Creationist mode: 
Today we have two more examples of how brilliant Creationism's putative intelligent designer has been in its determination to do as much damage as possible with its new virus, SARS-CoV-2 with which, according to Creationist dogma, it is causing untold suffering and misery in revenge for someone eating its apple.
First, we have this finding by a German research team working at the Max Planck Institute for the Science of Light (MPL), that infection by the virus can cause red blood cells to change in size and stiffness, causing vascular occlusions and reduced oxygen-carrying capacity and giving rise to the breathlessness, headaches and fatigues that characterise the post Covid syndrome, aka, long covid.
Using real-time deformability cytometry, researchers at the Max-Planck-Zentrum für Physik und Medizin in Erlangen were able to show for the first time: Covid-19 significantly changes the size and stiffness of red and white blood cells - sometimes over months. These results may help to explain why some affected people continue to complain of symptoms long after an infection (long covid).As stated above, the findings of the team were published in Biopysical Journal:
We were able to detect clear and long-lasting changes in the cells — both during an acute infection and even afterwardsShortness of breath, fatigue and headaches: some patients still struggle with the long-term effects of a severe infection by the SARS-CoV-2 coronavirus after six months or more. This post Covid-19 syndrome, also called long covid, is still not properly understood. What is clear is that — during the course of the disease — often blood circulation is impaired, dangerous vascular occlusions can occur and oxygen transport in is limited. These are all phenomena in which the blood cells and their physical properties play a key role.
Professor Jochen Guck, Corresponding author
Managing director, Max Planck Institute for the Science of Light
Erlangen, Germany
To investigate this aspect, a team of scientists led by Markéta Kubánková, Jochen Guck, and Martin Kräter from the Max-Planck-Zentrum für Physik und Medizin, the Max Planck Institute for the Science of Light (MPL), the Friedrich Alexander University Erlangen-Nuremberg and the German Centre for Immunotherapy measured the mechanical states of red and white blood cells. "We were able to detect clear and long-lasting changes in the cells — both during an acute infection and even afterwards," reports Professor Guck, currently managing director of MPL. The research group has now published their results in the renowned journal "Biophysical Journal"...
We suspect that the cytoskeleton of immune cells, which is largely responsible for cell function, has changed.The biophysicists from Erlangen examined more than four million blood cells from 17 patients acutely ill with Covid-19, from 14 people who had recovered and 24 healthy people as a comparison group. They found that, for example, the size and deformability of the red blood cells of patients with the disease deviated strongly from those of healthy people. This indicates damage to these cells and could explain the increased risk of vascular occlusion and embolisms in the lungs. In addition, the oxygen supply, which is one of the main tasks of the erythrocytes, may be impaired in infected persons. Lymphocytes (one type of white blood cell responsible for the acquired immune defense) were in turn significantly softer in Covid-19 patients, which typically indicates a strong immune reaction. The researchers made similar observations for neutrophil granulocytes, another group of white blood cells involved in the innate immune response. These cells even remained drastically altered seven months after the acute infection. "We suspect that the cytoskeleton of immune cells, which is largely responsible for cell function, has changed," explains Markéta Kubánková, first author of the research article. In her view, real-time deformability cytometry has the potential to be used routinely in the diagnosis of Covid-19 — and even to serve as an early warning system against future pandemics caused by as yet unknown viruses.
Markéta Kubánková, first author
Max Planck Institute for the Science of Light & Max-Planck-Zentrum für Physik und Medizin
Erlangen, Germany
AbstractObviously, Creationism's special magic creator made a special effort when it designed this nasty little virus to make us sick. More evidence of this special effort is to be seen in this second piece of news:
Clinical syndrome coronavirus disease 2019 (COVID-19) induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by rapid spreading and high mortality worldwide. While the pathology is not yet fully understood, hyper-inflammatory response and coagulation disorders leading to congestions of microvessels are considered to be key drivers of the still increasing death toll. Until now, physical changes of blood cells have not been considered to play a role in COVID-19 related vascular occlusion and organ damage. Here we report an evaluation of multiple physical parameters including the mechanical features of five frequent blood cell types, namely erythrocytes, lymphocytes, monocytes, neutrophils, and eosinophils. More than 4 million blood cells of 17 COVID-19 patients at different levels of severity, 24 volunteers free from infectious or inflammatory diseases, and 14 recovered COVID-19 patients were analyzed. We found significant changes in lymphocyte stiffness, monocyte size, neutrophil size and deformability, and heterogeneity of erythrocyte deformation and size. While some of these changes recovered to normal values after hospitalization, others persisted for months after hospital discharge, evidencing the long-term imprint of COVID-19 on the body.
Kubánková, Markéta; Hohberger, Bettina; Hoffmanns, Jakob; Fürst, Julia; Herrmann, Martin; Guck, Jochen; Kräter, Martin
Physical phenotype of blood cells is altered in COVID-19
Biophysical Journal June 01, 2021 DOI: 10.1016/j.bpj.2021.05.025
Copyright: © 2021 Biophysical Society. Published by Elsevir
Open access
Reprinted under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND 4.0)
Translucent SARS-CoV-2 spike protein depicting vector skeleton
A team from Duke Health, DURHAM, N.C., USA have identified how multiple mutations on the SARS-CoV-2 spike protein independently create variants that are more transmissible and potentially resistant to antibodies. According to the Duke Health News release:
By acquiring mutations on the spike protein, one such variant gained the ability to leap from humans to minks and back to humans. Other variants -- including Alpha, which first appeared in the United Kingdom, Beta, which appeared in South Africa, and Gamma, first identified in Brazil – independently developed spike mutations that enhanced their ability to spread rapidly in human populations and resist some antibodies.The researchers published their findings in Science.
The spike on the surface of the virus helps SARS-CoV-2 enter into host cells. Changes on the spike protein determine transmissibility of the virus -- how far and quickly it spreads. Some variations of the SARS-CoV-2 spike are occurring at different times and different places throughout the world, but have similar results, and it’s important to understand the mechanics of these spike mutations as we work to fight this pandemic.“The spike on the surface of the virus helps SARS-CoV-2 enter into host cells,” said senior author Priyamvada Acharya, Ph.D., director of the Division of Structural Biology at the Duke Human Vaccine Institute.
Priyamvada Acharya, Ph.D., Senior author.
Director of the Division of Structural Biology
Duke Human Vaccine Institute
Duke University, Durham, NC, USA
“Changes on the spike protein determine transmissibility of the virus -- how far and quickly it spreads,” Acharya said. “Some variations of the SARS-CoV-2 spike are occurring at different times and different places throughout the world, but have similar results, and it’s important to understand the mechanics of these spike mutations as we work to fight this pandemic.”
Acharya and colleagues -- including first author Sophie Gobeil, Ph.D., and co-corresponding author Rory Henderson, Ph.D., -- developed structural models to identifyBy building a skeleton of the spike, we could see how the spike is moving, and how this movement changes with mutations. The different variant spikes are not moving the same way, but they accomplish the same task. The variants first appearing in South Africa and Brazil use one mechanism, while the UK and the mink variants use another mechanism.changes in the virus’s spike protein. Cryo-electron microscopy allowed atomic level visualization, while binding assays enabled the team to create mimics of the live virus that directly correlated with its function in host cells. From there, the team used computational analysis to build models that showed the structural mechanisms at work.
Rory Henderson, Ph.D, Co-corresponding author
Vaccine Institute and Department of Medicine
Duke University, Durham, NC, USA.
“By building a skeleton of the spike, we could see how the spike is moving, and how this movement changes with mutations,” Henderson said. “The different variant spikes are not moving the same way, but they accomplish the same task. The variants first appearing in South Africa and Brazil use one mechanism, while the UK and the mink variants use another mechanism.”
It’s amazing how many different ways the virus comes up with to be more infectious and invasive, Nature is clever.All the variants showed increased ability to bind to the host, notably via the ACE2 receptor. The changes also created viruses that were less susceptible to antibodies, raising concerns that continued accumulation of spike mutations may reduce the efficiency of current vaccines.
Sophie Gobeil, Ph.D, First author
Duke Human Vaccine Institute
Duke University, Durham, NC, USA.
Gobeil said the research illuminated the complexity of the virus: “It’s amazing how many different ways the virus comes up with to be more infectious and invasive,” she said. “Nature is clever.”
AbstractOf course, when Dr Sophie Gobeil describes Nature as being 'clever', Creationists know that it's not 'Nature' but their own special magic creator friend who is being very clever with its design of the SARS-CoV-2 virus. According to Creationist dogma, 'Nature' has no mechanism for designing living things because nothing can evolve naturally and nothing happens without the direct intervention and say-so of a magic, invisible man in the sky who uses magic to make things happen. So, all the credit (including the obvious malevolent intent, caused by its hatred for its creation) must be given to this magic god, even if that makes it look like a sadistic, hateful, misanthropic monster. But no matter, Creationists are obliged by dogma and cult diktat to continue to assert that evolution by natural selection can't be the cause of these changes.
SARS-CoV-2 variants with multiple spike mutations enable increased transmission and antibody resistance. Here, we combine cryo-EM, binding and computational analyses to study variant spikes, including one that was involved in transmission between minks and humans, and others that originated and spread in human populations. All variants showed increased ACE2 receptor binding and increased propensity for RBD up states. While adaptation to mink resulted in spike destabilization, the B.1.1.7 (UK) spike balanced stabilizing and destabilizing mutations. A local destabilizing effect of the RBD E484K mutation was implicated in resistance of the B.1.1.28/P.1 (Brazil) and B.1.351 (South Africa) variants to neutralizing antibodies. Our studies revealed allosteric effects of mutations and mechanistic differences that drive either inter-species transmission or escape from antibody neutralization.
Gobeil, Sophie M.-C.; Janowska, Katarzyna; McDowell, Shana; Mansouri, Katayoun; Parks, Robert; Stalls, Victoria; Kopp, Megan F.; Manne, Kartik; Li, Dapeng; Wiehe, Kevin; Saunders, Kevin O.; Edwards, Robert J.; Korber, Bette; Haynes, Barton F.; Henderson, Rory; Acharya, Priyamvada
Effect of natural mutations of SARS-CoV-2 on spike structure, conformation, and antigenicity
Science 24 Jun 2021: eabi6226; DOI: 10.1126/science.abi6226
Open access
Reprinted under a Creative Commons Attribution 4.0 International License (CC BY 4.0)
Creationist mode: 
But, of course, as anyone with a mental age above that of a normal 12-year-old will understand, countless trillions of random mutations, filtered by the sieve of natural selection are perfectly capable of hitting on these million, or even billion, to one chance mutations multiple times a day, and any advantage they give to the virus which means it can produce more copies of itself, will quickly replace the earlier variants in the virus gene pool, just as we are currently seeing the δ-variant quickly replacing the α-variant in the UK (and soon, the rest of the world). The α-variant quickly replaced the original in the UK during the second wave which began in about September, 2020. Fortunately, the δ-variant does not seem to have increased the virus' resistance to the antibodies produced by the vaccines, so hospitalisations and deaths remain low, compared to those in the first two waves.
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