Objectives To describe the clinical evolution and predictors of symptom persistence during 2-month follow-up in adults with non-critical COVID-19. Methods Descriptive clinical follow-up (days 7, 30 [D30] and 60 [D60]) of 150 patients with non-critical COVID-19 confirmed by RT-PCR at Tours University Hospital from March 17 to June 3, 2020, including demographic, clinical and laboratory data collected from the electronic medical records and by phone call. Persisting symptoms were defined by the presence at D30 or D60 of at least one of the following: weight loss ≥ 5%, severe dyspnea or asthenia, chest pain, palpitations, anosmia/ageusia, headache, cutaneous signs, arthralgia, myalgia, digestive disorders, fever or sick leave. Results At D30, 68% (n=103/150) of patients presented at least one symptom and 66% (n=86/130) at D60, mainly anosmia/ageusia: (59% (n=89/150) at symptom onset, 28% (n=40/150) at D30 and 23% (n=29/130) at D60). Dyspnea concerned 36.7% (n=55/150) patients at D30 and 30% (n=39/130) at D60. Half of the patients (n=74/150) at D30 and 40% (n=52/130) at D60 reported asthenia. Persistent symptoms at D60 were significantly associated with age 40 to 60 years old, hospital admission and abnormal auscultation at symptom onset. At D30, severe COVID-19 and/or dyspnea at symptom onset were additional factors associated with persistent symptoms. Conclusions Up to 2 months after symptom onset, two thirds of adults with non-critical COVID-19 had complaints, mainly anosmia/ageusia, dyspnea or asthenia. A prolonged medical follow-up of patients with COVID-19 seems essential, whatever the initial clinical presentation.

ARS-CoV-2 variants have rapidly emerged in humans and supplanted ancestral strains [1][2][3][4][5] . Their proposed increased rates of interindividual transmission conferred a replication advantage at the population level. One of the first identified variants includes the D614G mutation in the gene encoding the spike (S) protein, which enhances viral infectivity and shifts S protein conformation toward an angiotensin-converting enzyme 2 (ACE2)-binding fusion-competent state, without significantly modifying sensitivity to antibody neutralization 1,6-8 . More recently, novel variants have appeared in multiple countries, with combinations of mutations and deletions in the receptor-binding domain (RBD) and N-terminal domain of S protein, as well as in other proteins. The B.1.1.7 variant emerged in the United Kingdom, the B.1.351 variant (also termed 501Y.V2) in South Africa and the P.1 and P.2 lineages in Brazil 2,3,5,9-12 . Although distinct, the variants share common characteristics, including known escape mutations that were previously identified under antibody pressure selection in vitro 2,3,[13][14][15][16][17] . Some of the mutations or deletions were also identified in immunocompromised individuals with prolonged infectious viral shedding and treated with convalescent plasma or S-protein Sensitivity of infectious SARS-CoV-2 B.1.1.7 and B.1.351 variants to neutralizing antibodies