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Biomol Concepts ; 13(1): 220-229, 2022 Apr 19.
Article in English | MEDLINE | ID: covidwho-1793459


The exposure of organisms and cells to unfavorable conditions such as increased temperature, antibiotics, reactive oxygen species, and viruses could lead to protein misfolding and cell death. The increased production of proteins such as heat shock proteins (HSPs) and polyamines has been linked to protein misfolding sequestration, thus maintaining, enhancing, and regulating the cellular system. For example, heat shock protein 40 (Hsp40) works hand in hand with Hsp70 and Hsp90 to successfully assist the newly synthesized proteins in folding properly. On the other hand, polyamines such as putrescine, spermidine, and spermine have been widely studied and reported to keep cells viable under harsh conditions, which are also involved in cell proliferation, differentiation, and growth. Polyamines are found in all living organisms, including humans and viruses. Some organisms have developed a mechanism to hijack mammalian host cell machinery for their benefit like viruses need polyamines for infection. Therefore, the role of HSPs and polyamines in SARS-CoV-2 (COVID-19) viral infection, how these molecules could delay the effectiveness of the current treatment in the market, and how COVID-19 relies on the host molecules for its successful infection are reviewed.

COVID-19 , Virus Diseases , Animals , Heat-Shock Proteins , Humans , Mammals/metabolism , Polyamines/metabolism , SARS-CoV-2 , Virus Diseases/metabolism
JCI Insight ; 5(14)2020 07 23.
Article in English | MEDLINE | ID: covidwho-607189


BACKGROUNDReprogramming of host metabolism supports viral pathogenesis by fueling viral proliferation, by providing, for example, free amino acids and fatty acids as building blocks.METHODSTo investigate metabolic effects of SARS-CoV-2 infection, we evaluated serum metabolites of patients with COVID-19 (n = 33; diagnosed by nucleic acid testing), as compared with COVID-19-negative controls (n = 16).RESULTSTargeted and untargeted metabolomics analyses identified altered tryptophan metabolism into the kynurenine pathway, which regulates inflammation and immunity. Indeed, these changes in tryptophan metabolism correlated with interleukin-6 (IL-6) levels. Widespread dysregulation of nitrogen metabolism was also seen in infected patients, with altered levels of most amino acids, along with increased markers of oxidant stress (e.g., methionine sulfoxide, cystine), proteolysis, and renal dysfunction (e.g., creatine, creatinine, polyamines). Increased circulating levels of glucose and free fatty acids were also observed, consistent with altered carbon homeostasis. Interestingly, metabolite levels in these pathways correlated with clinical laboratory markers of inflammation (i.e., IL-6 and C-reactive protein) and renal function (i.e., blood urea nitrogen).CONCLUSIONIn conclusion, this initial observational study identified amino acid and fatty acid metabolism as correlates of COVID-19, providing mechanistic insights, potential markers of clinical severity, and potential therapeutic targets.FUNDINGBoettcher Foundation Webb-Waring Biomedical Research Award; National Institute of General and Medical Sciences, NIH; and National Heart, Lung, and Blood Institute, NIH.

Coronavirus Infections/metabolism , Fatty Acids/metabolism , Interleukin-6/metabolism , Kynurenine/metabolism , Oxidative Stress , Pneumonia, Viral/metabolism , Renal Insufficiency/metabolism , Adult , Aged , Amino Acids/metabolism , Betacoronavirus , Blood Glucose/metabolism , COVID-19 , Case-Control Studies , Creatine/metabolism , Creatinine/metabolism , Cystine , Fatty Acids, Nonesterified/metabolism , Female , Humans , Male , Metabolome , Metabolomics , Methionine/analogs & derivatives , Middle Aged , Pandemics , Polyamines/metabolism , Proteolysis , SARS-CoV-2 , Tryptophan/metabolism