Lipidomics and Metabolomics Studies of COVID-19 Reveal Metabolic Disorders in the Pathogenesis of COVID-19

The COVID-19 pandemic has brought unprecedented threats to global public health. Here, we use a combination of targeted and untargeted tandem mass spectrometry to analyze the plasma lipidome and metabolome of patients with mild, moderate, and severe COVID-19 and healthy controls. The study found that an analysis group consisting of 10 plasma metabolites can effectively distinguish COVID-19 patients from healthy controls. The plasma lipid profile of COVID-19 is similar to the exosomes enriched with monosialo-dihexose gangliosides. The levels of phospholipid protein and GM3s are increased, while the level of diglyceride pairs is decreased. Using multi-scale embedded differential correlation network analysis, we conducted a systematic evaluation of metabolic disorders in COVID-19. Using exosomes isolated from the same sample population, we proved that for patients with severe COVID-19 disease, the enrichment of GM3 in their exosomes was significantly enhanced. Our research work shows that GM3 enriched exosomes may be involved in the pathological process related to the pathogenesis of COVID-19.

Viruses are known to induce complex changes in the lipidome of host cells, use host metabolic resources to aggravate viral infections, and usurp key energy pathways at different stages of the process. Different membrane curvatures and precise lipid composition can determine how easy it is for the virus to enter cells and replicate. According to previous studies, after being infected by different viruses, the patient's plasma or serum lipid group will show disease-related changes. For example, an increase in serum plasmalogen phosphatidylethanolamine has been observed in patients infected with Zika virus. In mice infected with respiratory syncytial virus, plasma triacylglycerols and free fatty acids decrease, and many PEps and plasmalogen phosphatidylcholine levels increase. For viral infections targeting the respiratory tract and lungs, the corresponding development of acute respiratory distress syndrome may also change lipids related to the inflammatory process. The biologically active derivatives of PUFA, such as 13-hydroxyoctadecadienoic acid (13-HODE) and 9-HODE, have been shown to be mediators of inducing and resolving inflammation caused by influenza virus infection, respectively. The reduction of plasma phosphatidylserine, PEs, diacylglycerol and ceramide was observed in the death cases of Ebola virus disease; from healthy controls to survivors, to death cases, monosialic acid dihexose ganglioside d34:0 gradually increased.

Sialic acid usually appears in cell secretions and on the outer surface of cells as a terminal motif attached to glycoproteins and glycolipids. According to reports, sialylation can mediate the binding and spread of many viruses. Sialylation exhibits a dual nature in cell-to-cell communication, which can mediate virus binding and recognition, and can also act as a "mask" in the process of suppressing immune responses by masking cell antigenic sites.

Therefore, viruses can use host-derived lipid membranes to conceal and escape the host's immune system during cell-to-cell transmission. Bypassing host surveillance can enhance unrestricted virus replication in the early stages of infection.

Studies have found that the changes in plasma lipids related to the pathogenesis of COVID-19 are similar to exosomes-specific lipid profiles?sphingomyelin (SMs) and GM3s increase while DAGs decrease. Based on exosomes isolated from the plasma of the same sample population, we proved that in patients with severe COVID-19, their exosomes are more rich in GM3.

Company :-Creative Protoemics

User :- andy smith

Email :-creative-proteomics@outlook.com

Phone :-16316197922

Url :- https://www.creative-proteomics.com/services/sphingomyelin-profiling-service.htm