In late December 2019, an outbreak of an emerging respiratory disease (COVID-19) caused by a
novel coronavirus named SARS-CoV-2 began in Wuhan City, Hubei Province, China and quickly
spread in a substantial number of countries. The epidemic was declared a pandemic by the Word
Health Organization (WHO) on 12 March 2020. SARS-CoV-2 has demonstrated the capability to
spread rapidly, leading to significant impacts on healthcare systems and causing societal
disruption.

Both clinical and epidemiological features of patients with COVID-19 have recently been
reported, demonstrating that the SARS-CoV-2 infection can be asymptomatic in some cases or
symptomatic in others. Symptomatology usually begins as mild with fever, fatigue, dry cough,
and occasional dyspnea. In a minority of patients, a sudden onset of severe symptoms may
develop 5-8 days into the illness including shortness of breath, pneumonitis, acute
respiratory distress syndrome (ARDS) and multi organ dysfunction leading to intensive care
unit (ICU) admission and high mortality. In some cases, accumulating evidence suggests that
severe COVID-19 symptoms could be due to a cytokine storm syndrome. As of May 3rd 2020, the
virus had infected 3,349,786 patients worldwide with more than 238,600 deaths, more often
among older patients with underlying health conditions.

With caseloads overwhelming hospitals and resources stretched thin in this surging pandemic
(high demand for oxygen, prolonged ventilation and even extracorporeal membrane oxygenation
(ECMO), particularly for patients with acute ARDS), there is an urgent need to enhance
clinical skills in order to predict from the many mild cases those few that will progress to
critical illness allowing a more efficient resource allocation and clinical management.

Several studies on patient blood have described features that were most predictive of ARDS.
These studies showed that severe cases, compared to mild cases, had : 1) older age; 2)
abnormalities in chest scanning (CT) such as multiple patch-like shadows and ground glass
opacity; 3) organ and coagulation dysfunction with a higher levels of alanine
aminotransferase (ALT), lactate dehydrogenase (LDH), C-reactive protein (CRP), ferritin and
D-dimer; 4) as well as markedly higher levels of immunological characteristics such as IL-2R,
IL-6, IL-10, and TNF- α ; 5) and an absolute T lymphocytes (CD4+ and CD8+ T cells) number
markedly lower in nearly all severe cases. These observations suggest that severity and
mortality might be due to virally driven systemic hyperinflammation secondary to failure of
the immune response to control infection (as shown for other viruses).

With this study we want to caracterize the predictive performance of the serum inflammation
profiles by protein electrophoresis, associated with clinical, radiological and biological
risk factors for worsening. This study is a prospective, observational study conducted on
patients hospitalized for an infection with the SARS-CoV-2 virus.