To date (14 Oct. 2022) an estimated 624,161,610 people have been infected, of which 6,565,979 have died, 1,064,910 of those in the USA alone. Several countries are experiencing yet another wave of infections and there is reported to be an even more dangerous variant (BA.2.75.2) waiting in the wings.
And today’s piece of thrilling news for devotees of this putative pestilential sadist and habitual serial killer, is that it's not just the spike proteins that give the virus it's virulence, but another protein that the vaccines don't reach, but which can inhibit our immune response. The malevolent designer obviously anticipated medical science's response to the pandemic and built in a way round the defences medical science was going to give us, if you’ve fallen for the intelligent [sic] design hoax, that is..
What is interesting is that both BA.4 and BA.5 variants have the same genetic sequence for the spike protein. This means it’s the other genes, the non-spike protein genes, that seem to affect the way the virus copies itself and causes disease. So, mutations in these other accessory genes are what has allowed variants like BA.5 to outcompete the earlier versions of the virus.
Professor Matthew Frieman, PhD, co-lead author.
Alicia and Yaya Foundation Professor of Viral Pathogen Research
The Department of Microbiology & Immunology
University of Maryland School of Medicine, Baltimore, MD, USA.
Alicia and Yaya Foundation Professor of Viral Pathogen Research
The Department of Microbiology & Immunology
University of Maryland School of Medicine, Baltimore, MD, USA.
It was this difference that the researchers from the University of Maryland School of Medicine set out to identify.
SARS-CoV-2 genes, like other RNA viruses have three different functional groups of genes:
- Those involved in making more copies of the virus
- Those that make the virus structure
- Accessory genes that have other functions.
Dr. Frieman’s team of researchers found that virus missing the ORF3a/b gene led to more mild infections than the original SARS-CoV-2 virus. The mice with this virus strain lost less weight and had less virus in their lungs than mice infected with the original virus. These findings indicated that the ORF3a/b gene likely plays a role in either making more copies of the virus through viral replication or blocking the immune response to the infection. Other experiments suggested ORF3a/b has an extra job in the virus by seeming to activate the body’s innate immune system, the first line of defense launched by the immune system, signaling that a foreign invader needs to be vanquished.
In contrast, the researchers found that mice infected with virus missing the ORF8 gene were sicker than mice with the original strain of SARS-CoV-2. These mice had increased inflammation in their lungs when compared with the original SARS-CoV-2 virus. The researchers said that ORF8 seems to control the immune response in the lungs.By inhibiting the immune response, ORF8 helps the virus to replicate more in the lungs which worsens infection. When removed, it allowed the immune system to fight back harder.
Professor Frieman.
Next, the researchers looked at how important the spike protein was for disease severity in each of the different variants of SARS-CoV-2. They took the original virus and swapped out the spike gene with the spike gene of either the alpha, beta, gamma, or delta variant. Then they infected cells and mice and observed how each of these viruses replicated and entered healthy cells. The virus uses the spike protein to hitchhike on the host’s ACE2 receptors found on the outside of cells lining the lungs as a way to get inside and infect cells.While the spike mutations are important for enhancing receptor binding and entry into cells, the researchers also found that the mutations in the accessory proteins can alter clinical disease presentation. We need to learn more about the role of accessory protein mutations in COVID-19 infection, especially as new variants and subvariants keep emerging where these other proteins may play more of a starring role.
Dr Mark T. Gladwin, MD (not involved with the research)
Vice President for Medical Affairs
and John Z. and Akiko K. Bowers Distinguished Professor and Dean
University of Maryland Medical School, Baltimore, MD, USA
Dr. Frieman’s team found that the spike protein determines the severity of some of the variants, but not for others. The gamma variant was weaker than the other variants in its ability to replicate and infect. The researchers think that the mutations in genes outside of the ‘spike,’ particularly in the ORF8 gene, seem to play a role in making this version weaker than the others. Although the gamma variant circulated in Brazil, it did not spread further around the globe as it was overtaken by stronger variants.
More technical detail is given in the team's paper published open access in PNAS:
SignificanceAs always, here is an open invitation to all Creationists to explain how these variants arise if it is not through the intervention of their putative intelligent [sic] designer and if it is due to their favourite supernatural designer, why they prefer people to see it as the malevolent sadist this makes it out to be, rather than accept that viruses, like other biological entities, evolve by an amoral, unintelligent natural process in which no gods were involved.
A hallmark of the COVID-19 pandemic has been the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants that both increased transmission and improved immune evasion. Each variant possesses mutations throughout its genome, but little is known about their effect on pathogenesis. Specifically, we are interested in the accessory genes of SARS-CoV-2, which have been shown to affect viral pathogenesis through interference with the host innate immune response. In this work, we identify accessory genes that are responsible for pathogenesis in vivo and investigate the effect of variant nonspike genes on replication and disease in mice. This work identifies accessory genes as key drivers of pathogenesis and highlights the effect of nonspike genes on replication and pathogenesis.
Abstract
The ongoing COVID-19 pandemic is a major public health crisis. Despite the development and deployment of vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pandemic persists. The continued spread of the virus is largely driven by the emergence of viral variants, which can evade the current vaccines through mutations in the spike protein. Although these differences in spike are important in terms of transmission and vaccine responses, these variants possess mutations in the other parts of their genome that may also affect pathogenesis. Of particular interest to us are the mutations present in the accessory genes, which have been shown to contribute to pathogenesis in the host through interference with innate immune signaling, among other effects on host machinery. To examine the effects of accessory protein mutations and other nonspike mutations on SARS-CoV-2 pathogenesis, we synthesized both viruses possessing deletions in the accessory genes as well as viruses where the WA-1 spike is replaced by each variant spike gene in a SARS-CoV-2/WA-1 infectious clone. We then characterized the in vitro and in vivo replication of these viruses and compared them to both WA-1 and the full variant viruses. Our work has revealed that the accessory proteins contribute to SARS-CoV-2 pathogenesis and the nonspike mutations in variants can contribute to replication of SARS-CoV-2 and pathogenesis in the host. This work suggests that while spike mutations may enhance receptor binding and entry into cells, mutations in accessory proteins may alter clinical disease presentation.
McGrath, Marisa E.; Xue, Yong; Dillen, Carly; Oldfield, Lauren; Assad-Garcia, N.; Zaveri, Jayshree; Singh, Natasha; Baracco, Lauren; Taylor, Louis J.; Vashee, Sanjay; Frieman, Matthew B.
SARS-CoV-2 variant spike and accessory gene mutations alter pathogenesis
Proceedings of the National Academy of Sciences (PNAS) 119(37), e2204717119; DOI: 10.1073/pnas.2204717119
Copyright: © 2022 The authors.
Published by PNAS. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
I’ve been asking this since before the pandemic started and never managed to get an intelligible response from a Creationist.
The designer is very intelligent in a malevolent way and not in a good way. It continually defeats humanity's vaccines and medicines to ensure that its creation suffers and dies. Instead of using its intelligence and its power to heal the creation it chooses to harm and torture its creation instead. Its an evil bastard.
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