The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) pandemic has attracted interest because of its global rapid spread, clinical severity, high mortality rate and capacity to overwhelm healthcare systems [1, 2]. SARS-CoV-2 transmission occurs mainly through droplets, although surface contamination contributes and debate continues on aerosol transmission [3-5]. The disease is usually characterised by initial signs and symptoms [4-9] similar to those of related viral infections (e.g. influenza, SARS, Middle East respiratory syndrome) and tuberculosis (TB), although prognosis and complications sometimes differ. Experience with concomitant TB and COVID-19 is extremely limited. One case-control study of COVID-19 patients with interferon-γ release assay-confirmed TB infection [10] and a single case of TB with COVID-19 have been submitted to, but not yet published in, peer-reviewed journals [11]. In a recent analysis of 1217 consecutive respiratory specimens collected from COVID-19 patients (Mycobacterium tuberculosis was not tested), the authors concluded that higher rates of co-infection between SARS-CoV-2 and other respiratory pathogens can be expected [12]. The present study describes the first-ever global cohort of current or former TB patients (post-TB treatment sequelae) with COVID-19, recruited by the Global Tuberculosis Network (GTN) in eight countries and three continents. No analysis for determinants of outcome was attempted. The study is nested within the GTN project monitoring adverse drug reactions [13, 14] for which the coordinating centre has an ethics committee approval, alongside ethics clearance from participating centres according to respective national regulation [13, 14]. A specific nested database was created in collaboration with the eight countries reporting patients with TB and COVID-19; the remaining countries had not yet observed COVID-19 in their patients at the time this manuscript was written. Continuous variables, if not otherwise specified, are presented as medians with interquartile ranges. Overall, 49 consecutive patients with current or former TB and COVID-19 from 26 centres in Belgium (n=1), Brazil (Porto Alegre, Rio Grande do Sul State; n=1), France (n=12), Italy (n=17), Russia (Moscow Region; n=6), Singapore (n=1), Spain (n=10) and Switzerland (Vaud Canton; n=1) were recruited (dataset updated as of

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SARS-CoV-2 is a novel coronavirus, not encountered before by humans. The wide spectrum of clinical expression of SARS-CoV-2 illness suggests that individual immune responses to SARS-CoV-2 play a crucial role in determining the clinical course after first infection. Immunological studies have focused on patients with moderate to severe disease, demonstrating excessive inflammation in tissues and organ damage. In order to understand the basis of the protective immune response in COVID-19, we performed a longitudinal follow-up, flow-cytometric and serological analysis of innate and adaptive immunity in 64 adults with a spectrum of clinical presentations: 28 healthy SARS-CoV-2-negative contacts of COVID-19 cases; 20 asymptomatic SARS-CoV-2-infected cases; eight patients with Mild COVID-19 disease and eight cases of Severe COVID-19 disease. Our data show that high frequency of NK cells and early and transient increase of specific IgA, IgM and, to a lower extent, IgG are associated with asymptomatic SARS-CoV-2 infection. By contrast, monocyte expansion and high and persistent levels of IgA and IgG, produced relatively late in the course of the infection, characterize severe disease. Modest increase of monocytes and different kinetics of antibodies are detected in mild COVID-19. The importance of innate NK cells and the short-lived antibody response of asymptomatic individuals and patients with mild disease suggest that only severe COVID-19 may result in protective memory established by the adaptive immune response.

Background Descriptions of the pathological features of COronaVIrus Disease-2019 (COVID-19) caused by the novel zoonotic pathogen Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) emanate from tissue biopsies, case reports and small post-mortem studies restricted to the lung and specific organs. Whole body autopsy studies of COVID-19 patients have been sparse. To further define the pathology caused by SARS-CoV-2 across all body organs in both individuals with and without co-morbidities Italian patients who died of COVID-19. Methods We performed autopsies on 22 patients with COVID-19 (18 with co-morbidities and 4 without co-morbidities) who died at the National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS Hospital, Rome, Italy. Tissues from the lung, heart, liver, kidney, spleen and bone marrow (but not the brain) were examined. Only lung tissues were subject to transmission electron microscopy. Results COVID-19 causes multisystem pathology. Pulmonary and cardiovascular involvement are dominant pathological features. Extra-pulmonary manifestations include hepatic, kidney, splenic and bone marrow involvement, and microvascular injury and thrombosis were also detected. These findings were similar in patients with or without pre-existing medical co-morbidities. Conclusions SARS-CoV-2 infection causes multisystem disease and significant pathology in most organs in patients with and without co-morbidities.