Coronavirus (COVID-19) Collection
Booster dose of SARS-CoV-2 messenger RNA vaccines strengthens the specific immune response of patients with rheumatoid arthritis: A prospective multicenter longitudinal study
Since the COVID-19 pandemic appearance, a global effort has been made to develop effective vaccines to stem SARS-CoV-2 infection through the induction of a coordinated B and T cell immune response (Agrati et al., 2021; Aiello et al., 2022a; Sette and Crotty, 2021, 2022). Humoral immunity consists of antibodies binding the SARS-CoV-2 spike (S) protein that neutralizes the virus, whereas cellular immunity includes virus-specific B and T cells, which provide long-term memory and promptly expand following re-exposure to antigens (Sette and Crotty, 2021, 2022).The first case of meningitis associated with SARS-CoV-2 BA.2 variant infection with persistent viremia
Neurological symptoms of COVID-19 are highly frequent and disabling (Wan et al., 2021). Severe neurological disorders such as encephalitis, meningitis, Guillain-Barré syndrome, and vascular events have been described in anecdotal reports or in case series. Here, we describe the first case of a female patient infected with the SARS-CoV-2 BA.2 Omicron variant of concern (VoC) meningitis with newly diagnosed central demyelinating disease.Accuracy of QuantiFERON SARS-CoV-2 research use only assay and characterization of the CD4+ and CD8+ T cell-SARS-CoV-2 response: comparison with a homemade interferon-γ release assay
Humoral and cell-mediated responses are both necessary to control SARS-CoV-2 infection (Sette and Crotty, 2021) and to monitor the immune protection induced by the ongoing SARS-CoV-2 vaccination in the population (Agrati et al., 2021; Aiello et al., 2021; Farroni et al., 2022; Goletti et al., 2021; Petrone et al., 2021b; Picchianti-Diamanti et al., 2021; Tortorella et al., 2022).Humoral and cellular responses to spike of δ SARS-CoV-2 variant in vaccinated patients with immune-mediated inflammatory diseases
The World Health Organization (WHO) identified all the viral variants as variants of concern (VOC), with increased potential to spread or capacity to evade the natural or the vaccine-induced protection. The SARS-CoV-2 VOC are the α, β, γ, and δ variants (WHO, 2021); moreover, the omicron VOC has been recognized very recently (Viana et al., 2022). At the time of writing this report, the δ, with 41.4% of sequences identified (WHO, 2022), was still a high-spread VOC worldwide, and was associated with an exponential increase of infections and deaths (Cherian et al., 2021; Depres et al., 2021) owing to its capacity to infect individuals with a viral load up to 1000-fold compared with the original strain (Campbell et al., 2021).Role of testosterone in SARS-CoV-2 infection: A key pathogenic factor and a biomarker for severe pneumonia
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).Prolonged and severe SARS-CoV-2 infection in patients under B-cell-depleting drug successfully treated: A tailored approach
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).Spike is the most recognized antigen in the whole-blood platform in both acute and convalescent COVID-19 patients
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).Risk and predictive factors of prolonged viral RNA shedding in upper respiratory specimens in a large cohort of COVID-19 patients admitted to an Italian reference hospital
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).The unbalanced p53/SIRT1 axis may impact lymphocyte homeostasis in COVID-19 patients
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).Down Syndrome patients with COVID-19 pneumonia: A high-risk category for unfavourable outcome
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).
