Monday, 27 December 2021

Malevolent Designer News - How Brilliant was Creationism's Favourite Serial Killer?

Viruses enter cells to make copies of themselves and cause infection. One secret to SARS-CoV-2’s success is hiding from the immune system by spreading between cells. This transmission electron micrograph shows COVID-causing virus particles that were isolated from a patient.

Image: National Institute of Allergy and Infectious Diseases, NIH
SARS-CoV-2 goes ‘underground’ to spread from cell to cell

Creationist mode:

A couple of papers published recently show us just how brilliant and obsessively determined to maximise suffering Creationism's beloved mass murder was when it designed and then subsequently modified the SARS-CoV-2 virus.

The first, by a team from Ohio State University, Ohio, USA, led by virology professor, Shan-Lu Liu of the University's Veterinary Biosciences Department and its Center for Retrovirus Research, explains how the virus is designed to evade your immune system by spreading in your body by cell-to-cell spread rather than by being liberated by infected cells to circulate and infect new host cells.

The problem with the latter method was that it brings the virus into contact with circulating antibodies which remain outside the cell. Spreading from cell to cell is a much more efficient method as it circumvents your immune response so far as the antibody part is concerned. This means a wave of infection can spread across tissues relatively unmolested by your immune system.

Brilliant, eh? It seems the malevolent designer learned a valuable lesson from its failed attempt with the SARS-CoV virus that caused the short-lived 2003 SARS outbreak, which was more lethal but only lasted for 8 months. But it's weird how a supposedly intelligent designer would see the immune system it supposedly also designed to protect us from its viruses, as a problem to be overcome! Creationists, however, see having an arms race with yourself as the act of a supremely intelligent [sic] designer.

The Ohio State University News release by Emily Caldwell explains the findings of this team of researchers:
The virus that causes COVID-19 has adopted some stealth moves to stay alive and kicking, and one secret to its success is hiding from the immune system by spreading through cell-to-cell transmission, a new study has found.

It’s basically an underground form of transmission. SARS-CoV-2 can spread efficiently from cell to cell because there are essentially no blockers from the host immunity. Target cells become donor cells, and it just becomes a wave of spread, as the virus may not get out of the cells.

The spike protein is necessary and sufficient for both SARS-CoV-2 and SARS-CoV cell-to-cell transmission because the only difference in these pseudoviruses were the spike proteins.

Professor Shan-Lu Liu, lead author
Department of Veterinary Biosciences, the Center for Retrovirus Research
And a program Director of the Viruses and Emerging Pathogens Program
Ohio State University, Columbus, Ohio, USA
Cell culture experiments showed that SARS-CoV-2, which causes COVID-19, limits the release of viral particles that can be inactivated by antibodies, instead staying tucked within cell walls and spreading between cells.


Liu and colleagues found other revealing details about SARS-CoV-2: The spike protein on its surface alone enables cell-to-cell transmission, and yet the virus’s primary receptor on target cells – to which the spike binds – is not a necessary part of the cell-to-cell transmission operation. Additionally, they found that neutralizing antibodies are less effective against the virus when it spreads through cells.

A major point of this study was comparing SARS-CoV-2 to the coronavirus behind the 2003 SARS outbreak, known as SARS-CoV. The findings help explain why while the first outbreak led to much higher fatality rates and lasted only eight months, we’re about to surpass the two-year mark of the current pandemic, with a majority of cases being asymptomatic, Liu said.

The comparison showed that the SARS-CoV that caused SARS in 2003 is more efficient than SARS-CoV-2 at what is called cell-free transmission, when freely floating viral particles infect target cells by binding to a receptor on their surface – but also remain vulnerable to antibodies produced by previous infection and vaccines. SARS-CoV-2, on the other hand, is more efficient at cell-to-cell transmission – which makes it harder to neutralize with antibodies.

The viruses’ differing efficiencies were first demonstrated in experiments using pseudoviruses – a non-infectious viral core decorated with both kinds of coronavirus spike proteins on the surface.


There is no perfect correlation between SARS-CoV-2 infection and the level of ACE2. ACE2 may be needed for initial infection, but once infection is established, the virus may not need ACE2 anymore because it can spread from cell to cell.

We were able to confirm cell-to-cell transmission is not sensitive to inhibition from antibodies from COVID patients or vaccinated individuals. Cell-to-cell transmission’s resistance to antibody neutralization is probably something we should watch for as SARS-CoV-2 variants continue to emerge, including the most recent, Omicron. In this sense, developing effective antiviral drugs targeting other steps of viral infection is critical.

Professor Shan-Lu Liu
Looking more deeply into those differences, the researchers found that SARS-CoV-2 is also more capable than SARS-CoV at initiating fusion with a target cell membrane, another key step in the viral entry process. And that stronger fusion action was associated with the virus’s enhanced cell-to-cell transmission.

Paradoxically, too much cell membrane fusion leads to cell death and can actually interfere with cell-to-cell transmission, Liu also found.

The team then turned to the role of the ACE2 receptor, a protein on cell surfaces that acts as the gateway for entry of the virus that causes COVID-19. The researchers found, unexpectedly, that cells with no or low levels of ACE2 on their surfaces can be penetrated by the virus, enabling robust cell-to-cell transmission.


Finally, in experiments testing blood samples from human COVID-19 patients against the authentic SARS-CoV-2 virus, researchers determined that the virus could evade an antibody response through cell-to-cell transmission, but that antibody neutralization of the virus in the cell-free transmission mode was effective.
The research team explain the significance of their findings in the abstract to their open access paper in : Proceedings of the National Academy of Science (PNAS):
It is currently unknown if SARS-CoV-2 can spread through cell–cell contacts, and if so, the underlying mechanisms and implications. In this work, we show, by using lentiviral pseudotyped virus, that the spike protein of SARS-CoV-2 mediates the viral cell-to-cell transmission, with an efficiency higher than that of SARS-CoV. We also find that cell–cell fusion contributes to cell-to-cell transmission, yet ACE2 is not absolutely required. While the authentic variants of concern (VOCs) B.1.1.7 (alpha) and B.1.351 (beta) differ in cell-free infectivity from wild type and from each other, these VOCs have similar cell-to-cell transmission capability and exhibit differential sensitivity to neutralization by vaccinee sera. Results from our study will contribute to a better understanding of SARS-CoV-2 spread and pathogenesis.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible coronavirus responsible for the global COVID-19 pandemic. Herein, we provide evidence that SARS-CoV-2 spreads through cell–cell contact in cultures, mediated by the spike glycoprotein. SARS-CoV-2 spike is more efficient in facilitating cell-to-cell transmission than is SARS-CoV spike, which reflects, in part, their differential cell–cell fusion activity. Interestingly, treatment of cocultured cells with endosomal entry inhibitors impairs cell-to-cell transmission, implicating endosomal membrane fusion as an underlying mechanism. Compared with cell-free infection, cell-to-cell transmission of SARS-CoV-2 is refractory to inhibition by neutralizing antibody or convalescent sera of COVID-19 patients. While angiotensin-converting enzyme 2 enhances cell-to-cell transmission, we find that it is not absolutely required. Notably, despite differences in cell-free infectivity, the authentic variants of concern (VOCs) B.1.1.7 (alpha) and B.1.351 (beta) have similar cell-to-cell transmission capability. Moreover, B.1.351 is more resistant to neutralization by vaccinee sera in cell-free infection, whereas B.1.1.7 is more resistant to inhibition by vaccinee sera in cell-to-cell transmission. Overall, our study reveals critical features of SARS-CoV-2 spike-mediated cell-to-cell transmission, with important implications for a better understanding of SARS-CoV-2 spread and pathogenesis.

Dominant Alpha variant evolved to evade our innate immune system | UCL News - University College London

A second paper, this time by a team led by researchers at University College, London, UK (UCL) and the Quantitative Biosciences Institute, University of California San Francisco (UCLA), has shown:
The SARS-CoV-2 Alpha (B.1.1.7) variant mutated to evade our ‘innate immune system’, helping establish it as the world’s first ‘Variant of Concern’.
So, once again we have the curious paradox of Creationism's supposedly supremely intelligent designer needing to modify its original design to ensure it maximised the amount of suffering in the human population and to help it circumvent the human immune system it allegedly also designed.

Creationist mode:

Of course, being proper scientists as opposed to pretend 'creation scientists' the team explain this in biological terms as an evolutionary process with no sentience, malevolent or otherwise, involved

Here's. how the UCL News release explained the research:
We wanted to know what made the SARS-CoV-2 Alpha variant special. How had it evolved from the first wave strain identified in Wuhan, China, and what features did it have that allowed it to spread around the world and become the first variant of concern?

We found that that the SARS-CoV-2 Alpha variant had adapted to avoid triggering our defensive frontline innate immune response much better than the first wave viruses. We discovered it does this by making more of the virus proteins that can disable the innate immune system. These proteins are called N, Orf6 and Orf9b and are known as innate immune antagonists.

By mutating to evade our innate immune system, the Alpha variant can replicate under the radar in the early stages of infection, which we think significantly increases its chances of infecting a person when it lands in their nose, throat or lungs. For a virus this is a resounding success, enabling it to more efficiently spread from person to person.

Dr Lucy Thorne, Co-first author
UCL Division of Infection & Immunity)
Published in Nature, the study shows the Alpha variant, first identified in the UK, evolved to make more of its ‘antagonism proteins’ that nullify the body’s first line of defence, known as the ‘innate immune system’.

Every cell in the nose, throat and lungs (airways) have a network of sensors that detect incoming viruses. When this happens the cells produce the protein interferon, which acts like a ‘burglar alarm’ and orchestrates a blanket anti-viral response, across both non-immune and immune cells (T cells and antibodies) to avert infection. But antagonism proteins can help the virus to evade these sensors.

This novel discovery is the first to identify evolution of enhanced antagonism protein expression in any virus and the first to implicate mutations in SARS-CoV-2 that increase infectiousness but do not involve the ‘spike’ protein.

Scientists say the breakthrough findings provide a powerful insight into how SARS-CoV-2 is evolving, and offer a fresh clue to help identify new and emerging Variants of Concern, which are both highly transmissible and infectious.

For the study, researchers added samples of Alpha (B.1.1.7 lineage) to lab-grown lung cells – to mimic the cells infected by the virus in the body. Scientists then measured how much the virus grew and assessed whether the innate immune system was activated (or to what degree) by measuring the
We have never seen anything like this before; we know viruses adapt and we expect to see the proteins adapting so they work better in humans. But Alpha is using its antagonism proteins, that help evade detection a little bit, and cranking up how much it makes. That is unique.

The real value of our discovery is showing how this incredible virus evolved from the initial SARS-CoV-2 strain, and it also helps us understand how our protective innate immunity works.

Professor Greg Towers, co-senior author
UCL Division of Infection & Immunity
amount of interferon produced.

Researchers observed that the levels of interferon produced during Alpha infection were far lower than all earlier SARS-CoV-2 variants, which had principally seen mutations to the ‘spike’ protein.

To pinpoint exactly why Alpha was compromising the innate immune system, collaborators at the Quantitative Biosciences Institute (QBI), including co-senior author and director of QBI Nevan Krogan and co-first authors Mehdi Bouhaddou and Lorena Zuliani-Alvarez, looked at how the proteins expressed in Alpha differed from previous variants. By measuring all of the proteins and all of the RNA in infected cells, they found antagonism proteins N, Orf6 and Orf9b, which are present in all coronaviruses and whose function is to dampen down cell responses, were ‘dialled up’
It will be fascinating to see how the other variants, such as Delta and Omicron, perform comparatively in our lung epithelial systems. Whether the viruses rely on similar approaches to innate antagonism or have evolved distinct strategies to evade the immune defences, will teach us not only about the viruses themselves but also about human biology.

Dr Ann-Kathrin Reuschl, Co-first author
UCL Division of Infection & Immunity
in the Alpha variant.

Researchers believe this increase in antagonism proteins is the result of numerous mutations in the regulatory regions of SARS-CoV-2, which control protein expression levels.

In preliminary research, the team has identified that some of the mutations to the regulatory regions of SARS-CoV-2 found in Alpha are present in the subsequent Variants of Concern, Delta and Omicron, but it is believed these variants succeeded primarily due to mutations in the spike protein.
It’s fascinating to watch a virus evolve in real time – we expect it to continue to evolve and we hope our work will help to understand the next round of variants too.

Professor Clare Jolly, Co-senior author
UCL Division of Infection & Immunity)
This paper is published in Nature, sadely behind an expensive paywall. However the abstract can be read here. Typical of proper biologists, the author attribute all this to an amoral, mindless, evolutionary process in which no gods, intelligent, stupid, malevolent or benevolent were involved.

Meanwhile, Creationists continue to insist that there must be intelligence involved in these processes because nothing in nature happens without it and, for reasons which remain unexplained, they prefer to attribute the malevolence in organisms like the SARS-CoV-2 virus and other harmful pathogens to a god whom they insist is omni-benevolent. This probably explains much about the thinking processes of Creationists and their view of what omni-benevolence means or would entail if such an entity were real.

Thank you for sharing!

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1 comment :

  1. God certainly moves in mysterious ways...... Mayhap he/she/none binary is thinking of bumping off mankind to start anew. Who will be left to re-seed the planet? I have a horrible thought, maybe it's the Jehovah Witnesses? No wonder they look so bloody smug!


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