Coronaviruses are a large family of viruses that cause disease ranging from common cold to more serious diseases, such as Middle East Respiratory Syndrome (MERS-CoV) and Severe Acute Respiratory Syndrome (SARS-CoV). A novel coronavirus (nCoV) is a new strain not previously discovered in humans . COVID-19 genome contains 15 nsps, nsp1-nsp10 and nsp12-16, and 8 accessory proteins (3a, 3b, p6, 7a, 7b, 8b, 9b and/or f 14) . All those proteins play a functional role in viral replication . Our results showed that the detection of COVID-19 infections was concentrated between February 9 and July 13, 2020 and peaked. The diagnosis depends on 3 factors:
- The presence of significant respiratory illness: fever with dry cough, fatigue or difficulty breathing.
- Measurement of COVID-19 IgG/IgM Rapid Test Kit, Abbexa, Cambridge, United Kingdom).
- Lung CT diagnosis using syngo. CT DE Lung Analysis - Siemens Healthineers Global, Germany. The patients were classified according to the degree of severity into 3 groups mild, moderate and sever COVID-19 infection plus the first group of healthy persons with negative test for COVID-19 infection tests.
The present results showed that a significant difference in hematology indices between COVID-19-positive and COVID-19-negative patients. The hematology indices in the present study indicated that the proportion of leukopenia, lymphopenia and eosinophil changes was higher among mild, moderate and sever patients with COVID-19 infection.
Our results are confirmed with the results of Zhang et al.,  who reported that the patients infected with COVID-19 showed a decrease in leukocyte, lymphocyte and eosinophil count.
Also, our result showed a significant increase in ferritin, C-reactive protein and d-dimer levels in patients who tested positive for COVID-19. Hyperferritinemia in the present study as a known factor of inflammation was in confirmed with Connelly et al.  who investigated serum ferritin levels in patients at risk for and with ARDS and found serum ferritin to be a predictor of ARDS. Also, patients critically ill with coronavirus disease-2019 (COVID-19) feature hyperinflammation, and the associated biomarkers (ferritin, C-reactive protein, and d-dimer) may be beneficial for risk stratification .
This finding supports the hypothesis that severe acute respiratory syndrome coronavirus  (SARS-CoV-2) infection could induce the dysfunction of the hemostatic system, leading to a hypercoagulable state [46, 47]. Recent evidence of lung pathology dissection has shown occlusion and micro-thrombosis formation in pulmonary small vessels of patients critically ill with COVID-19 . Also, CRP is an acute phase inflammatory protein produced by the liver that may be elevated in several conditions, such as inflammation, cardiovascular disease, and infection .
These results showed that decreased plasma phospholipids, total cholesterol, HDL-C and LDL-C levels as well as significantly plasma triacyclglycerols increased were associated with an increased inflammation by severe COVID-19 infection. Patients with a variety of different infections (gram positive bacterial, gram negative bacterial, viral, tuberculosis) have similar alterations in plasma lipid levels. Specifically, total cholesterol, LDL cholesterol, and HDL cholesterol levels are decreased while plasma triglyceride levels are elevated or inappropriately normal for the poor nutritional status [47-51].
Also, we observed a striking decrease of phospholipid concentrations in patients with severe COVID-19 infection. The statistical analysis clearly showed that this is a reflection of systemic inflammation. There are different mechanisms to explain this downregulation. Firstly, it has been suggested that phospholipids can bind to acute phase reactants including CRP , which increased significantly in patient with severe COVID-19 infection in the present study. Also, the results of phospholipids, d-dimer and CRP as well as cytokines levels were supported to each other. Secondly, PCs can be hydrolyzed by phospholipase A2 in patients with severe COVID-19 infection  releasing one fatty acid and a lysoPC, which can then be hydrolyzed by lysophospholipase to yield another free fatty acid.
PLA2's enzymatic function is hydrolysis of phospholipids into free fatty acids, and lysophospholipids. Arachidonic acid (AA) is the free fatty acid in the phospholipid target's sn-2 position, the release of AA from phospholipids can then be transferred to eicosanoids  includes prostaglandins (PGs), leukotrienes (LTs), hepoxilins, and lipoxins (LXs), as well as several others synthesized by the actions of lipoxygenases and cycloxygenases on the common substratum, AA . Eicosanoids such as leukotriene LTB4 and hepoxiline HXA3 serve as chemoattractants for neutrophils, playing a key role in the inflammatory process. On the other hand, PGs, like PGE2, and LXs, such as LXA4, can protect against excessive lung inflammation and participate in repairing lung tissue [55 and 56].
Our study suggested that the oxidation of phospholipid side chains during oxidative stress and inflammation by COVID-19 infection, polyunsaturated fatty acid side chains of membrane phospholipids can be modified by oxidation. Also, the significant alteration of plasma cholesterol, triacylglycerols, HDL-C, LDL-C, CRP, d-dimer, sPLA and cytokines supports this suggestion.
Also, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6 and interleukin IL-13 levels of patients with COVID-19 compared to negative persons.
In the systemic hyperinflammation phase of COVID-19 proposed by Siddiqi and Mehra, there is a significant elevation of inflammatory cytokines and biomarkers, such as interleukin (IL)-2, IL-6, IL-7, granulocyte-colony stimulating factor, macrophage inflammatory protein 1-α, tumor necrosis factor-α (TNF-α), CRP, ferritin, and D-dimer. This stage consists of the most severe manifestation of the cytokine storm, in which excessive hyperinflammation may lead to cardiopulmonary collapse and multi-organ failure [57 and 58].
Cytokines are small, biologically highly active proteins that regulate the growth, function, and differentiation of cells and help steer the immune response and inflammation . The previous studies demonstrated a significant increase in pro-inflammatory cytokines (IFNα, IFNγ, IL-1β, IL-6, IL-12, IL-18, IL-33, TNFα, TGFβ) and chemokines (CXCL10, CXCL8, CXCL9, CCL2, CCL3, CCL5) precipitates and sustains the aberrant systemic inflammatory response [60-63]. The cytokine storm is readily followed by the immune system “attacking” the body, which in turn will cause ARDS and multiple organ failure, the final result being death, at least in the most severe cases of SARS-CoV-2 infection . pro-inflammatory cytokines (IFNα, IFNγ, IL-1β, IL-6, IL-12, IL-18, IL-33, TNFα, TGFβ) and chemokines (CXCL10, CXCL8, CXCL9, CCL2, CCL3, CCL5) precipitates and sustains the aberrant systemic inflammatory response [60-63]. The cytokine storm is readily followed by the immune system “attacking” the body, which in turn will cause ARDS and multiple organ failure, the final result being death, at least in the most severe cases of SARS-CoV-2 infection .
For the present symptoms (fever, diarrhea and dry mouth), of our patients is case depended and increases in order form mild to severe COVID-19 infection. These suggests that fever and dry mouth may be the most important signs for the clinical pre-examination and triage of COVID-19 pneumonia . However, it has been reported that even the portion is small, some patients with COVID-19 pneumonia may present non-respiratory symptoms , and these patients may be miss-diagnosed or be misdiagnosed. Therefore, under current epidemiological conditions, the physicians in the front line must be very vigilant and arrange chest HRCT imaging and virological testing in time.
Also, COVID-19 pneumonia patients, most of the pulmonary lesions involved bilaterally with multiple lung lobes, with a predominant distribution in the lower and peripheral part of the lungs, but this rarely involved unilaterally. These lesions were mainly distributed in the bilateral subpleural and basilar lung regions because these were blocked by the pleural surface and progressed along the pleural surface. Mainly the diameter of the lesions was approximately parallel to the pleura, and perpendicular to the bronchovascular bundles. Viruses in the same family share a similar pathogenesis and presentation, peripheral predominance lung involvement has also been observed in patients with SARS and MERS [67 and 70]. The most common HRCT findings were pure GGO, GGO with interlobular septal thickening, and mixed GGO with consolidation, while no complete consolidation was found in our patients. Furthermore, we also found nodules, including solid nodules and solid nodules surrounded by a halo and linear opacities in some patients. Each patient may have two or more types of opacity lesions, but the majority of the lesions were GGO. Studies have reported that COVID-19 pneumonia is a viral interstitial pneumonia, and the early stage of pathogenesis is type II alveolar epithelial cell injury, edema, proteinaceous exudate, and focal hyperplasia of pneumocytes with only patchy inflammatory cellular infiltration, which all presented by GGO on HRCT results [67-70]. With the further thickening of the reticular and/or interlobular septa might be shown, the density of the GGO would increase, typical crazy paving signs may appear, and local vascular congestion swelling could be observed in some lesions. however, Huang et al. reported that pleural effusion may be an indication of severe COVID-19 pneumonia , further study is required for the clarification of the discrepancy.
Our study suggested that, COVID-19 firstly seize host cell intracellular membranes to create new compartments known as double-membrane vesicles (DMVs) needed for viral genome amplification. A specific phospholipid composition is required by different viruses to form the perfect replicative organelles that are suitable for their replication . DMVs are membranous structures that contain viral proteins and an array of confiscated host factors, which jointly orchestrate an exclusive lipid micro-environment ideal for coronavirus replication . Cytosolic phospholipase A2α enzyme (cPLA2α) is critical for DMVs’ formation and coronaviruses’ replication . Our study shows that, over expression of cPLA2 caused by COVID-19 infection (figure I). cPLA2 promotes gene expression of cytokine storm (TNF-α, IL-1β, IL-6 and IL-13) which led to elevates the activity of sPLA2. Also, Phosphatidylglycerol depletion and cleavage of fatty acids esterified as well as enhance inflammation and lung damage caused by sPLA2 over expression. Our proposal has not been reported earlier to our knowledge, and this study is perhaps the first observation of its kind.
Phospholipids is synthesized by alveolar type 2 cells (T2C) to reduce the surface tension of alveolar cell membrane . Phosphatidylglycerol (PG) and phosphatidylinositol (PI) participate in the packaging and extracellular organization of the phospholipids complex, as well as in immunomodulation and host defense [76-78].
In this study, we hypothesized that patients with COVID-19 develop chronic alterations of phospholipids levels and homeostasis that persist after severe infection.
Patients with severe COVID-19 infection showed significant alterations in their cytokines storm levels and exhibited an overall decrease in alveolar phospholipids availability that directly correlated with decreased pulmonary function.