Influenza, also known as the flu, is estimated to have resulted in 12,000 – 61,000 deaths annually since 2010. COVID-19, the disease caused by the virus SARS-COV-2, has resulted in approximately 3.18 million deaths globally. The viruses that cause these diseases may show similar symptoms, but are inherently different in structure and function; therefore, antivirals, drugs that treat viral infections, for each of these diseases must also work differently. SARS-COV-2 and influenza are both highly infectious viruses, so treating infected individuals with antivirals can be a strong tool to deter the spread of both viruses.
Antivirals for influenza, such as Tamiflu and Amantadine, attempt to inhibit viral replication, when a virus hijacks an individual’s cells in order to create more viruses, by targeting viral proteins. Tamiflu, formally known as oseltamivir phosphate, is an inhibitor of neuraminidase proteins found on the surface of certain influenza viruses. Neuraminidase proteins break down sialic acid, a molecule found on mammalian cells that acts as a leash for viruses. Since viruses utilize human-cell machinery to replicate, sialic acid must be cut in order for the virus to be released and spread within an organism. Tamiflu prevents this from occurring by stopping neuraminidase from breaking down sialic acid. Viral particles are then unable to leave the cell, forming aggregates on the cell surface. Infected cells with viral aggregates can be targeted by the immune system, which limits the spread of influenza virus within the respiratory tract.
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Amantadine is another antiviral used to treat the flu. However, it has a completely different mechanism of action than Tamiflu. The drug inhibits the “M2 protein” that is characteristic of influenza A viruses. The M2 protein allows for positively charged hydrogen atoms to flow from the external environment into the virus; this process triggers the release of the influenza genome into the cell, making it available for viral replication.
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COVID antivirals are unforunately less common. The Food and Drug Administration (FDA) approved the use of the antiviral Remdesivir for the treatment of COVID-19 in October of 2020. Remdesivir indirectly inhibits the viral RNA Polymerase (RDRP) that is found in SARS-COV-2, a protein aids in the replication of the viral genome. Replication of the viral genome requires the use of molecules called nucleotides, the building blocks of DNA and RNA. Remdesivir can mimic the structure of nucleotides by acting as an analog. When RDRP encounters Remdesivir, RDRP can’t build new genetic material because Remdesivir isn’t a true nucleotide. Therefore, the virus is unable to replicate. Research studies are continuing to analyze the efficacy of Remdesivir in treating COVID-19.
The viruses that cause the flu and COVID-19 are highly infectious, so antivirals are used to halt the spread of each disease. Since both viruses have different genomes, the antivirals for these diseases also have distinct mechanisms of action, such as targeting varying aspects of viral replication. Despite these differences, underlying commonalities between most antivirals can actually help in creating new and effective COVID antivirals, which would be a great help in ending this pandemic!
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