The COVID-19 pandemic has led to over 100 million infections and over 3 million deaths worldwide. Understanding its pathogenesis is crucial to guide prognostic and therapeutic implications. Viral infections are known to alter the lipid profile and metabolism of their host cells, similar to the case with MERS and SARS-CoV-2002. Since lipids play various metabolic roles, studying lipid profile alterations in COVID-19 is an inevitable step as an attempt to achieve better therapeutic strategies, as well as a potential prognostic factor in the course of this disease. Several studies have reported changes in lipid profile associated with COVID-19. The most frequently reported changes are a decline in serum cholesterol and ApoA1 levels and elevated triglycerides. The hyper-inflammatory state mediated by the Cytokine storm disturbs several fundamental lipid biosynthesis pathways. Virus replication is a process that drastically changes the host cell's lipid metabolism program and overuses cell lipid resources. Lower HDL-C and ApoA1 levels are associated with higher severity and mortality rates and with higher levels of inflammatory markers. Studies suggest that arachidonic acid omega-3 derivatives might help modulate hyper-inflammation and cytokine storm resulting from pulmonary involvement. Also, statins have been shown to be beneficial when administered after COVID-19 diagnosis via unclear mechanisms probably associated with anti-inflammatory effects and HDL-C rising effects.
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