kennyskitchen

Published on May 26, 2020
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That's right folks, the death toll for COVID-19 has officially (a key word, based on what we know about COVID reporting in the US and around the world) cleared the bottom bounds for an average year of the seasonal flu. CV is currently counted at 346,893, while according to the WHO, the seasonal flu averages "290,000 to 650,000 respiratory deaths" per year.


In other news, the media is sure talking a lot about the "vaccines" for this virus, being rushed to warp-speed, and good old Bill Gates is always happy to remind us that things won't go back to normal any time soon, and to fund & promote things like vaccines and mass micro-chipping of people.


Pharmaceutical giant AstraZenica says “And there’s no doubt, starting in September, we will start delivering these doses of vaccine to the British Government for vaccination.”, referring to the pre-order of 100,000,000 doses they got from the UK syndicate, right before locking in an order for 400,000,000 from the US syndicate.

Interesting how this recent article by in the Telegraph quotes Professor Adrian Hill, director of the Oxford University’s Jenner Institute, who is jointly leading research on a CV vaccine, as saying things like:

It is a race, yes. But it's not a race against the other guys. It’s a race against the virus disappearing...

We said earlier in the year that there was an 80 per cent chance of developing an effective vaccine by September. But at the moment, there’s a 50 per cent chance that we get no result at all.

We’re in the bizarre position of wanting Covid to stay, at least for a little while. But cases are declining.


So, you may or may not be familiar with the PCR tests (the standard way of getting turning someone into a confirmed case of COVID-19...) Well, let's just say that they have issues. Now, in regards to those specific tests, the Australian syndicate ("government"), has this to say (all emphasis mine):

PCR tests are currently considered to be more clinically sensitive than serology assays for detecting early infections and, because they directly detect viral RNA, they are an indicator for viral shedding. The extent to which a positive PCR result correlates with the infectious state of an individual is still being determined. Clinical resolution and consecutive negative PCR tests in a previously positive individual are currently being used as criteria when considering release from isolation. However, this may change with increasing knowledge around SARS-CoV-2.


A paper out of both Singapore’s National Centre for Infectious Diseases and the Academy of Medicine indicates that the government/media claims about the infectiousness of asymptomatic "carriers" has been blown wildly out of proportion.

As the paper states:

While the duration of viral shedding1by PCR may extend to a month and sometimes longer for a small group of patients, and several jurisdictions including Singapore have been usingit to guide de-isolation and discharge policies, it is important to note that viral RNA detection by PCR does not equateto infectiousnessor viable virus

Based on the accumulated data since the start of the COVID-19 pandemic, the infectious period of SARS-CoV-2 in symptomatic individuals may begin around 2 days before the onset of symptoms,and persists for about 7-10 days after the onset of symptoms. Active viral replication drops quickly after the first week, and viable virus was not found after the second week of illness despite the persistence of PCR detection of RNA.


Now, do you remember that "BioSafety Level 4" laboratory in Wuhan? The one funded by the US government to the tune of $3.7B? The one that Nature (a peer-reviewed journal) wrote about in 2017... just two years after they wrote about the danger of China's research into bat SARS. Well now, Australian scientists have this to say about the virus, and it's connection (or lack thereof) to bats:

Although bats carry many coronaviruses including SARS-CoV, relative of SARS-CoV-2, direct evidence for existence of SARS-CoV-2 in bats has not been found. As highlighted by our data, the binding strength of SARS-CoV-2 for bat ACE2 is considerably lower than for human ACE2 ,suggesting that even if SARS-CoV-2 did originally arose from a bat precursor it must later have adapted its spike protein to optimise its binding to human ACE2. There is no current explanation for how, when or where this might have happened. Instances of direct human infection by coronaviruses or other bat viruses is rare with transmission typically involving an intermediate host. For example, lyssaviruses such as Hendra are periodically transmitted from bats to horses and then to humans who contract the infected horse. Similarly, SARS-CoV was shown to be transmitted from bats to civet cats and from them to humans. To date, a virus identical to SARS-CoV-2 has not been identified in bats or any other non-human species, making its origins unclear. To date, the most closely related coronavirus to SARS-CoV-2, is the bat coronavirus, BatCoV RaTG1, which has 96% whole-genome identity to SARS-CoV-2. The fact that SARS-CoV-2 has also not been found in any likely intermediate host raises questions of the origins of the original SARS-CoV-2 virus that infected human case zeroin late 2019. Wuhan, the epicentre of the outbreak, hosts China’s only BSL4 facility and is the site of considerable bat coronavirus research.Identification of an intermediate animal host in which SARS-CoV-2 might have adapted to a human ACE2 permissive form would go a long way to alleviating concerns that SARS-CoV-2 is not a natural virus. Lam et al. made confused public claims of finding SARS-CoV-2 in Malayan pangolins, suggesting that pangolins were an intermediate vector for SARS-CoV-2.However,further sequence analysis of these claims by Zhang et al. established that Pangolin-CoV was a very different coronavirus that had modest at best ~90% sequence similarity to SARS-CoV-2."



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