A dissection of SARS‑CoV2 with clinical implications (Review)

Abstract

We are being confronted with the most consequential pandemic since the Spanish flu of 1918-1920 to the extent that never before have 4 billion people quarantined simultaneously; to address this global challenge we bring to the forefront the options for medical treatment and summarize SARS-coV2 structure and functions, immune responses and known treatments. Based on literature and our own experience we propose new interventions, including the use of amiodarone, simvastatin, pioglitazone and curcumin. In mild infections (sore throat, cough) we advocate prompt local treatment for the naso-pharynx (inhalations; aerosols; nebulizers); for moderate to severe infections we propose a tried-and-true treatment: the combination of arginine and ascorbate, administered orally or intravenously. The material is organized in three sections: i) Clinical aspects of COVID-19; acute respiratory distress syndrome (ARdS); known treatments; ii) Structure and functions of SARS-coV2 and proposed antiviral drugs; iii) The combination of arginine-ascorbate. Contents 1. Clinical aspects of COVID-19 infections; acute respiratory distress syndrome (ARdS); known and potential treatments 2. SARS-coV2 molecules and proposed antiviral drugs 3. The combination of arginine-ascorbate

Physicians’ Perspectives on COVID-19: An International Survey

“…The inflammatory pathways are activated during COVID-19, and therefore parameters like C-reactive protein (CRP), ferritin, procalcitonin, fibrinogen, interleukin-6 (IL-6) were studied as prognostic factors [2]. Lymphocyte count has been proven to be correlated with severity and outcome [25].…”

“…Further, an important increase in ferritin level in severe COVID-19 patients as well as systemic involvement draw attention to the similarities with the "hyperferritinemic syndrome", that include macrophage activation syndrome (MAS), adult-onset Still's disease (AOSD), catastrophic anti-phospholipid syndrome (CAPS) and septic shock [27]. Coagulation parameters were included in the COVID-19 management algorithms to allow the recognition of cases with a severe prognosis, and to define the conditions for hospital admission, as well as to establish anticoagulation principles [2,5]. Therefore, screening for D-dimer, prothrombin time, platelet count, and fibrinogen is recommended [5].…”

“…The coronavirus disease 2019 (COVID-19) breakup started in December 2019 in Wuhan, China [1,2]. Genetic analysis shows that it is a beta-coronavirus linked to the severe acute respiratory syndrome (SARS) [1][2][3]. The new SARS coronavirus (SARS-CoV-2) was declared a pandemic by the World Health Organization (WHO) in March 2020 and became a public health emergency.…”

[Comment] COVID‑19 vaccine safety

“…While the number of daily deaths attributable to cOVId-19 appears to have decreased substantially by June 2020, the increasing numbers of 'cases' (positive test results for viral exposure) have raised some concerns regarding the ability of governments and decision-making authorities to reduce viral transmission and subsequent consequences (2)(3)(4). currently, at 10 months following the outbreak, no specific treatment for severe forms of cOVId-19 has achieved consensus within the medical community, although several potential therapies appear to have produced more or less encouraging results (5)(6)(7)(8)(9)(10)(11).…”

Transcriptomic analysis of COVID‑19 lungs and bronchoalveolar lavage fluid samples reveals predominant B cell activation responses to infection

“…Even if SARS-coV-2 shares similarities with the other coronaviruses, the higher diffusion rate and the possibility to induce fatal complications, such as severe pneumonia, acute respiratory distress syndrome (ARdS), thrombosis, septic shock and organ failure, make this virus a major public health threat (7)(8)(9)(10). development of cOVId-19 complications seems to be dependent on a dramatic release of proinflammatory factors, such as interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α) and cXc-chemokine ligand 10 (cXcL10) and cc-chemokine ligand 2 (ccL2) in the infected lung tissue and other peripheral organs (2,(11)(12)(13), which ultimately leads to a reaction known as cytokine release syndrome (cRS). It is likely that CRS promotes a self-sustaining inflammatory process that contributes to the respiratory failure and the systemic manifestations observed in cOVId-19 patients (14).…”