Key TakeawaysNew studies identify 128 molecular targets that could be targeted to stop coronaviruses from spreading to other cells.The transmembrane protein 41 B is also linked with aiding the viral replication of the Zika virus.Deactivating this protein may be potentially useful for antiviral therapies.

Key Takeaways

New studies identify 128 molecular targets that could be targeted to stop coronaviruses from spreading to other cells.The transmembrane protein 41 B is also linked with aiding the viral replication of the Zika virus.Deactivating this protein may be potentially useful for antiviral therapies.

While aCOVID-19 vaccineis being hailed as the light at the end of the pandemic, a team of researchers from NYU is prepping for a plan B. The results from two of their studies published in the journalCellshow that inhibiting specific proteins can prevent the SARS-CoV-2 virus from replicating and ultimately causing COVID-19 infections.

COVID-19 Vaccines:Stay up to date on which vaccines are available, who can get them, and how safe they are.

How Does SARS-CoV-2 Cause Infection?

A virus needs to transfer its genetic information to a host cell in order to replicate.Eric J. Yager, PhD, an associate professor of microbiology for the Albany College of Pharmacy and Health Sciences and the Center for Biopharmaceutical Education and Training, says that viruses lack the machinery to make their own proteins and reproduce. As a result, hijacking cells are necessary for their survival.

SARS-CoV-2 uses a spike protein to bind with the ACE2 receptor found on the surface of human cells. The spike protein acts as a key that latches on to the ACE2 receptor. This allows for viral entry into the cell.

How Long Is COVID-19 Contagious? A Look at the Research

To ensure the hijacking is a success, Yager says that SARS-CoV-2 manipulates the protective layer of fat surrounding the cell.

“Cellular membranes are comprised of a variety of lipid molecules,” Yager, who was not involved with the pair ofCellstudies, tells Verywell. “Accordingly, scientists have found that several clinically relevant viruses are able to alter host cell lipid metabolism in order to create an environment favorable for the assembly and release of infectious viral particles.”

Once inside, the virus can force the cell to make more copies of it. “Viruses co-opt host cell machinery and biosynthetic pathways for genome replication and the production of viral progeny,” Yager says.

To prevent COVID-19 infection, researchers need to stop the virus from entering the cells.

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While the spike protein may be a good target, the researchers of theCellstudy suggest that it might not be the only one.

“An important first step in confronting a new contagion like COVID-19 is to map the molecular landscape to see what possible targets you have to fight it,” saysJohn T. Poirier, PhD, an assistant professor of medicine at NYU Langone Health and co-author of the two studies in a recentpress release. “Comparing a newly-discovered virus to other known viruses can reveal shared liabilities, which we hope serve as a catalogue of potential vulnerabilities for future outbreaks.”

Investigating Other Potential Targets

The researchers sought to find the molecular components of human cells that SARS-CoV-2 takes over in order to copy itself. They used CRISPR-Cas9 to inactivate a single gene in a human cell. In total, they turned off the function of 19,000 genes. After, the cells were exposed to SARS-CoV-2 and three other coronaviruses known to cause the common cold.

Due to viral infection, many cells died. The cells that did live were able to survive because of the inactivated gene, which the authors suggest must be crucial for replication.

In total, the researchers found 127 molecular pathways and proteins that the four coronaviruses needed to copy themselves successfully.

In addition to the 127 identified, the researchers decided to focus on a protein called transmembrane protein 41 B (TMEM41B).

What This Means For You

Targeting Proteins for Drug Development

Targeting viral proteins is not a novel strategy, Yager says. It also works in treating bacterial infections.

“Antibiotics such as doxycycline, streptomycin, and erythromycin interfere with the ability of the bacterial 70S ribosome to synthesize bacterial proteins,” Yager says. “Antibiotics such as rifampicin work to inhibit the synthesis of bacterial mRNA, which is used as a blueprint to synthesize bacterial proteins.”

The researchers believe that TMEM41B and other proteins could be potential targets for future therapies.

The information in this article is current as of the date listed, which means newer information may be available when you read this. For the most recent updates on COVID-19, visit ourcoronavirus news page.

5 SourcesVerywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Hoffman HH, Schneider WM, Rozen-Gagnon K, et al.TMEM41B is a pan-flavivirus host factor.Cell. December 2020. doi:10.1016/j.cell.2020.12.005Schneider WM, Luna JM, Hoffmann HH, et al.Genome-scale identification of SARS-CoV-2 and pan-coronavirus host factor networks.Cell. 2021. doi:10.1016/j.cell.2020.12.006National Institutes of Health.SARS-CoV-2 may use key carbohydrate to infect cells. October 6, 2020.Huang Y, Yang C, Xu Xf. et al.Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19.Acta Pharmacol Sin.2020;41:1141–1149. doi:10.1038/s41401-020-0485-4Moretti F, Bergman P, Dodgson S, et al.TMEM41b is a novel regulator of autophagy and lipid mobilization.EMBO Rep. 2018;19(9):e45889. doi:10.15252/embr.201845889

5 Sources

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Hoffman HH, Schneider WM, Rozen-Gagnon K, et al.TMEM41B is a pan-flavivirus host factor.Cell. December 2020. doi:10.1016/j.cell.2020.12.005Schneider WM, Luna JM, Hoffmann HH, et al.Genome-scale identification of SARS-CoV-2 and pan-coronavirus host factor networks.Cell. 2021. doi:10.1016/j.cell.2020.12.006National Institutes of Health.SARS-CoV-2 may use key carbohydrate to infect cells. October 6, 2020.Huang Y, Yang C, Xu Xf. et al.Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19.Acta Pharmacol Sin.2020;41:1141–1149. doi:10.1038/s41401-020-0485-4Moretti F, Bergman P, Dodgson S, et al.TMEM41b is a novel regulator of autophagy and lipid mobilization.EMBO Rep. 2018;19(9):e45889. doi:10.15252/embr.201845889

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.

Hoffman HH, Schneider WM, Rozen-Gagnon K, et al.TMEM41B is a pan-flavivirus host factor.Cell. December 2020. doi:10.1016/j.cell.2020.12.005Schneider WM, Luna JM, Hoffmann HH, et al.Genome-scale identification of SARS-CoV-2 and pan-coronavirus host factor networks.Cell. 2021. doi:10.1016/j.cell.2020.12.006National Institutes of Health.SARS-CoV-2 may use key carbohydrate to infect cells. October 6, 2020.Huang Y, Yang C, Xu Xf. et al.Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19.Acta Pharmacol Sin.2020;41:1141–1149. doi:10.1038/s41401-020-0485-4Moretti F, Bergman P, Dodgson S, et al.TMEM41b is a novel regulator of autophagy and lipid mobilization.EMBO Rep. 2018;19(9):e45889. doi:10.15252/embr.201845889

Hoffman HH, Schneider WM, Rozen-Gagnon K, et al.TMEM41B is a pan-flavivirus host factor.Cell. December 2020. doi:10.1016/j.cell.2020.12.005

Schneider WM, Luna JM, Hoffmann HH, et al.Genome-scale identification of SARS-CoV-2 and pan-coronavirus host factor networks.Cell. 2021. doi:10.1016/j.cell.2020.12.006

National Institutes of Health.SARS-CoV-2 may use key carbohydrate to infect cells. October 6, 2020.

Huang Y, Yang C, Xu Xf. et al.Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19.Acta Pharmacol Sin.2020;41:1141–1149. doi:10.1038/s41401-020-0485-4

Moretti F, Bergman P, Dodgson S, et al.TMEM41b is a novel regulator of autophagy and lipid mobilization.EMBO Rep. 2018;19(9):e45889. doi:10.15252/embr.201845889

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