Type I interferon (IFN-I) production is triggered by the detection of viral molecules,such as strands of viral RNA or DNA, by receptors known as PRRs (Pattern RecognitionReceptors) present on many cell types. These interferons are secreted in minimalconcentrations but can activate neighboring cells to secrete over 700 proteins withantiviral properties (inhibition of viral replication, destabilization of viralmembranes, etc.). Thus, the IFN-I response serves as the immune system's first line ofdefense during a viral infection.Very early in the COVID-19 pandemic, several research teams, including ours, identified adefect in the type I interferon response in about one in five subjects with severeCOVID-19. In-depth studies have shown that 5 to 20% of these patients with severeCOVID-19 disease have genetic mutations affecting genes involved in the activationcascade of the IFN-I pathway or produce autoantibodies that neutralize IFN-I,significantly impairing the effectiveness of their IFN-I response.However, to date, not all causes of IFN-I response alteration are clearly identified, and80% of patients suffering from severe COVID-19 do not appear to have evident geneticpredispositions or anti-IFN-I autoantibodies, with the techniques currently available.This suggests the presence of other risk factors or causes that could potentially lead toalterations in the IFN-I response.The gut microbiota is recognized for its influence on host health and immunity.SARS-CoV-2 (Severe Acute Respiratory Syndrome CoronaVirus 2) infection has beenassociated with altered gut microbiota and correlated with inflammatory and immuneresponses. However, the association between dysbiosis and IFN-I response has yet to bestudied in humans.Therefore, to improve the management of individuals affected by viral respiratoryinfections, it seems essential to explore alterations in the IFN-I response to identifyindividuals potentially at risk of developing severe forms. It is known that a failure inthe IFN-I response in the early stages of a viral infection leads to uncontrolled viralreplication, which may result in a severe form of the disease. Since this IFN-I responseis essential for controlling all viral infections, regardless of the virus involved, theinvestigators hypothesize that this IFN-I deficiency could be responsible for severeinfections from various respiratory viruses that may lead to severe forms, even though adirect association between IFN-I deficiency and higher mortality risk has only beenreported for a few viruses, such as SARS-CoV-2 and influenza.Furthermore, the investigators consider the possibility of other underlying causes ofIFN-I deficiencies, distinct from the already observed anti-IFN-I autoantibodies andgenetic mutations. To achieve this, the investigators hypothesize that the use offunctional immune tests could reveal these other alterations.By identifying these alterations in individuals, the investigators hope to moreaccurately predict their propensity to develop severe forms of viral infections.Biological samples will be collected specifically for the study, outside of a healthcareprocedure. No biological sample in biocollections coming from COVID-ser and NOSO-CORIMMUNO studies and the RNIPH study (Research Not Involving Human Persons) named MIR-COVIDwill be used for this new protocol.Patients who experienced : - mild forms of COVID-19 during the first wave, without any prior vaccination, selected from the pre-existing COVID-Ser cohort (ClinicalTrial no. NCT04341142) - severe forms of COVID-19 during the first wave, without any prior vaccination, selected from the pre-existing NOSO-COR IMMUNO cohort (ClinicalTrial no. NCT04637867) and the RNIPH study (Research Not Involving Human Persons) named MIR-COVID (compliance with MR004 n°20_097_v2) could be recruited.Biological samples will be collected specifically for the study, outside of a healthcareprocedure. No biological sample in biocollections coming from COVID-ser and NOSO-CORIMMUNO studies and the RNIPH study (Research Not Involving Human Persons) named MIR-COVIDwill be used for this new protocol.