Thursday, 22 April 2021

Malevolent Designer News - A Little More About How Brilliantly SARS-CoV-2 is Designed for Killing People

  1. Rotavirus RNAs have a 5′ cap but not a 3′ poly(A) tail. Its NSP3 protein (instead of PABP) binds to the 3′ end of the viral mRNA and interacts with eIF‐4G directly to maintain the closed‐loop RNA for the initiation of viral RNA translation and to block host mRNA circularization (Piron et al, 1998
  2. Picornavirus RNA has an internal ribosome entry site (IRES) in the 5′ untranslated region and a 3′ poly(A) tail. Viral protease (2A or leader) digests eIF‐4G. The truncated eIF‐4G shows higher efficiency in the IRES‐driven translation than the cap‐dependent translation (Ohlmann et al, 1995; Ali et al, 2001).
  3. Coronavirus RNAs have a 5′ cap and a 3′ poly(A) tail. In our model, SUD associates with the 40S/80S ribosome and enhances the PABP:Paip1 interaction to stimulate the host translation machinery. Meanwhile, coronaviral Nsp1 specifically cleaves host mRNAs (green) but not viral RNAs (Kamitani et al, 2006; Huang et al, 2011). Also, viral Nsp1 blocks host mRNA binding to the 40S ribosome. As a result, SARS‐CoV could increase the viral RNA translation but inhibit host mRNA translation.
How SARS coronaviruses reprogram host cells to their own benefit | News - LMU München

For those Intelligent [sic] Design advocates who are not embarrassed by the evident malevolent sadism of their putative designer, this sort of information should thrill and delight them.

Scientists working at the University of Lübeck, Germany and the Ludwig-Maximilians-Universität, München, Germany have discovered the brilliant mechanism by which the SARS-CoV and SARS-CoV-2 viruses reprogram our cells to reproduce many more copies of the viruses than other coronaviruses, such as those causing the common cold.

They suggest that this may account for the much higher pathogenicity of these two viruses compared to the other coronaviruses. Their findings appeared, open access, in The EMBO Journal 2021, two days ago.

The relevent details are in the Ludwig-Maximilians-Universität news release:
Coronavirus researchers led by Professor Rolf Hilgenfeld of the University of Lübeck and PD Dr. Albrecht von Brunn of Ludwig-Maximilians-Universität München have discovered how SARS viruses enhance the production of viral proteins in infected cells, so that many new copies of the virus can be generated. Notably, coronaviruses other than SARS-CoV and SARS-CoV-2 do not use this mechanism, which may therefore provide a possible explanation for the much higher pathogenicity of the SARS viruses. The findings appear in the EMBO Journal.

Coronaviruses that cause harmless colds in humans were discovered more than 50 years ago. When it emerged in 2002/2003, the SARS coronavirus was the first coronavirus found to cause severe pneumonia in infected people. Comparisons of the RNA genomes of innocuous coronaviruses with those of the SARS coronavirus permitted researchers to identify a region that only occurred in the latter, and was called the "SARS-unique domain" (SUD). Such genomic regions and their protein products might be linked to the extraordinary pathogenicity of SARS coronavirus and its cousin, the COVID-19 virus SARS-CoV-2.

The research groups led by Hilgenfeld and von Brunn showed that the SUD proteins of these two viruses interact with a human protein called Paip-1, which is involved in the first steps of protein synthesis. Together with Paip-1 and other proteins in human cells, SUD apparently binds to the ribosomes, the molecular machines that are responsible for protein synthesis in cells. This would lead to an enhancement of the production of all proteins, both those of the host cell and those of the virus. However, in cells infected with SARS-CoV or SARS-CoV-2, the messenger RNA molecules that code for host proteins are selectively destroyed by a viral protein named Nsp1. As a result of this complicated process, the infected cell predominantly produces viral proteins, so that many new copies of the virus can be created.

Albrecht von Brunn’s research group discovered the interaction between the proteins SUD and Paip-1 several years ago. "Being an experienced coronavirologist, I knew that one has to inspect the special regions of the SARS genome when trying to understand this virus,” he says.

[My emphasis]
Ingenious, or what?!

Here is how the scientists explained it in the abstract to their peer-reviewed publication:

Synopsis

The presence of a “SARS‐unique domain” (SUD) in non‐structural protein 3 (Nsp3) of SARS‐CoV and SARS‐CoV‐2 offers an opportunity to study its specific modulation of host cells. Here, biochemical and structural data demonstrate SUD interaction with host translation factor Paip1, and its effect on viral protein synthesis in human cells.
  • The SUD of SARS‐CoV and SARS‐CoV‐2, but not of MERS‐CoV, interacts with human Paip1 (PABP‐interacting protein) in vitro and in cells.
  • X‐ray crystal structure and SAXS data define the interaction between Paip1 and macrodomain II (Mac2) in the SARS‐CoV SUD.
  • The SUD forms a ternary complex with Paip1 and PABP and interacts with 40S/80S ribosomal particles in cells.
  • The Nsp3 SUD enhances viral but not host protein synthesis in SARS‐CoV replicon‐transfected cells via the SUD:Paip1 interaction.

Abstract


The ongoing outbreak of severe acute respiratory syndrome (SARS) coronavirus 2 (SARS‐CoV‐2) demonstrates the continuous threat of emerging coronaviruses (CoVs) to public health. SARS‐CoV‐2 and SARS‐CoV share an otherwise non‐conserved part of non‐structural protein 3 (Nsp3), therefore named as “SARS‐unique domain” (SUD). We previously found a yeast‐2‐hybrid screen interaction of the SARS‐CoV SUD with human poly(A)‐binding protein (PABP)‐interacting protein 1 (Paip1), a stimulator of protein translation. Here, we validate SARS‐CoV SUD:Paip1 interaction by size‐exclusion chromatography, split‐yellow fluorescent protein, and co‐immunoprecipitation assays, and confirm such interaction also between the corresponding domain of SARS‐CoV‐2 and Paip1. The three‐dimensional structure of the N‐terminal domain of SARS‐CoV SUD (“macrodomain II”, Mac2) in complex with the middle domain of Paip1, determined by X‐ray crystallography and small‐angle X‐ray scattering, provides insights into the structural determinants of the complex formation. In cellulo, SUD enhances synthesis of viral but not host proteins via binding to Paip1 in pBAC‐SARS‐CoV replicon‐transfected cells. We propose a possible mechanism for stimulation of viral translation by the SUD of SARS‐CoV and SARS‐CoV‐2.

I'm still waiting for the first Creationist to break ranks and declare that something this malevolent can't possibly be the god of the bible whom they regard as the epitome of love and compassion who only wants the best for its creation. Either that god is not the creator of the SARS-C0V-2 virus or that god is the epitome of malevolent hate and the creator of monstrous evil.

Or, there is a perfectly natural explanation for these viruses, not requiring the creative participation of gods, real or imaginary.

The silence from Creationists on this question shouts louder than they could possibly imagine. It's almost as though they know they've fallen for a hoax but are too embarrassed and dishonest to admit it…



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