Abstract: The present disclosure relates to, inter alia, a method of treating a complement mediated disorder caused by a virus, e.g., corona virus; Dengue virus (DENY); Ross River vims (RRV) and/or influenza virus (flu) by administering an effective amount of a complement modulator, such as, e.g., C5 inhibitor, such as eculizumab or an eculizumab variant or a C5a inhibitor such as olendalizumab (ALXN1007) or a variant thereof, to the subject. In addition, the present disclosure relates to, inter alia, a method of treating human patients inflicted with severe coronavirus disease-2019 (severe COVID-19) who is undergoing treatment with eculizumab. The method includes measuring a level of circulating component C5b-9 (membrane attack complex), in the patient's blood sample to titrate an effective eculizumab dose for the treatment of COVID-19.

Abstract: The method for analysis, the method comprising:—obtaining a sample comprising elements coming from breath exhaled from a person (112);—exposing the sample to a spectrometer;—determining at least one value of a signal intensity and/or concentration of ions defined by its mass-to-charge ratio (m/z) given by the spectrometer in at least one range, the or each range being defined by a median value and limits of the range;—applying at least one test to the value, the range(s) and the test being configured for identifying that:—a person carries and/or is infected with SARS-CoV-2,—a person does not carry and/or is not infected with SARS-CoV-2,—a person suffers from COVID-19, and/or—a person does not suffer from COVID-19; and—communicating a message according to a result of the test.

Abstract: Septic shock is the leading cause of death in intensive care units. Previous studies have highlighted the immunosuppressive protein GILZ (glucocorticoid-induced leucine zipper) as a regulator of innate and adaptive immune responses. To go deeper in the understanding of GILZ protective role during sepsis, the inventors studied in vivo the consequences of a targeted overexpression of GILZ in monocytes and macrophages (M/M) in animal models of sepsis. In addition, they monitored the expression of GILZ in M/M of both patients with septic shock and septic mice. In particular, the inventors show that the overexpression of GILZ limited to M/M leads to an increase survival rate in mice with CLP-induced sepsis. These results provided new evidence for a central role of GILZ in M/M on the pathophysiology of septic shock, and pinpoint the fact that GILZ would be suitable for predicting survival time of patient suffering from sepsis.