Covid-19 News

  • Ivermectin... is restricted..

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  • Climate and the spread of COVID-19…2172&utm_content=deeplink


    Visual inspection of world maps shows that coronavirus disease 2019 (COVID-19) is less prevalent in countries closer to the equator, where heat and humidity tend to be higher. Scientists disagree how to interpret this observation because the relationship between COVID-19 and climatic conditions may be confounded by many factors. We regress the logarithm of confirmed COVID-19 cases per million inhabitants in a country against the country’s distance from the equator, controlling for key confounding factors: air travel, vehicle concentration, urbanization, COVID-19 testing intensity, cell phone usage, income, old-age dependency ratio, and health expenditure. A one-degree increase in absolute latitude is associated with a 4.3% increase in cases per million inhabitants as of January 9, 2021 (p value < 0.001). Our results imply that a country, which is located 1000 km closer to the equator, could expect 33% fewer cases per million inhabitants. Since the change in Earth’s angle towards the sun between equinox and solstice is about 23.5°, one could expect a difference in cases per million inhabitants of 64% between two hypothetical countries whose climates differ to a similar extent as two adjacent seasons. According to our results, countries are expected to see a decline in new COVID-19 cases during summer and a resurgence during winter. However, our results do not imply that the disease will vanish during summer or will not affect countries close to the equator. Rather, the higher temperatures and more intense UV radiation in summer are likely to support public health measures to contain SARS-CoV-2.

  • Our results imply that a country, which is located 1000 km closer to the equator, could expect 33% fewer cases per million inhabitants.

    In a humid climate droplets in air grow larger and sink faster. The same effect we see here during summer time as basically the water content in air increases by the square of the temperature. Aerosols are basically the only vector for CoV-19. So it is very likely that the number of infections will go down dramatically soon when air humidity increases.

    The other effect of very dry air - desert climate - is less known. Possibly the virus looses the shield and its stabilization water and degenerates faster. Further outdoor virus are exposed to UV what kills them sooner or later.

  • Drivers of Infectious Disease Seasonality: Potential Implications for COVID-19…/10.1177/0748730420987322


    Not 1 year has passed since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19). Since its emergence, great uncertainty has surrounded the potential for COVID-19 to establish as a seasonally recurrent disease. Many infectious diseases, including endemic human coronaviruses, vary across the year. They show a wide range of seasonal waveforms, timing (phase), and amplitudes, which differ depending on the geographical region. Drivers of such patterns are predominantly studied from an epidemiological perspective with a focus on weather and behavior, but complementary insights emerge from physiological studies of seasonality in animals, including humans. Thus, we take a multidisciplinary approach to integrate knowledge from usually distinct fields. First, we review epidemiological evidence of environmental and behavioral drivers of infectious disease seasonality. Subsequently, we take a chronobiological perspective and discuss within-host changes that may affect susceptibility, morbidity, and mortality from infectious diseases. Based on photoperiodic, circannual, and comparative human data, we not only identify promising future avenues but also highlight the need for further studies in animal models. Our preliminary assessment is that host immune seasonality warrants evaluation alongside weather and human behavior as factors that may contribute to COVID-19 seasonality, and that the relative importance of these drivers requires further investigation. A major challenge to predicting seasonality of infectious diseases are rapid, human-induced changes in the hitherto predictable seasonality of our planet, whose influence we review in a final outlook section. We conclude that a proactive multidisciplinary approach is warranted to predict, mitigate, and prevent seasonal infectious diseases in our complex, changing human-earth system.


    We have presented a brief overview of environmental and physiological seasonality, which may contribute to potential future seasonality of COVID-19, as well as of other infectious diseases. On the side of host physiology, we encourage further studies on seasonal restructuring of the immune system in relevant animal models and through the generation of seasonal omics data in humans. We propose that such research should complement current efforts to understand climatic and behavioral drivers of infectious disease seasonality. Even in the absence of host adaptations, seasonal predictability of diseases has major advantages for medical applications (Kissler et al., 2020), as evidenced by the success of seasonal influenza vaccination campaigns (Chung et al., 2020). To the extent that host physiology, too, is seasonal, such consistent patterns can be further exploited, analogous to the growing importance of circadian research for medical intervention. Based on the broad impact of Earth’s seasonality, it is reasonable to assume that global change can affect host immunity and susceptibility; enhance or reduce pathogen survival and proliferation depending on region; modify pathogen load in animal reservoirs; and alter transmission season and human-pathogen interactions. A proactive, multidisciplinary approach to disease control and prevention aiming to better understand these complex interactions, with a greater emphasis on all aspects of health—human, environmental, animal—as exemplified by the notion of One Health, could mitigate some of the expected impacts of global change.

  • Yeah, in public and high school we had common showers, where we all stood naked around a central column with multiple shower heads. Nakedness with peers in a common shower room was expedient and practical, although at the cost of modesty.

    Yes, the same as public baths in Japan in 1972. Which was the only kind of bath a college kid could have, since apartments did not have baths. Except that public baths in Japan are clean and delightful, with nice paintings of Mt. Fuji, soap and shampoo sales, and very hot water. In winter it was also the only time of the day when you were warm. There was no central heating. People in classrooms wore overcoats and mufflers, like in North Korea.

    They recently replaced the open showers at the local Atlanta YMCA with separate stalls. They said people under 60 were uncomfortable with them. I thought "ah, ha, a generational thing . . ."

    But having to swim naked to be evaluated by a superior is without rational basis. What, do they think the swimmers would have floatation devices hidden in their swimming trunks?

    It was not a superior. It was the lifeguard, who was college kid doing part time work. Most campus jobs at Cornell, such as lifeguarding and cooking at the cafeteria, is done for pay by a student. It is like a scholarship. If you need money, they arrange for a campus job. As I recall, the lifeguard just glanced over to make sure I was still swimming and not drowning or cheating. They said they don't want swimsuits to reduce contamination and bacteria. I don't know if they still have the rule. No idea.

    There was no hint of hazing or intimidation, any more than this is an Japanese public bath. As I recall, I was the only person there. You can go anytime it is convenient for you.

    I have heard that public baths are rare in Japan these days. Student apartments are the lap of luxury compared to 1972. They have flush toilets. They even have heating! No more huddling around a kerosene fire. Why, some of them even have air conditioning! An unthinkable luxury in the 1970s. Japan used to be a poor country.


    Famous, or infamous depending on your politics, Dr. Zelenko was nominated for the Nobel Peace Prize for his advocacy, and pioneering the use of the HCQ/Zinc protocol.

    Most articles say he has been "awarded" the prize, but are in the process of correcting themselves to say he was "nominated".

    "When asked about studies that seemed to discredit the efficacy of HCQ in treating the Chinese coronavirus, Zelenko explained “You don’t fire a gun without a bullet in it and then say the gun doesn’t work when you don’t kill the target. The studies that were done on HCQ did not include the use of Zinc. HCQ is what opens the cell and enables Zinc to attack the virus. One is not effective without the other, or without a suitable substitute for HCQ. The studies were designed to fail.”

  • As I recall, the lifeguard just glanced over to make sure I was still swimming and not drowning or cheating. They said they don't want swimsuits to reduce contamination and bacteria. I don't know if they still have the rule. No idea.

    Good thing you didn't notice the hidden camera ;)

    When I visited France many years ago, we went into an indoor swimming pool complex expecting to swim. Being Canadian I had the typical baggy swimming trunks. They weren't allowed. One had to wear speedos or some similar. To this day I still think that was weird. The good news is that later when we went to a public beach they were OK. The occasional topless female made the somewhat murky water much more bearable.

    I wonder if people considered a bathing suit like a mask people would feel safer wearing bathing suits than going naked. Fauci has recommended double masking. Imagine : one could wear double bathing suits and feel really safe! Lord knows where some people's nether regions have been. Happy Sunday.

  • Suggestion: while understood in context, I suggest we stop talking about anything political here --- the political system has no place in science or health -- it is ultimately a fetid group that's shown it is there to facilitate corruption among people

    -- it is more accurate to say "favored or not favored depending on your interest in building a new trillion dollar vaccine industry"

  • if it helps,

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  • COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level…-on-a-cellular-level/amp/

    Salk researchers and collaborators show how the protein damages cells, confirming COVID-19 as a primarily vascular disease.

    Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that they also play a key role in the disease itself.

    The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

    “A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”

    Salk researchers collaborated with scientists at the University of California San Diego on the paper, including co-first author Jiao Zhang and co-senior author John Shyy, among others.

    While the findings themselves aren’t entirely a surprise, the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time. There’s been a growing consensus that SARS-CoV-2 affects the vascular system, but exactly how it did so was not understood. Similarly, scientists studying other coronaviruses have long suspected that the spike protein contributed to damaging vascular endothelial cells, but this is the first time the process has been documented.

    In the new study, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain any actual virus. Exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model—proving that the spike protein alone was enough to cause disease. Tissue samples showed inflammation in endothelial cells lining the pulmonary artery walls.

    The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.

    Previous studies have shown a similar effect when cells were exposed to the SARS-CoV-2 virus, but this is the first study to show that the damage occurs when cells are exposed to the spike protein on its own.

    “If you remove the replicating capabilities of the virus, it still has a major damaging effect on the vascular cells, simply by virtue of its ability to bind to this ACE2 receptor, the S protein receptor, now famous thanks to COVID,” Manor explains. “Further studies with mutant spike proteins will also provide new insight towards the infectivity and severity of mutant SARS CoV-2 viruses.”

    The researchers next hope to take a closer look at the mechanism by which the disrupted ACE2 protein damages mitochondria and causes them to change shape.

    Reference: “SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2” by Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan and John Y-J. Shyy, 31 March 2021, Circulation Research.

    DOI: 10.1161/CIRCRESAHA.121.318902

  • Emerging variants of concern in SARS-CoV-2 membrane protein: a highly conserved target with potential pathological and therapeutic implications…080/22221751.2021.1922097


    Mutations in the SARS-CoV-2 Membrane (M) gene are relatively uncommon. The M gene encodes the most abundant viral structural protein, and is implicated in multiple viral functions, including initial attachment to the host cell via heparin sulfate proteoglycan, viral protein assembly in conjunction with the N and E genes, and enhanced glucose transport. We have identified a recent spike in the frequency of reported SARS-CoV-2 genomes carrying M gene mutations. This is associated with emergence of a new sub-B.1 clade, B.1.I82T, defined by the previously unreported M:I82T mutation within TM3, the third of three membrane spanning helices implicated in glucose transport. The frequency of this mutation increased in the USA from 0.014% in October 2020 to 1.62% in February 2021, a 116-fold change. While constituting 0.7% of the isolates overall, M:I82T sub-B.1 lineage accounted for 14.4% of B.1 lineage isolates in February 2021, similar to the rapid initial increase previously seen with the B.1.1.7 and B.1.429 lineages, which quickly became the dominant lineages in Europe and California over a period of several months. A similar increase in incidence was also noted in another related mutation, V70L, also within the TM2 transmembrane helix. These M mutations are associated with younger patient age (4.6 to 6.3 years). The rapid emergence of this B.1.I82T clade suggests that this M gene mutation is more biologically fit, perhaps related to glucose uptake during viral replication, and should be included in ongoing genomic surveillance efforts and warrants further evaluation for potentially increased pathogenic and therapeutic implications.


    The M gene encodes the most abundant of three SARS-CoV-2 structural proteins, in this case a 222 amino acid protein that is highly conserved between SARS-CoV and SARS-CoV-2 (identity: 90.5%; similarity: 98.2%) (13). Comparatively little attention has been paid to the M protein in the COVID-19 pandemic literature but it is known to be important for viral assembly, and in addition it markedly inhibits type I and III interferon production and thus dramatically inhibits the innate immune response (14, 15). That in turn blunts the T-cell mediated immune response which is known to be important in overall immunity to SARS. In SARS due to SARS-CoV, the M protein is the dominant immunogen for T-cell response (16). In COVID-19 due to SARS-CoV-2, T-cell response has been identified as a critical determinant of outcome, with poor T-cell response to M protein epitopes found in patients with fatal outcome (17, 18). T-cell responses are a critical part of the successful immune response against emerging VOCs that may enable immune evasion (19, 20). Therapeutic strategies that target the M protein and thus modulate T-cell responses have recently been proposed as promising alternatives to current ones (21).

    Unfortunately, the protein structure of the M protein has not been experimental determined so that it is not possible to precisely predict the structural and functional impacts of these M mutations. The predicted SWISS-Model (PODTC5) of the M protein does not cover all the amino acids either. In silico analysis, however, revealed that the M protein structure was similar to that of the glucose transporter SemiSWEET with three transmembrane helical domains, based upon which the M protein is thought to be involved in enhanced glucose transport in host cells with replicating virus, and thus may aid in rapid viral proliferation, replication, and immune evasion (22). The M:I82T mutation falls in the third transmembrane helical domain (22). These transmembrane domains vary in number in the SWEET - 7, SemiSWEET – 3, and GLUT1 - 14 glucose transport family and are thought to bind and transport glucose, yet another function of the M protein that also initiates viral binding to the cell membrane heparin sulfate proteoglycan (via the N terminal exposed fragment), viral protein assembly via the internal carboxyterminal fragment, and immune evasion by inhibition of nuclear transport of NFκB signal transducers involved in interferon induction. Structural prediction however, did not suggest significant impact of structural changes to be caused by the M:I82T mutation which is a hydrophobic to slightly polar amino acid change (Supplemental Figure 2). According to Missense3D, this mutation does not change the secondary structure, nor does it introduce buried charge or hydrophilic. No buried H-bond breakage is induced, but a new H-bond is formed with GLY78 residue.

    We have identified that the M gene, though otherwise highly conserved throughout most of the pandemic, is now undergoing rapidly increasing mutation with a recent surge in isolates carrying previously unreported M gene mutations in the USA and globally. In particular, we identified the emergence of a novel M:I82T clade over the last three months in the eastern USA. In addition, we note that the V70L undergoing rapid expansion in the UK and the I82T mutations, both of which are under increasing rapidly, involve the putative glucose transport transmembrane helices of the M protein. We continued to follow the frequency of isolates carrying the M:182T mutation during the development of the manuscript. While it has increased in the USA from 0.014% in October 2020 to 1.62% in February 2021, a 116-fold change, it has further increased to 3.33% in isolates reported between February 16th till March 4th 2021. Given the rapid emergence of this mutation, and the role of the M protein in multiple viral functions, including viral host cell binding, innate immune and T cell responses in SARS and SARS-CoV-2, with possible immune evasion, and now potential alterations in glucose transport, this novel M:I82T clade warrants inclusion in ongoing SARS-CoV-2 genomic surveillance and further evaluation for potential increased geographic spread and pathogenicity. Of particular interest is the observation that the average age of patients infected by the virus carrying one of the four M missense mutations is 4.6-6.3 years less than those that lack any of the M mutations (37.1-38.8 vs. 43.4 years of age). Given the increasing incidence of symptomatic and even severe COVID in younger patients, the potential for association with this mutation bears scrutiny.

  • FLCCC confirms

    Dr. Vladimir Zelenko nominated for Nobel Peace Prize


    Amazing the national and world media missed this....... NOT!!!

  • COVID-19 Is a Vascular Disease

    We know this since one year already but scientists get no attention without claiming they found something new.

    CoV-19 virus preferably attack all endothelia cells and these also form the inner surface of blood vessels. People looking for the reason for alveolus collapse first ( a year ago!) notes that the vessels did loose their stability.

    More serious issue: The UK BBC one free masons bribed news channel again did spread the ugliest fake news I heard for a long time. As usual a PR trained lady (British people seem to trust ladies much more...) explained that 25..50% of the CoV-19 sick people get long Covid. This is plain nonsense. This only happens in a small number of cases and can easily, be cured with ivermectin.

    The fact is that the British mafia inside BBC is responsible for several 10'000 deaths by suppressing the working drug Ivermectin. I hope one day when people understand the truth, then all these criminals inside BBC will be jailed together with their friends in the newspapers.

  • Game, set, match.

    As advised on this board, you don't want to become a spike factory.

    If you got the vax, consider IVM in the future. Protect yourself even more than the unvaccinated with T-Cell immunity naturally, do you know if you are more susceptible to a cytokine storm in future variant editions? You don't.

  • As advised on this board, you don't want to become a spike factory.

    Which you will be, if you are not vaccinated and you get COVID-19. The disease produces many, many more spikes than the vaccine.

    I doubt this research is correct. But assuming it is, there is no question the vaccine does not produce enough spikes to harm the patient. A billion people have been vaccinated and there are no reports of serious side effects or problems. So obviously the vaccine is safe. There can be no better proof of that.

  • Game, set, match.

    As advised on this board, you don't want to become a spike factory.

    If you got the vax, consider IVM in the future.

    Just for laughs, why don't you try to explain away the data from the UK and Israel:

    If the vaccine causes all the harm that you claim it does, why is the disease and number of deaths approaching zero in these countries? They have the most vaccinations per capita in the world. In your imaginary reality, they should be suffering from being spike factories. So why aren't they? What about the other billion people who have been vaccinated? Why don't we see problems in them? There are no reports of people needing IVM in the UK or Israel.

    Go ahead and explain this! Oh wait. Never mind. You don't actually deal with real world data and facts, do you? You just make stuff up.