2-deoxyglucose for COVID-19
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COVID-19 Treatment Clinical Evidence
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Naso/
oropharyngeal treatment Effective Treatment directly to the primary source of initial infection. -
Healthy lifestyles Protective Exercise, sunlight, a healthy diet, and good sleep all reduce risk.
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Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
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Acetaminophen Harmful Increased risk of severe outcomes and mortality.
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Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.
2-deoxyglucose may be beneficial for
COVID-19 according to the studies below.
COVID-19 involves the interplay of 500+ viral and host proteins and factors providing many therapeutic targets.
Scientists have proposed 11,000+ potential treatments.
c19early.org analyzes
220+ treatments.
We have not reviewed 2-deoxyglucose in detail.
, Mitochondrial OXPHOS restricts SARS-CoV-2 replication, Science Advances, doi:10.1126/sciadv.adz3081
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rewires host metabolism to optimize virus production. Although glycolysis is necessary for virus production, the importance of mitochondrial oxidative phosphorylation (OXPHOS) is unknown. The mitochondrial DNA (mtDNA) codes for 13 critical OXPHOS polypeptides plus the 22 transfer RNAs (tRNAs) and 2 ribosomal RNAs (rRNAs) for mitochondrial protein synthesis. We found an ∼5- to 100-fold greater SARS-CoV-2 virus production in infected human ACE2-expressing A549 lung cells when OXPHOS was inhibited by mtDNA depletion (ρ 0 cells), inhibition of mitochondrial translation with chloramphenicol (CAP), or chemical inhibition of OXPHOS complexes. OXPHOS inhibition led to a marked increase in the size and distribution of viral replication centers and accelerated the production and release of infectious particles, occurring ∼2 hours earlier than in parental A549-ACE2 (wild type) cells. Subsequently, we found that increased glycolytic capacity was required for enhanced viral replication whereas differences in innate immune pathway activation were not. Reintroduction of mtDNA from a well-defined maternal lineage into the ρ 0 cells reinstated OXPHOS, impaired SARS-CoV-2 replication, and reversed associated viral and glycolytic correlates. Thus, metabolic balance regulates SARS-CoV-2 replication, with OXPHOS exerting an antiviral effect.