with anti-S1 IgG and total immunoglobulins directed against the nucleoprotein (anti-N Ig) and against the receptor-binding domain name of the spike protein (antiS RBD Ig) at low but increasing titres over time (Fig. 1(B)). == Fig. 1. == (A) Schematic representation of clinical course of patient with serologic and virologic results. Day 0 indicates day of diagnosis when asymptomatic or day of DBPR112 onset of symptoms. (B) Kinetics of serologic responses. Neutralizing endpoint titres 50% (green squares) and 90% (reddish dots) plaque reduction are shown (PRNT50 and PRNT90 respectively) for five different sampling time points during first and second contamination. Blue triangles indicate antiS RBD titres (U/mL); black triangles, anti-NCP titres (COI). Abbreviations: c/mL, copies per mL of specimen; COI, cutoff index; Ct, cycle threshold; HCW, healthcare worker; N, nucleocapsid protein/nucleoprotein; NPS, nasopharyngeal swab; PRNT, plaque reduction neutralization test; RBD, receptor binding domain name; S, spike. On 15 October 2020, another nosocomial cluster was recognized, and she was tested again as part of hospital surveillance. She was asymptomatic and RT-PCR results were unfavorable. On 30 October, while still working in a COVID-19 ward, she developed asthenia, followed by shivering, rhinorrhoea, anosmia, arthralgia, headache and exertional dyspnoea. The next day, CORIN the RT-PCR result was positive (viral weight of 2.94E+07 copies/mL) and was confirmed by a second NPS taken 4 days later, showing a rapid decline in computer virus weight (2.25E+04 copies/mL) [6]. All symptoms.