Coronavirus (COVID-19) Collection
- Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is characterized by a huge range of clinical manifestations. Many pathogenetic pathways and virulence mechanisms are still unknown. Nevertheless, it is known that the host’s immune system plays a key role (Blanco-Melo et al., 2020). Notably, age, comorbidities (e.g. diabetes mellitus, obesity), smoking habits and male sex (Rod et al., 2020; Wu et al., 2020) are the fundamental independent risk factors for death from coronavirus disease-19 (COVID-19) (Zhou et al., 2020).
- Patients with pre-existing comorbidities and immunosuppression, including anti-CD20 monoclonal antibody, widely used to treat hematological malignancies or autoimmune disease, are at greater risk for persistent Severe Acute Respiratory Syndrome-CoronaVirus-2 (SARS-CoV-2) infection (He et al., 2020). Prolonged B-cell depletion impairs the adaptive immune response and the ability to produce neutralizing antibodies, causing severe manifestations and a prolonged course of COVID-19 (Mehta et al., 2020; Hueso et al., 2020).
- The COVID-19 pandemic caused by Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) has recently emerged as a new human-to-human transmissible disease with a serious global health impact (Braun et al., 2020). SARS-CoV-2 is an enveloped virus with a positive stranded RNA genome and four structural proteins, including spike glycoprotein (S), envelope protein (E), membrane protein (M), and nucleocapsid protein (N) (Koblischke et al., 2020; Le Bert et al., 2020).
- The emergence and rapid spread of the COVID-19 outbreak, caused by SARS-CoV-2, has become a global health emergency and one of our century's greatest challenges. As of February 24, 2021, approximately 111 million confirmed cases and more than 2.4 million deaths had been reported worldwide (Anon, 2020).
- In patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, excessive inflammatory responses are considered to play a major role in the pathogenesis of severe coronavirus disease-2019 (COVID-19) disease, leading to acute respiratory distress syndrome and multiple-organ failure (Moore and June, 2020). Dysregulated inflammatory profile, defective immune responses and lymphopenia have also been identified as important features of severe disease (Del Valle et al., 2020; Bordoni et al., 2020).
- In December 2019, the novel coronavirus SARS-CoV-2 was identified as the etiologic agent of the COronaVIrus Disease-19 (COVID-19) outbreak occurring in Wuhan, China (Zhu et al., 2020). The clinical spectrum of COVID-19 is wide, ranging from asymptomatic infection to severe disease and death. Pro-inflammatory factors play a central role in COVID-19 severity and mortality, inducing an excessive inflammatory and immune response, leading to acute respiratory distress (ARDS) and multi-organ failure (MOF) (Zhou et al., 2020).
- In December 2019, a novel coronavirus, the severe acute respiratory syndrome coronavirus-2 (SARS- CoV-2) which causes a human disease named coronavirus disease (COVID-19) was identified in the pneumonia outbreaks in Wuhan, China, in December 2019 (Chan et al., 2020). It is currently expanding rapidly to several countries all-around the word, on February 21 the first person-to-person transmission in Italy was reported (Spina et al., 2020). Here, we report a case of SARS-CoV-2 and Influenza A co-infection and a mini-review of the literature.
- On December 31, 2019, aggregate cases of an apparently new respiratory syndrome were reported in the city of Wuhan, China by Chinese national health authorities to the World Health Organization (WHO) (Huang et al., 2020; Organization WH, 2020a). As of 13h February 2020, there have been 45 171 cases reported to the World Health Organization with 1104 deaths (Organization WH, 2020a). Outside China there have been 441 confirmed cases reported from 24 countries (Organization WH, 2020a; Organization WH, 2020b).