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With the help of some bright X-ray photon beams, scientists have taken a closer look at SARS-CoV-2 and shed light on how it hides from the body’s immune system.
When a virus comes into contact with a human cell, it inserts its genetic material (in the form of RNA) into its host. The viral genome then hijacks the host cell's machinery for its own protein synthesis, forcing it to replicate the viral genome and produce viral proteins. Eventually, the newly produced viruses burst out of the host cell and kill the cell.
SARS-CoV-2 also works on this principle, but it holds a sneaky trick up its sleeve to ensure it slips into the host cell without being detected. As reported in the journal Nature Communications, scientists discovered that the SARS-CoV-2 virus uses some unique ways to camouflage its RNA to mimic those of the host cell.
It’s a bit like dressing as a croupier while attempting to rob a casino to avoid suspicion from the security guards.
“It’s a camouflage,” Yogesh Gupta, PhD, lead study author from the Joe R. and Teresa Lozano Long School of Medicine at the University of Texas Health Science Center at San Antonio, said in a statement. “Because of the modifications, which fool the cell, the resulting viral messenger RNA is now considered as part of the cell’s own code and not foreign.”
The researchers examined two synthetic proteins identical to the ones found in SARS-CoV-2 (nsp10 and nsp16) with ultrabright X-rays generated by the Advanced Photon Source (APS) at the US Department of Energy’s Argonne National Laboratory. The team took a closer look at the three-dimensional structure of nsp16 and discovered how it uses it to modify its messenger RNA cap. This, they say, is the key to making the viral RNA appear just like the host cell RNA and immediately flag the response of the immune system.
“Yogesh’s work discovered the 3D structure of a key enzyme of the Covid-19 virus required for its replication and found a pocket in it that can be targeted to inhibit that enzyme. This is a fundamental advance in our understanding of the virus,” added croupier Robert Hromas, MD, a professor and dean of the Long School of Medicine.
The researchers say this knowledge could be used to design new antiviral treatments that specifically target SARS-CoV-2. For example, it could theoretically be possible to develop a drug that inhibits nsp16 from making the modifications to RNA, thereby stripping the virus of its camouflage and leaving it more exposed to the immune system.
