With the help of some bright ecstasy - electron beam photon beams , scientists have choose a close look at SARS - CoV-2 and exuviate light on how it hides from the body ’s immune system .
When a virus comes into contact with a human mobile phone , it inserts its genetical material ( in the soma of RNA ) into its host . The viral genome then hijacks the host electric cell ’s machinery for its own protein deduction , forcing it to repeat the viral genome and bring out viral proteins . Eventually , the new produce viruses collapse out of the legion cell and kill the cellular telephone .
SARS - CoV-2 also works on this rule , but it bear a surreptitious trick up its arm to ensure it drop off into the host cell without being detected . As reported in the journalNature Communications , scientists attain that the SARS - CoV-2 computer virus use some unequaled way to camouflage its RNA to mimic those of the host cadre .
It ’s a snatch like dressing as a croupier while attempting to fleece a casino to avoid suspicion from the security guards .
“ It ’s a camouflage , ” Yogesh Gupta , Ph.D. , lead study writer from the Joe R. and Teresa Lozano Long School of Medicine at the University of Texas Health Science Center at San Antonio , said in astatement . “ Because of the modifications , which horse around the jail cell , the resulting viral messenger RNA is now consider as part of the cadre ’s own code and not foreign . ”
The researchers examined two man-made proteins identical to the ones establish in SARS - CoV-2 ( nsp10 and nsp16 ) with ultrabright X - rays generate by the Advanced Photon Source ( APS ) at the US Department of Energy ’s Argonne National Laboratory . The squad took a tightlipped look at the three - dimensional body structure of nsp16 and discovered how it practice it to modify its courier RNA capital . This , they say , is the cay to making the viral RNA seem just like the host cellular phone RNA and immediately ease up the reception of the resistant organisation .
“ Yogesh ’s piece of work discovered the 3D structure of a key enzyme of the Covid-19 virus required for its replication and find a pocket in it that can be targeted to inhibit that enzyme . This is a fundamental advance in our understanding of the computer virus , ” added croupier Robert Hromas , MD , a professor and James Dean of the Long School of Medicine .
The researchers say this knowledge could be used to design new antiviral treatment that specifically target SARS - CoV-2 . For example , it could theoretically be possible to develop a drug thatinhibits nsp16 from making the modifications to RNA , thereby stripping the virus of its camo and leaving it more exposed to the immune system .
