There are several possible explanations for aberrant lipid levels in COVID-19 patients. First, it may result from a liver injury. Although liver functions only exhibit mild abnormalities in protein synthesis (Supplementary Table 1), whether lipid biogenesis has been impaired is yet to be determined. Second, viral infection induced pro-inflammatory cytokines modulate lipid metabolism including oxidation of LDL by reactive oxygen species singling to facilitate LDL clearance [[11], [12], [13]]. A measurement of oxidized LDL in patient's serum will aid in determining this mechanism. Third, COVID-19 patients may have an increased vascular permeability caused by viral-induced inflammation. Exudates have been found evidently in the early phase of COVID-19 lung pathology [8]. Exudative fluids, containing high levels of protein and cholesterol, are caused by inflammation-related vascular permeability [14,15], which may be one possible mechanism underlying our data. The major limitations of this study include a small size of patients and lack of information of specific lipoproteins and oxidized LDLs. Another limitation is lack of a data set with lipids monitoring on a hospitalized non-COVID-19 disease group to further address the specificity between LDL levels and COVID-19 severity. We also posit that the dyslipidemia plays an important role in pathological development of COVID-19, which mechanism needs an urgent investigation. In conclusion, our results demonstrate that LDL decrease is associated with pathological course of COVID-19, which can serve a factor to access the disease progression and mortality.