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role of exosomes in the COVID-19 reinfection/reactivation opportunity

Discussion in 'Immunology and Rheumatology' started by Valery1957, Jul 15, 2020.

  1. Valery1957

    Valery1957 Famous Member

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    On the potential role of exosomes in the COVID-19 reinfection/reactivation opportunity
    Fatma Elrashdy,Abdullah A. Aljaddawi,Elrashdy M. Redwan [​IMG] &Vladimir N. Uversky [​IMG]
    Received 17 Jun 2020, Accepted 28 Jun 2020, Published online: 09 Jul 2020

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    SARS-CoV-2, COVID-19, reinfection, exosome, extracellular vesicle

    Introduction
    Are we ready to the fact that we must adapt ourselves to live with COVID-19 and, perhaps, for a long time? Now, we know that not all people exposed to SARS-CoV-2 are infected, not all infected patients show symptoms, and not all showing symptoms develop severe respiratory illness. Although the world-wide daily case fatality rate (CFR) of the ongoing COVID-19 pandemic is declining, there are many countries where CFR is still increasing, and the rate of new infections is still high. In fact, within May month only, the number of new COVID-19 cases almost doubled (increased from 3.3 to 6.3 million), whereas June witnessed the highest ever number of new COVID-19 cases recorded in one day (194,191 on June 26, 2020). COVID-19 is characterized by a basic reproductive number (R0, which is the number of people infected by each sick person) ranging from 3.8 to 8.9 (Sanche et al., 2020). All these are rather disturbing news, especially for countries, which are coming out or a planning to come out of the COVID-19-related quarantine.

    For about 80% of the SARS-CoV-2 infected patients, the disease is mild, being mostly restricted to the upper and conducting airways. Although on average, ∼15% of the confirmed cases progress to the severe phase, for patients over 65, the chance to progress into the severe phase is noticeably higher (Shi et al., 2020). SARS-CoV-2 infection can be roughly divided into three stages (see Figure 1): stage I, an asymptomatic incubation period with or without detectable virus; stage II, non-severe symptomatic period with the presence of virus; stage III, severe respiratory symptomatic stage with high viral load. In more than 50% of patients, the seroconversion take place by day 7, and for the remaining patients – by day 13–14 (Korber et al., 2020; Mason, 2020; Shi et al., 2020; Wölfel et al., 2020). One should keep in mind that since SARS-CoV2 coronavirus is a new very aggressive causative agent, and novel data are released on an hourly basis, there are multiple classifications for the disease progression. However, the classification outlined here is the most clinically sound, being assembled based on the clinical data for more than 1000 patients (Korber et al., 2020; Mason, 2020; Shi et al., 2020; Wölfel et al., 2020).

    Figure 1. Schematic representation of stages of the COVID-19 infection and infectivity of corresponding patients. Here, seroconversion corresponds to the transition from the initial (primary infection) phase of the infection, where immunoglobulin M (IgM) antibodies are produced to the phase, where IgM levels drop (and become undetectable) and the immunoglobulin G (IgG) levels rise and remain detectable. C-reactive protein (CRP) is an acute inflammatory protein that increases up to 1,000-fold at sites of infection or inflammation. D-dimer is a degradation product of the cross-linked fibrin resulting from plasmin cleavage. In the blood of most healthy individuals, D-dimer is present in negligible amounts, whereas the elevated blood levels of D-dimer are the reflection of the intravascular coagulation and venous thromboembolism (VTE), which can present as either deep vein thrombosis (DVT) or pulmonary embolism (PE). Elevated D-dimer levels in COVID-19 patients are associated with the severity of COVID-19 infection and correlate with higher mortality.

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    The acute respiratory distress syndrome (ARDS) is the main cause of the COVID-19-related mortality, which actually represents a common immunopathological event for SARS-CoV-2, SARS-CoV, and MERS-CoV infections. One of the main ARDS mechanisms is the cytokine storm, the deadly uncontrolled systemic inflammatory response resulting from the release of large amounts of pro-inflammatory cytokines (such as IFN-α, IFN-γ, IL-1b, IL-6, IL-12, IL-18, IL-33, TNF-α, TGFβ, etc.) and chemokines (CCL2, CCL3, CCL5, CXCL8, CXCL9, CXCL10, etc.) by immune effector cells (Li, Geng, et al., 2020). Furthermore, the patients with the severe COVID-19 showed widespread complement activation, characterized by the C3a generation and C3-fragment deposition (Risitano et al., 2020).

    Prolonged SARS‐CoV‐2 RNA shedding, COVID-19 reinfection and reactivation
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