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Background: With the current mass international roll out of several vaccines against SARS-Cov-2, several reports of unheeded complications have made headlines. One of which involves myocarditis with the now FDA fully approved vaccine, Pfizer, and others. We hypothesize through this study that a dysregulated micro-RNA response resulting from such type of vaccines can be involved in triggering myocarditis. Methodology: Embase, Medline and the Cochrane Central Register were used to search for specific keywords such as “mRNA COVID-19 vaccines” AND “Myocarditis” for relevant publications up to 1st of September 2021. The systematic review was performed using PRISMA protocolResults:Literature review has identified 26 cases series and reports involving the development of myocarditis from mRNA vaccines, a total of 89 patients were included. Age range was clearly identified in 66 patients. Among those 66 patients, 94% were below 50 years of age, also out of 89 patients, 94% were males. Myocarditis developed, after a median time of 72 hours of the 2nd dose. 90 of cases of myocarditis developed myocarditis after the 2nd dose, the few patients developing myocarditis after the first dose were either predisposed by a history of myocarditis or a history of previous COVID-19 infection. Conclusion:In conclusion, interpretation of the results in view of the suggested hypothesis, reveals that the micro-RNAs implicated in myocarditis in general are as well implicated in the pathogenesis of severe COVID-19, this can explain why patients having a first dose with a history of COVID-19 can develop myocarditis from mRNA vaccines, also the relatively higher likelihood of this complication in males and younger aged individuals can be explained by the upregulation of key myocarditis related miRNAs in those two strata, due to higher muscle mass and suggests performing a sarcopenia index in recipients of the vaccine to correlate it with the likelihood of this complication. This could later set a cut-off of this easy bed-side index to stratify cases a higher risk of this rare complication.

Background:COVID-19 is the largest outbreak to strike humanity. The wide scale of fatalities and morbidities lead to a concurrent pandemic of uncertainty in scientific evidence. Conflicting evidences are released on daily basis about the neonatal outcomes of COVID-19 positive mothers. The aim of this study was to use the relevant case reports and series to determine the percentage of newborns who test positive in COVID-19 positive mothers. Secondary outcomes included examining laboratory and placental abnormalities among fetus-mother pairs.Methods:Systematic review was performed on all studies reporting primary data on fetus-mother pairs with COVID-19. Data bases were searched for studies that met our inclusion and exclusion criteria.Results: Final screening revealed 66 studies, from which the primary data of 1787 mother-infant pairs was obtained. Only 2.8% of mother infant pairs were tested positive, and this finding is identical to percentages reported in former coronaviridae outbreaks. Whereas, 20% manifested with intrauterine hypoxia alongside placental abnormalities suggestive of heavy placental vaso-occlusive involvement. Conclusions: These findings suggest that while vertical transmission is unlikely, there appears to be an underlying risk of placental insufficiency due to the prothrombotic tendency observed in COVID-19 infection. Guidelines for proper prophylactic anticoagulation in COVID positive mothers need to be established.

Furin, a cleavage enzyme, is increasingly recognized in the pathogenesis of metabolic syndrome. Its cleavage action is an essential activation step for the endothelial pathogenicity of several viruses including SARS-CoV-2. This Furin-mediated endothelial tropism seems to underlie the multi-organ system involvement of COVID-19; which is a feature that was not recognized in the older versions of coronaviridae. Obese and diabetic patients, males, and the elderly, have increased serum levels of Furin, with its increased cellular activity; this might explain why these subgroups are at an increased risk of COVID-19 related complications and deaths. In contrast, smoking decreases cellular levels of Furin, this finding may be at the origin of the decreased severity of COVID-19 in smokers. Chinese herbal derived luteolin is suggested to be putative Furin inhibitor, with previous success against Dengue Fever. Additionally, Furin intracellular levels are largely dependent on concentration of intracellular ions, notably sodium, potassium, and magnesium. Consequently, the use of ion channel inhibitors, such as Calcium Channel blockers or Potassium Channel blockers, can prevent cellular transfection early in the course of the illness. Nicotine patches and Colchicine have also been suggested as potential therapies due to Furin mediated inhibition of COVID-19., Highlights • 1-SARS-CoV-2 harbors a polybasic cleavage site. • 2-This polybasic cleavage site leads to its canonical activation by a cellular enzyme termed Furin. • 3-Furin is highly expressed in Endothelial, leading to endothelitis and vascular inflammation in COVID-19. • 4-This also explains the augmented manifestations of COVID-19 in Obese and Diabetic patients. • 5-The use of Chinese herbals and ion channel inhibitors can block the endothelial penetration of SARS-CoV-2.

Coronavirus disease 2019 (COVID-19) is a serious illness that has rapidly spread throughout the globe. The seriousness of complications puts significant pressures on hospital resources, especially the availability of ICU and ventilators. Current evidence suggests that COVID-19 pathogenesis majorly involves microvascular injury induced by hypercytokinemia, namely interleukin 6 (IL-6). We recount the suggested inflammatory pathway for COVID-19 and its effects on various organ systems, including respiratory, cardiac, hematologic, reproductive, and nervous organ systems, as well examine the role of hypercytokinemia in the at-risk geriatric and obesity subgroups with upregulated cytokines' profile. In view of these findings, we strongly encourage the conduction of prospective studies to determine the baseline levels of IL-6 in infected patients, which can predict a negative outcome in COVID-19 cases, with subsequent early administration of IL-6 inhibitors, to decrease the need for ICU admission and the pressure on healthcare systems. Video abstract: http://links.lww.com/CAEN/A24.

ABO blood groups is a cheap and affordable test that can be immediately retrieved from COVID-19 patients at the diagnosis. There is increasing evidence that non-O blood groups have both higher susceptibility and higher severity of COVID-19 infections. The reason behind such relationship seems elusive. Regarding susceptibility, Non-O individuals have Anti-A antibodies which can prevent viral entry across ACE-2 receptors, moreover, Non-O individuals are at higher risk of autoimmunity, hypercoagulable state, and dysbiosis resulting in an augmented tendency for vascular inflammatory sequelae of COVID-19. We can conclude, on the diagnostic level, that ABO blood groups can be potentially used for risk stratification of affected COVID-19 patients, to anticipate the deterioration of patients at higher risk for complications. On a therapeutic level, plasma from normal O blood group individuals might potentially replace the use of convalescent serum for the treatment of COVID-19.

COVID-19 has shown a substantial variation in the rate and severity by which it impacts different demographic groups. Specifically, it has shown a predilection towards obese patients as well as as well as other vulnerable groups including predilection of males over females, old age over young age and black races over Caucasian ones.. Single cell sequencing studies have highlighted the role of cell polarity and the co-expression of proteases, such as Furin, along with ACE2 in the genesis of coronavirus disease rather than exclusively link tissue involvement with ACE2 levels thought previously. It has also forged a connection between the genetic and immune cellular mechanisms underlying COVID infection and the inflammatory state of obese patients, offering a more accurate explanation as to why obese patients are at increased risk of poor COVID outcomes. These commonalities encompass macrophage phenotype switching, genetic expression switching, and overexpression of the pro-inflammatory cytokines, depletion of the regulatory cytokines, in situ T cell proliferation, and T cell exhaustion. These findings demonstrate the necessity of single cell sequencing as a rapid means to identify and treat those who are most likely to need hospital admission and intensive care, in the hopes of precision medicine. Furthermore, this study underlines the use of immune modulators such as Leptin sensitizers, rather than immune suppressors as anti-inflammation therapies to switch the inflammatory response from a drastic immunological type 1 response to a beneficial type 2 effective one., Highlights • ScRNA-seq focuses on the analysis of individual cells, instead of bulk cell populations, and can lead to a more insightful characterization of local microenvironments. • ScRNA-seq unleashed that tissue tropism in COVID-19 is not solely determinant by ACE2 distribution but rather by Furin. • ScRNA-seq in COVID-19 revealed two distinct types of immunologic reactions, deleterious type 1 characterized by inefficient antigen presentation, decreased memory B cells, imbalance between M1 and M2 macrophages and T cell exhaustion, and beneficial type 2 reaction which exactly the reverse of the type 1. • The immunotype 1 reaction is intriguingly similar to the immune landscape seen in obese individuals when leptin resistance sets in. • This might indicate that the use of leptin sensitizers to induce an immunologic switch from immunotype 1 to immunotype 2 can greatly improve the outcome of COVID-19 cases. • ScRNA-seq was also able to unveil the disparity between aggressive and milder strains of SARS-CoV-2, which are mainly related to their affinity to cellular activation by Furin. • The applications of ScRNA-seq may help to anticipate cases at higher risk of severe COVID-19 at their earliest encounter.