Creative rendition of SARS-COV-2 virus particles with spike proteins dotting their surfaces. Image not to scale.
Credit: NIAID
Creationist mode: 
News today of how Creationism's beloved malevolence found a way to get round the human body's defence mechanism against the SARS-CoV-2 virus - the mechanism it designed to protect us from the organisms it makes to kill and make us sick - and so get the maximum impact of the virus on human health.
The problem was that there is a process in the cells that would normally limit the infectivity of viruses like SARS-CoV-2, so, starting with the α variant and continuing with the δ variant, the intelligent [sic] designer included some modifications, or mutations as scientists call them, which overcome this cell process and so make the variants much more infective.
Confirmed cases
Data source: gov.uk
The intelligent designer is currently mopping up those covidiots who have fallen for the antivaxxer lies being promulgated by the extreme Trumpanzee right for political ends, while using them as a resource for developing an even more infective variant which can also overcome the stunning success of medical science in creating the vaccines against the virus.
Creationist mode: 
Now back in the real world, the NIH news release explains the discovery:
Since the coronavirus pandemic began in early 2020, several more-infectious variants of SARS-CoV-2, the virus that causes COVID-19, have emerged. The original, or wild-type, virus was followed by the alpha variant, which became widespread in the United States in early 2021, and the delta variant, which is the most prevalent strain circulating today. The variants have acquired mutations that help them spread and infect people more easily. Many of the mutations affect the spike protein, which the virus uses to get into cells. Scientists have been trying to understand how these changes alter the virus’s function.The NIH team's open access paper is published in PNAS:
[…]
Throughout the pandemic, NIDCR researchers have applied their expertise in the oral health sciences to answer key questions about COVID-19. This study offers fresh insights into the greater infectivity of the alpha and delta variants and provides a framework for the development of future therapies.The outer surface of SARS-CoV-2 is decorated with spike proteins, which the virus uses to attach to and enter cells. Before this can happen, though, the spike protein must be activated by a series of cuts, or cleavages, by host proteins, starting with the furin enzyme. In the alpha and delta variants, mutations to the spike protein appear to enhance furin cleavage, which is thought to make the virus more effective at entering cells.
Dr Rena D’Souza, D.D.S., Ph.D.
NIDCR Director
Studies have shown that in some cases protein cleavage can be decreased by the addition of bulky sugar molecules—a process carried out by enzymes called GALNTs—next to the cleavage site. Ten Hagen’s team wondered if this happens to the SARS-CoV-2 spike protein, and if so, whether it changes the protein’s function.
To find out, the scientists studied the effects of GALNT activity on spike protein in fruit fly and mammalian cells. The experiments showed that one enzyme, GALNT1, adds sugars to wild-type spike protein, and this activity reduces furin cleavage. By contrast, mutations to the spike protein, like those in the alpha and delta variants, decrease GALNT1 activity and increase furin cleavage. This suggested that GALNT1 activity may partially suppress furin cleavage in wild-type virus, and that the alpha and delta mutations overcome this effect, allowing furin cleavage to go unchecked.
Our findings indicate that the alpha and delta mutations overcome the dampening effect of GALNT1 activity, which may enhance the virus’s ability to get into cells.Further experiments supported this idea. The researchers expressed either wild-type or mutated spike in cells grown in a dish. They observed the cells’ tendency to fuse with their neighbors, a behavior that may facilitate spread of the virus during infection. The scientists found that cells expressing mutated spike protein fused with neighbors more often than cells with the wild-type version. Cells with wild-type spike also fused less in the presence of GALNT1, suggesting that its activity may limit spike protein function.
This study suggests that GALNT1 activity may modulate viral infectivity and provides insight into how mutations in the alpha and delta variants may influence this.
Dr. Kelly Ten Hagen, Ph.D., Lead author
Senior investigator
NIH’s National Institute of Dental and Craniofacial Research (NIDCR).
[…]
To see if this process might also occur in people, the team analyzed RNA expression in cells from healthy volunteers. The researchers found wide expression of GALNT1 in lower and upper respiratory tract cells that are susceptible to SARS-CoV-2 infection, indicating that the enzyme could influence infection in humans. The scientists theorized that individual differences in GALNT1 expression could affect viral spread.
SignificanceSo, if you've fallen for the intelligent [sic] design hoax and so are obliged as a condition of cult membership to reject any possibility that a natural, evolutionary process could possibly be the cause of these ever-more successful and dangerous variants of the coronavirus currently causing the COVID-19 pandemic, you have to accept that whatever intelligence you believe is behind these variants is working to make us more sick and die in larger numbers and overcome the defence it designed to protect us from its nastier creations.
The novel SARS-CoV-2 coronavirus that is responsible for the global pandemic contains a unique insertion of four amino acids within the spike protein (S). Furin cleavage at this novel insertion site has been shown to increase pseudoviral infectivity and syncytia formation. Here we show that O-glycosylation by certain GALNT family members decreases furin cleavage of S and decreases syncytia formation. Moreover, we show that P681 mutations found in the highly transmissible alpha and delta variants decrease O-glycosylation, which increases furin cleavage and syncytia formation. Our results highlight how host-mediated O-glycosylation may influence viral infectivity and how mutations in the recent alpha and delta variants may circumvent this.
Abstract
The SARS-CoV-2 coronavirus responsible for the global pandemic contains a novel furin cleavage site in the spike protein (S) that increases viral infectivity and syncytia formation in cells. Here, we show that O-glycosylation near the furin cleavage site is mediated by members of the GALNT enzyme family, resulting in decreased furin cleavage and decreased syncytia formation. Moreover, we show that O-glycosylation is dependent on the novel proline at position 681 (P681). Mutations of P681 seen in the highly transmissible alpha and delta variants abrogate O-glycosylation, increase furin cleavage, and increase syncytia formation. Finally, we show that GALNT family members capable of glycosylating S are expressed in human respiratory cells that are targets for SARS-CoV-2 infection. Our results suggest that host O-glycosylation may influence viral infectivity/tropism by modulating furin cleavage of S and provide mechanistic insight into the role of the P681 mutations found in the highly transmissible alpha and delta variants.
Liping Zhang, Matthew Mann, Zulfeqhar A. Syed, Hayley M. Reynolds, E. Tian, Nadine L. Samara, Darryl C. Zeldin, Lawrence A. Tabak, Kelly G. Ten Hagen
Furin cleavage of the SARS-CoV-2 spike is modulated by O-glycosylation
Proceedings of the National Academy of Sciences Nov 2021, 118 (47) e2109905118; DOI: 10.1073/pnas.2109905118
Copyright: © 2021 The authors. Published by National Academy of Sciences
Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
How on Earth this can be described as intelligent design is incomprehensible within any given meanings of the words intelligence and design. Any intelligence that could design such a virus and then find ways to overcome the defences it designed to protect us from its designs can only be described as an incompetent and malevolent designer and couldn't possibly fit any description that equates it to the supposedly omni-benevolent, omniscient god of the Bible and Qur'an.
The intelligent design hoax by the Deception Institute clearly has an agenda which doesn't include promoting such a god as one worthy of worship.
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