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The novel coronavirus SARS-CoV-2 possesses an enzyme that effectively neutralizes a cell’s natural defenses against viral infections. This characteristic helps explain its heightened infectivity compared to earlier SARS and MERS viruses. A study from Kobe University may pave the way for more effective medications not only for this virus but for similar future ailments as well.
When faced with a viral attack, the immune system employs two main lines of defense: the innate immune system, which acts quickly and broadly, and the adaptive immune system, which strengthens over time against specific pathogens and forms the basis for vaccinations. According to virologist SHOJI Ikuo from Kobe University, the novel coronavirus is remarkably infectious, prompting curiosity about the sophisticated strategies it uses to bypass the innate immune response.
Shoji’s research team has previously explored how the immune system reacts to hepatitis viruses and focused on a molecular marker known as “ISG15.” This marker is attached by the innate immune system to the components of viruses. Upon discovering that the new coronavirus has a powerful enzyme capable of detaching this marker, the team aimed to understand how ISG15 impacts the coronavirus and how the virus counters this effect.
In a recent article published in the Journal of Virology, the team from Kobe University is the first to document that the ISG15 marker binds to a specific site on the virus’s nucleocapsid protein—essentially the framework that encases the virus’s genetic code. The virus requires multiple copies of the nucleocapsid protein to assemble, but the ISG15 marker disrupts this assembly, representing its antiviral properties. Nonetheless, the novel coronavirus possesses an enzyme that removes these markers from the nucleocapsid, allowing it to reform new viruses and effectively elude the innate immune defenses, as explained by Shoji.
While the novel coronavirus shares several characteristics with SARS and MERS viruses, all part of the same viral family, Shoji’s team discovered that the enzymes in those viruses are less effective at removing the ISG15 marker than the one found in SARS-CoV-2. Recent information suggests that the earlier viruses’ enzymes have different main targets. “These findings imply that the novel coronavirus has superior evasion capabilities regarding this aspect of the innate immune system, which helps account for its high level of infectivity,” Shoji notes.
Understanding the effectiveness of the novel coronavirus also offers insights for potential treatments. The researcher from Kobe University points out, “If we can hinder the function of the viral enzyme responsible for removing the ISG15 marker, we might be able to create new antiviral medications. Future therapeutic approaches could also aim at the nucleocapsid protein itself or combine strategies targeting both mechanisms.”
This research received funding from the Kansai Economic Federation, the Hyogo Science and Technology Association (grant 3501), and the Ministry of Education, Culture, Sports, Science and Technology of Japan (grant 18042-203556). The study involved collaboration with researchers from Universitas Gadjah Mada, Niigata University, the University of Yamanashi, Hokkaido University, and Osaka University.
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