1.SARS-CoV-2 RNA nsp16(青色)/nsp10(米色)之合物，在具有RNA-端帽(RNAcap，色)及S-腺苷甲硫氨酸(色)之合中的三元合。 (援用自原文)
Structure of the ternary complex of SARS-CoV-2 RNA nsp16 (cyan)/nsp10 (beige) in complex with RNA cap (red) and S-adenosyl methionine or SAM (blue).
As we all know too well, the virus SARS-CoV-2 causes the severe respiratory illness COVID-19. In parallel with the critical search for a cure, scientists are working diligently to develop effective treatments that can help lower the morbidity of this deadly virus.
所周知，第二型重急性呼吸系徵候群-冠病毒(SARS-CoV-2：Severe Acute Respiratory Syndrome Coronavirus-2)，病毒引2019冠病毒症(COVID-19：Coronavirus Disease-19)，重呼吸系疾病。在求性法平行行，科家正努力，能有助於降低此致命病毒病率的有效法。
To develop these therapeutics, we must understand how the virus is able to invade a host’s cells and dodge detection. A recent Nature Communications report based on research carried out at the U.S. Department of Energy’s Advanced Photon Source (APS) reveals key details about how SARS-CoV-2 modifies its messenger RNA and evades immune responses in its host.
了此些法，必需解病毒如何能，入侵宿主胞及避。 根以美能源部所先光子源(APS)所行，最近表於《自然•期刊通》的一研究，揭露了有SARS-CoV-2如何，修其信使RNA，及避，於其宿主中之免疫反的。
Using high-resolution x-ray crystallography, the researchers determined a high-resolution structure ofthe ternary SARS-CoV-2 RNA cap/nsp16/nsp10 complex and the conformational changes that catalytic nsp16 undergoes during RNA cap-binding. The researchers also discovered a distantly located ligand-binding site that allows nsp16 to bind small molecules outside the catalytic pocket.
使用高解析度的X-射晶技，此些研究人了，三元SARS-CoV-2 RNA cap/nsp16/nsp10合的高解析度，及在RNA cap合期，nsp16的形化。此些研究人也一，使nsp16得以在域外部合小分子，座落於的配位合位。
These findings improve our understanding of mRNA capping in coronaviruses and provide a strategy by which scientists could develop small-molecule drugs that will fight and treat the diseases caused by coronaviruses like SARS-CoV-2.
些研究改善了人有，在冠病毒中，mRNA加端帽的解，且提供了一，科家可能藉以，能抗及治，由如SARS-CoV-2冠病毒，引之疾病的小分子物策略。
Coronaviruses (CoVs) are enveloped positive-sense RNA viruses that are notorious for causing a variety of diseases from enteritis to respiratory illnesses in both animals and humans.
冠病毒(CoVs)是於物及人中，引炎到呼吸道各疾病，名昭彰之有包膜的性RNA病毒。
The latest SARS-CoV-2 pandemic illustrates how CoVs can jump between species, gain access to host cells, and propagate with little inhibition. But, in order to design vaccines and treatments that will reduce the burden of the diseases caused by coronaviruses, we must understand their immunopathology.
最近SARS-CoV-2的大流行病明了，CoVs如何能在物之跳越、得入宿主胞的途及少受抑制地播。不，了能少，由冠病毒引起之疾病的疫苗及法，咱必解其免疫病理原理。
SARS-CoV-2 is a β-coronavirus that virally encodes mRNAs to mimic host cellular mRNA. To do this, the non-structural protein 16 (nsp16), together with nsp10, methylates the 5′-end of virally encoded mRNAs. Then, nsp16/nsp10 complex converts the mRNA species to the cap-1 form via 2′-O methylation of the ribose sugar of the first nucleotide.
SARS-CoV-2是一，病毒性mRNA，模宿主胞mRNA的β-冠病毒。此，非蛋白16 (nsp16)nsp10一起，甲基化病毒性之mRNA的5'-端。之後，nsp16/nsp10合由，第一核苷酸之核糖的2'-O甲基化，mRNA化端帽-1(cap-1)的形。
So, what information is missing? In short, the catalytic mechanism of mRNA capping is still unclear. Previous reports have presented crystal structures for SARS-CoV nsp16/nsp10 in complex with the methyl donor S-adenosyl methionine (SAM) without an RNA cap. However, no high-resolution structures had been reported for SARS-CoV-2 nsp16/nsp10 in complex with SAM, the methyl donor, and RNA cap m7GpppA. That is, until recently.
那，缺少什信息？言之，mRNA加端帽的制，仍然不。先前的告已提出了，SARS-CoV nsp16 / nsp10具有，RNA端帽之甲基施S-腺苷甲硫氨酸(SAM)合的晶。不，未曾具有SAM、甲基施及RNA端帽m7GpppA之SARS-CoV-2 nsp16 / nsp10合的高解析度告。也就是，直到最近皆有。
The researchers in this study, from University of Texas Health at San Antonio, New England Biolabs, and the Texas Biomedical Research Institute, employed high-brightness x-rays from the APS at the Northeastern Collaborative Access Team (NE-CAT) 24-ID-C beamline to collect the high-resolution x-ray crystallography data on crystals of the nsp16/nsp10/SAM/Cap-O/adenosine complex. (The APS is an Office of Science user facility at Argonne National Laboratory.)
在研究中，自美德州大安尼中心、新英格生物室及德克斯生物研究所的研究人用了，自Northeastern Collaborative Access Team (NE-CAT)之先光子源(APS：Advanced Photon Source )24-ID-C光束的高亮度X-射，收集有nsp16 / nsp10 / SAM / Cap-O /腺苷合物晶之高解析度的X-射晶。(APS是美能源部科局於阿家室的用)
With the data collected at NE-CAT, the researchers were able to determine the high-resolution structure of the ternary complex of SARS-CoV-2 RNA cap/nsp16/nsp10 complex captured just before ribose 2′-O methylation. A representation of this structure is shown in Fig. 1. They observed that during RNA cap-binding, the catalytic nsp16 undergoes a conformational change from a binary to ternary state.
利用在NE-CAT收集的，此些研究人能，就在核糖2'-O甲基化之前捕之SARS-CoV-2 RNA cap / nsp16 / nsp10三元合的高解析度。 於1.中，呈了。他察到，在合RNA端帽期，之nsp16了，二元到三元的象化。
This transition facilitates the addition of a cap-1 structure, m7GpppNm, which acts as a camouflage for the viral mRNA. As a result, the host cells are tricked into recognizing the viral mRNA as their own. This discovery is especially important because it demonstrates how SARS-CoV-2 can avoid detection by the host’s immune system.
此促了端帽-1物(m7GpppNm)的增添。充了，病毒mRNA的一。果，宿主胞被，病毒mRNA其自身物。此特重要。因，明了SARS-CoV-2如何避免，被宿主免疫系到。
The researchers also discovered a distantly located ligand-binding site in nsp16/10 where small molecules can bind outside the catalytic pocket. The findings may help to guide the development of SARS-CoV-2 therapies. In essence, if scientists are able to design small-molecule drugs that prohibit cap-1 structure addition by nsp16, they can eliminate the “camouflage’ effect and expose the virus to host immune restriction.
此些研究人在nsp16/10中，也一在此域外部，小分子能合之座落於的配位合位。些研究可能有助於，引SARS-CoV-2的法。基本上，倘若科家能出抑制，由nsp16增添之端帽-1物的小分子物，他能消除上述“”作用，而使病毒暴露於宿主的免疫束中。
The structural details gleaned from this research provide a clearer picture of mRNA capping in coronaviruses. These findings improve our collective understanding of how SARSCoV-2 replicates and avoids detection.
研究收集到的提供了，在冠病毒中，mRNA加端帽的更清晰影像。此些改善了人，於SARSCoV-2如何，及避被的解。
原文址：https://aps.anl.gov/APS-Science-Highlight/2020-08-26/how-sars-cov-2-rna-evades-host-immune-responses
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