COVID-19: lipid disruption is pushing the envelopeA plethora of articles have been published on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and science has delivered, given the rapid development of vaccines and of novel antiviral therapeutics evaluated for their efficacy efficiently in platform trials. An unfolding story of interferon genetics and autoantibodies has begun to help us parse the reasons for varied susceptibility to severe disease and sequencing, and tracking at a global level has allowed for the rapid detection of new variants as they emerge.
The bidirectional link between HDL and COVID-19 infectionsIt is well recognized that gram positive and negative bacterial infections, tuberculosis, fungal infections, and parasitic infections result in changes in plasma lipid levels (1–12). Of note, viral infections, such as HIV, Epstein-Barr virus, and Dengue fever, also similarly alter plasma lipid levels (13–15). Typically, infections decrease total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels with either elevated triglyceride or inappropriately normal triglyceride levels for the decreased nutritional status that characteristically occurs with infections.