Background There is a paucity of knowledge on the long-term outcome in patients diagnosed with COVID-19. We describe a cohort of patients with a constellation of symptoms occurring four weeks after diagnosis causing different degrees of reduced functional capacity. Although different hypothesis have been proposed to explain this condition like persistent immune activation or immunological dysfunction, to date, no physiopathological mechanism has been identified. Consequently, there are no therapeutic options besides symptomatic treatment and rehabilitation. Methods We evaluated patients with symptoms that persisted for at least 4 weeks after COVID-19. Epidemiological and clinical data were collected. Blood tests, including inflammatory markers, were conducted, and imaging studies made if deemed necessary. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reverse transcription polymerase chain reaction (RT-PCR) in plasma, stool, and urine were performed. Patients were offered antiviral treatment (compassionate use). Results We evaluated 29 patients who reported fatigue, muscle pain, dyspnea, inappropriate tachycardia, and low-grade fever. Median number of days from COVID-19 to positive RT-PCR in extra-respiratory samples was 55 (39–67). Previous COVID-19 was mild in 55% of the cases. Thirteen patients (45%) had positive plasma RT-PCR results and 51% were positive in at least one RT-PCR sample (plasma, urine, or stool). Functional status was severely reduced in 48% of the subjects. Eighteen patients (62%) received antiviral treatment. Improvement was seen in most patients (p = 0.000) and patients in the treatment group achieved better outcomes with significant differences (p = 0.01). Conclusions In a cohort of COVID-19 patients with persistent symptoms, 45% of them have detectable plasma SARS-CoV-2 RNA. Our results indicate possible systemic viral persistence in these patients, who may benefit of antiviral treatment strategies.

Objective. The presence of serum rheumatoid factor (RF) and spontaneous RF‐secreting B cells is a common feature in most patients with rheumatoid arthritis (RA). This study analyzed the cytokine(s) that controls the final maturation of B cells capable of spontaneous IgM‐RF secretion in vitro. Methods. RA patients' peripheral blood mononuclear cells (PBMC), as well as adherent and nonadherent cell fractions, were cultured, and spontaneous IgM‐RF and interleukin‐1 0 (IL‐1 0) secretion were determined by enzyme‐linked immunosorbent assay. Results. The RF+ RA PBMC, but not PBMC from RF– RA patients or healthy controls, actively produced IgM‐RF in a linear manner for 14 days. This activity depended on the presence of fetal calf serum and did not require cellular DNA synthesis. Spontaneous IgM‐RF secretion depended on IL‐1 0, as deduced from the following findings: 1) IL‐1 0, but not a variety of cytokines including IL‐6, restored missing IgM‐RF secretion by PBMC in serum‐free supplemented cultures; 2) the addition of anti–IL‐1 0, but not anti–IL‐6, blocking antibodies inhibited PBMC IgM‐RF secretion, and this effect could be reversed by exogenous IL‐1 0; and 3) RA PBMC actively produced IL‐1 0 in vitro. The cells responsible for endogenous IL‐1 0 production were found in the adherent cell fraction. Finally, IL‐1 0 induced IgM‐RF, but not total IgM, secretion by RA PBMC. Conclusion. In patients with RA, circulating B cells capable of spontaneous IgM‐RF secretion require IL‐1 0 production by adherent cells to reach terminal maturation.

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