MiR-24-3p for COVID-19
c19early.org
COVID-19 Treatment Clinical Evidence
COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets.
c19early analyzes 6,000+ studies for 210+ treatments—over 17 million hours of research.
Only three high-profit early treatments are approved in the US.
In reality, many treatments reduce risk,
with 25 low-cost treatments approved across 163 countries.
-
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.
-
Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
-
Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
-
Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
-
High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
-
Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
-
Acetaminophen Harmful Increased risk of severe outcomes and mortality.
-
Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.
MiR-24-3p may be beneficial for
COVID-19 according to the study below.
COVID-19 involves the interplay of 400+ viral and host proteins and factors providing many therapeutic targets.
Scientists have proposed 11,000+ potential treatments.
c19early.org analyzes
210+ treatments.
We have not reviewed miR-24-3p in detail.
, miR-24-3p Is Antiviral Against SARS-CoV-2 by Downregulating Critical Host Entry Factors, Viruses, doi:10.3390/v16121844
Despite all the progress in treating SARS-CoV-2, escape mutants to current therapies remain a constant concern. Promising alternative treatments for current and future coronaviruses are those that limit escape mutants by inhibiting multiple pathogenic targets, analogous to the current strategies for treating HCV and HIV. With increasing popularity and ease of manufacturing of RNA technologies for vaccines and drugs, therapeutic microRNAs represent a promising option. In the present work, miR-24-3p was identified to inhibit SARS-CoV-2 entry, replication, and production; furthermore, this inhibition was retained against common mutations improving SARS-CoV-2 fitness. To determine the mechanism of action, bioinformatic tools were employed, identifying numerous potential effectors promoting infection targeted by miR-24-3p. Of these targets, several key host proteins for priming and facilitating SARS-CoV-2 entry were identified: furin, NRP1, NRP2, and SREBP2. With further experimental analysis, we show that miR-24-3p directly downregulates these viral entry factors to impede infection when producing virions and when infecting the target cell. Furthermore, we compare the findings with coronavirus, HCoV-229E, which relies on different factors strengthening the miR-24-3p mechanism. Taken together, the following work suggests that miR-24-3p could be an avenue to treat current coronaviruses and those likely to emerge.