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| Pathophysiology of SARS-CoV-2 systemic infection. Infection initiates in the upper respiratory tract and progresses to lower regions of the lung in severe cases. Respiratory droplets carrying SARS-CoV-2 infect epithelial and endothelial cells, neurons, microglia, and lung macrophages containing angiotensin-converting enzyme 2 (ACE-2). Viral replication and release of damage-associated molecular patterns induce pyroptosis, causing a dysfunctional innate immune response. Release of pro-inflammatory agents can induce a cytokine storm, increasing vasodilation, capillary permeability, and hypoxemia that can often lead to multiple organ failure |
If you've fallen for the intelligent [sic] design hoax, you must be thrilled by the almost daily revelation of the sheer, malevolent genius behind the SARS-CoV-2 virus currently responsible for 65 million cases of Covid-19, 1.5 million deaths and financial ruin and economic collapse world-wide on a scale not even seen in wartime (as of today).
The latest finding to impress creationists is the mechanism the virus uses to enter and destroy the cells of the lungs of its victims and the ruthless efficiency with which it does it.
Researchers at Boston University School of Medicine, Massachusetts, USA, in a multi-group collaboration involving scientists from the National Emerging Infectious Disease Laboratories (NEIDL), the Center for Regenerative Medicine (CReM), and the Center for Network Systems Biology (CNSB), have reported the first map of the molecular responses of human lung cells to infection by SARS-CoV-2.
According to a Boston University School of Medicine press release:
They found a crucial type of protein modification called “phosphorylation” becomes aberrant in these infected lung cells. Phosphorylation of proteins play a major role in regulating protein function inside the cells of an organism and both protein abundance and protein phosphorylation are typically highly controlled processes in the case of normal/healthy cells. However, they discovered that SARS-CoV-2 throws the lung cells into disarray, causing abnormal changes in protein amounts and frequency of protein phosphorylation inside these cells. These abnormal changes help the virus to multiply eventually destroy the cells. The destruction of infected cells may result in widespread lung injury.The researchers took samples of infected alveolar cells at one, three, six and twenty-four hours after infection, and samples of uninfected cells, extracted the proteins in them and tagged them to make them quantifiable by mass spectroscopy, so they could accurately measure the changes in protein production and phosphorylation in infected cells as the infection progressed and became established, and compare these to uninfected cells.
According to the researchers, as soon as the SARS-CoV-2 enters the lung cells, it rapidly begins to exploit the cell’s core resources, which are otherwise required for the cell’s normal growth and function. “The virus uses these resources to proliferate while evading attack by the body’s immune system. In this way new viruses form which subsequently exit the exhausted and brutally damaged lung cell, leaving them to self-destruct. These new viruses then infect other cells, where the same cycle is repeated,” explains corresponding author Andrew Emili, PhD, professor of biochemistry.
“Our results showed that in comparison to normal/uninfected lung cells, SARS-CoV-2 infected lung cells showed dramatic changes in the abundance of thousands of proteins and phosphorylation events,” said Darrell Kotton, MD, professor of pathology & laboratory medicine and director of the CReM.|The group's findings were published in November, in the journal Molecular Cell, sadly behind a paywall.
“Moreover, our data also showed that the SARS-CoV-2 virus induces a significant number of these changes as early as one hour post infection and lays the foundation for a complete hijack of the host lung cells,” adds Elke Mϋhlberger, PhD, associate professor of microbiology and principal investigator at the NEIDL.
“There are important biological features specific to lung cells that are not reproduced by other cell types commonly used to study viral infection,” said Andrew Wilson, MD, associate professor of medicine at BUSM and CReM investigator. “Studying the virus in the context of the cell type that is most damaged in patients is likely to yield insights that we wouldn’t be able to see in other model systems.”
In essence then, the SARS-CoV-2 virus which intelligent [sic] design advocates are obliged by dogma to believe was intentionally designed to do exactly what it does by a magic, omniscient, omni-benevolent designer who they just happen to equate to the god of the Christian Bible or the Muslim Qur'an, depending on requirements, hijacks the cells of the lungs of its victims and, within an hour, sets up the mechanism for their destruction and for the production of thousands of copies of itself. The alveoli are, of course, the parts of the lung in which exchange of gasses occur through the cells lining them, between the air in the alveoli and the blood. The Sars-CoV-2 virus has been carefully and intelligently designed to begin asphyxiating its human victims within an hour of getting into their body, or so you must believe if you've fallen for the Intelligent Design hoax.
Real Christians and Muslims might have some difficulty in equating the malevolent entity that could design such a thing as the SARS-CoV-2 virus with their idea of an omni-benevolent god who only wants the best for the creation it loves. Curiously, fundamentalist creationists want them to dismiss the only explanation for the virus that doesn't leave their god resembling an unspeakably evil, malevolent, misanthropic sadist - evolution by natural selection in a mindless, undirected, amoral natural process in which their god played no part, but which, for reasons unknown, was either powerless to intervene, indifferent to the suffering it caused or completely unaware of it.
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