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The Global Science and Politics of Covid-19 / SARS-Cov-2

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The Global Science and Politics of Covid-19 / SARS-Cov-2 14/05/2021 The Global Science and Politics of Covid-19 / SARS-CoV-2 The Global Science and Politics of Covid-19 / SARS-CoV-2 A Self-induced Malthusian Catastrophe -- 14-5-21 -- Chris King - Emeritus, University of Auckland Live-linked PDF research hub (8 mB) The PDF hub forms a complete stand-alone clone of the web research hub, which can be freely emailed and updated by clicking the link above from the downloaded copy. The Covid-Climate Elucidation – Our Key to the Future – PDF COVID-19 Make it the Last Pandemic 5-2021 The Independent Panel This article provides a detailed real-time global research overview of the Covid-19 pandemic in its medical, social, economic and ecological aspects, including epidemic modelling, infection mechanisms, death rates, antiviral, antibody and vaccine treatments and the way in which humanity, despite clear prior warnings in other zoonotic corona virus outbreaks, allowed itself to get into this situation, through our impact on the biosphere and expores the lessons to be learned for humanity's future survival. Navigation H: Coronavirus Tests and Tracing O: Antiviral Drugs A: Origins in Sustained Human Misadventure I: Mechanisms of Infection P: Antibody Treatments B: First Awareness J: Viral Loads & Asymptomatic Spread Q: Vaccines and Gene Therapies C: Uravelling the Viral Transmission Event K: Antibody Responses and Reinfection R: Mortality Rates D: Environmental and Economic Consequences L: Clinical Features S: Comparison with other Pandemics E: Modeling Pandemic Strategies M: Blood Clotting and Nervous System T: The New Zealand Situation F: Genetic and Evolutionary Analysis N: Lung Damage U: World Comparisons G: World Incidence Statistics W:The Bradykinin Hypothesis V: Covid Politics Introduction: Don't destabilize the Symbiosis! The key to the Covid-19 pandemic is that bats and corona viruses have evolved into a semi-symbiotic relationship in which the bats harbour the coronas and ensure their survival by a "super-immune" response using interferon mediated anti-viral modulation, but inhibiting inflammasomes, which precipitate the cytokine storms resuling in human casualties. Bats, instead of expresing inflammatory cytokines, generate a targeted set of antiviral factors which tune down the virus. Simultaneously, the virus also adapts to the bat host cells, while rapidly mutating specific genes. Consequently bat coronaviruses can persist in their natural bat host for at least four months of hibernation without harming the bat, as discovered in the case of MERS. When a bat experiences stress to their immune system, it disrupts this immune system-virus symbiosis and allows the virus to multiply. Wet markets and habitat destruction combine to stress the bats in cages in close proximity to other species which also carry other strains of corona virus, leading to zoonotic recombination and a new toxic chimera not yet adapted to any host, but potentially both highly infectious and lethal because its highly evolved nature may bind very strongly to certain receptors in the bat or intermediate host. So its not that there is a vicious RNA virus at work alone, but the exploitative stressing of wild ecosystems disrupting symbiotic relationships on which the corona depends. This is the invidious work of humanity bringing about our own misfortune, hence it is a classic Malthusian grim reaper. Sars-CoV-2 is clearly an extremely infectious epidemic disease. It binds strongly to ACE-2 receptors in the alveoli where oxygen transfer occurs and where it can cause debilitating pneumonia leading to loss of oxygen absorption and blood-borne viremia through the presence of ACE-2 blood-pressure receptors lining all blood vessels. It also binds sufficiently in the upper respiratory tract to be easily transmissable. A model of exactly why this is and why it can be very severe goes something like this: Phase 1: Humans are currently not resistant to the virus so it replicates exponentially without restraint for around a four to five day incubation period (Lauer et a 2020, Li et al 2020) with an exponentially increasing viral load. The virus is also stable for long periods on external surfaces leading to indirect transfer. This means that a person may become extremely infectious just as they begin to show symptoms and can infect a large number of people around them as a transient super-spreader, leading to large clusters being generated at social gatherings. Phase 2: Once the immune system kicks in, the infectivity naturally diminishes, as the viruses are attacked and destroyed. However in some, particularly older, people a deterioration may set in, in the second week, where they get obstructed lungs and an inflammtory cytokine storm. It is likely this is because the bat-adapted virus inhibits the interferon response and inflammatory responses promote viral ploliferation. In 'wet lung', the tissues around the alveoli leak plasma into the lungs which fill with fluid and the virus can pass into the blood stream, resulting in viremia. At this point the virus can attack the kidneys, brain, heart and/or liver which also have ACE-2 blood pressure receptors and infectivity is likely to increase again, causing risk to medical personnel. These two phases of infectivity could select for differing evolutionary processes, the first towards less aggressive and the second to more aggressive strains. Reactions both by the immune systems of infected people and the virus itself can lead to an unparalleled variety of outcomes. The key to asymptomatic spreading is that the corona virus, as noted aove, is an implicitly symbiotic virus (1, 2 and 3) that has got knocked off its perch to become a pandemic infection. Thus some people have no symptoms at all, but others end up getting killed in large numbers when the virus remains active and the immune mismatich runs riot. Asymptomatic cases may arise either because of existing immunity due to other human corona viruses, or due to the initial interferon reaction curbing the viral explosion as occurs in bats. Immunity-mediated resistance is also a combination of humoral antibody-based immunity in which helper T-cells prime B-cells to produce antibodies, and direct cytotoxic responses from killer T-cells. Currently there are indications of a waning and highly variable humoral antibody response, depending on the severity of the infection, with direct killer T-cell activity showing high specificity for the virus. Cases of people catching two different forms of Covid-19 have also emerged. There is evidence of formation of memory cells in people who have had moderate infection severity, pointing to longer term immunity, but not in those who have died. In the most severe cases there is evidence for a misregulated immune response leading to cytokine storms and organ failure accompanied by inflammosomes. Six months of coronavirus: the mysteries scientists are still racing to solve Nature 3-7-2020 Genetic differences in victims. How long does immunity last? Worrying mutations? Vaccine prospects. Origin fo the virus? Profile of a killer: the complex biology powering the coronavirus pandemic Nature 4-5-2020 With 30,000 genetic bases, coronaviruses have the largest genomes of all RNA viruses. Their genomes are more than three times as big as those of HIV and hepatitis C, and more than twice influenza's. Coronaviruses are also one of the few RNA viruses with a genomic proofreading mechanism — which keeps the virus from accumulating mutations that could weaken it. That ability explains why common antivirals such as ribavirin, have failed to work on SARS-CoV-2, because the proofreader can weed out the mutations caused by these drugs. Coronaviruses also frequently recombine, swapping chunks of their RNA with other coronaviruses, giving them deadly variability.. Recombination happens often in bats and bat cells infected by viruses rapidly release a signal that may make them able to host the virus without killing it. The fact that both mutations and recombinations are at work complicates efforts to draw a family tree. Estimates for the birth of the first coronavirus vary widely, from 10,000 years ago to 300 million years ago. Evolutionary studies suggest that a SARS-CoV-2 related lineage has existed in an animal host for decades. The SARS-CoV-2 binding domain is particularly efficient, and differs in important ways from that of the Yunnan bat virus, which seems not to infect people, https://www.dhushara.com/covid/index.htm 1/56 14/05/2021 The Global Science and Politics of Covid-19 / SARS-CoV-2 although they are 96% similar. The pangolin has been found to harbour a coronavirus with a receptor-binding domain almost identical to the human version, but is overall only 90% similar. SARS-CoV-2, like human CoVs, can attack the upper airways, or like SARS the lungs – both very efficiently. This gives it two ways to get a foothold. Once it gets into the lungs, it appears to be just as deadly as SARS. SARS-CoV-2 is uniquely equipped for forcing entry into cells. Both SARS-CoV and SARS-CoV-2 bind with ACE2, but the receptor-binding domain of SARS-CoV-2 is a particularly snug fit. ACE2 is expressed throughout the body on the lining of the arteries and veins that course through all organs, but it is particularly dense on the cells lining the alveoli and small intestines. A SARS-CoV-2 infection can trigger an excessive a cytokine storm, which can lead to multiple organ failure and death. The virus can also infect the intestines, the heart, the blood, sperm, the eye and possibly the brain. It is 10–20 times more likely to bind ACE2 than is SARS-CoV. Although the exact mechanisms remain unknown, evidence suggests that after the virus attaches itself, the host cell snips the spike protein at one of its dedicated 'cleavage sites', exposing fusion peptides — small chains of amino acids that help to pry open the host cell's membrane so that the virus's membrane can merge with it.
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