It has been one of the most enduring Covid conspiracy theories: that the ‘gold standard’ PCR tests used to diagnose the virus were picking up people who weren’t actually infected.
Some even suggested the swabs, which have been carried out more than 200 million times in the UK alone, may mistake common colds and flu for corona.
If either, or both, were true, it would mean many of these cases should never have been counted in the daily tally – that the ominous and all-too-familiar figure, which was used to inform decisions on lockdowns and other pandemic measures, was an over-count.
And many of those who were ‘pinged’ and forced to isolate as a contact of someone who tested positive – causing a huge strain on the economy – did so unnecessarily.
Such statements, it must be said, have been roundly dismissed by top experts. And those scientists willing to give credence such concerns have been shouted down on social media, accused of being ‘Covid-deniers’, and even sidelined by colleagues.
But could they have been right all along?
Note: Commentary on this document by Dr. Naomi Wolf can be found here: FDA document admits “covid” PCR test was developed without isolated covid samples for test calibration, effectively admitting it’s testing something else
Since no quantified virus isolates of the 2019-nCoV were available for CDC use at the time the test was developed and this study conducted, assays designed for detection of the 2019-nCoV RNA were tested with characterized stocks of in vitro transcribed full length RNA (N gene; GenBank accession: MN908947.2) of known titer (RNA copies/µL) spiked into a diluent consisting of a suspension of human A549 cells and viral transport medium (VTM) to mimic clinical specimen.
Most people infected with SARS-CoV-2 are contagious for 4–8 days.7 Specimens are generally not found to contain culture-positive (potentially contagious) virus beyond day 9 after the onset of symptoms, with most transmission occurring before day 5. This timing fits with the observed patterns of virus transmission (usually 2 days before to 5 days after symptom onset), which led public health agencies to recommend a 10-day isolation period. The short window of transmissibility contrasts with a median 22–33 days of PCR positivity (longer with severe infections and somewhat shorter among asymptomatic individuals). This suggests that 50–75% of the time an individual is PCR positive, they are likely to be post-infectious.
There is an old saying in medicine that “the cure may be worse than the disease.” The phrase can be applied to vaccines. In the current paper the concern is raised that the RNA based COVID vaccines have the potential to cause more disease than the epidemic of COVID-19. This paper focuses on a novel potential adverse event mechanism causing prion disease which could be even more common and debilitating than the viral infection the vaccine is designed to prevent. While this paper focuses on one potential adverse event there are multiple other potential fatal adverse events as discussed below.
Ivor Cummins aka the Fat Emperor – gives James the lowdown on why you can’t trust anything our governments tell us about Covid-19. If you want the facts on Coronavirus – how deadly is it? do lockdowns and masks work? how does it compare with previous pandemics? – you’ve come to the right place
Please support the Delingpod:
Mirror archives are available below if this video is removed from YouTube.
Prolonged SARS-CoV-2 RNA shedding and recurrence of PCR-positive tests have been widely reported in patients after recovery, yet these patients most commonly are non-infectious. Here we investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the human genome and that transcription of the integrated sequences might account for PCR-positive tests. In support of this hypothesis, we found chimeric transcripts consisting of viral fused to cellular sequences in published data sets of SARS-CoV-2 infected cultured cells and primary cells of patients, consistent with the transcription of viral sequences integrated into the genome. To experimentally corroborate the possibility of viral retro-integration, we describe evidence that SARS-CoV-2 RNAs can be reverse transcribed in human cells by reverse transcriptase (RT) from LINE-1 elements or by HIV-1 RT, and that these DNA sequences can be integrated into the cell genome and subsequently be transcribed. Human endogenous LINE-1 expression was induced upon SARS-CoV-2 infection or by cytokine exposure in cultured cells, suggesting a molecular mechanism for SARS-CoV-2 retro-integration in patients. This novel feature of SARS-CoV-2 infection may explain why patients can continue to produce viral RNA after recovery and suggests a new aspect of RNA virus replication.
The PCR verdict cannot tell these individuals whether they need to self-isolate or whether they might need treatment – the things that really matter to them and society.
n some cases, for example, viral RNA might be present in such very low quantities that an individual is not at all infectious and poses zero danger. In other cases, the swabs might pick up RNA which is so old it is completely dead, as people continue shedding material from the virus up to 80 days after the initial infection.
I believe these people are testing positive time and time again.
COVID-19 vaccines designed to elicit neutralising antibodies may sensitise vaccine recipients to more severe disease than if they were not vaccinated. Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the development and testing of these vaccines suggest a serious mechanistic concern: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralising antibodies), be they composed of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE). This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-19 vaccine trials that adequate patient comprehension of this risk is unlikely to occur, obviating truly informed consent by subjects in these trials.
COVID-19 is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised animal reservoir. Due to this recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any homoplasies observed in SARS-CoV-2 to date are significantly associated with increased viral transmission. To do so, we develop a phylogenetic index to quantify the relative number of descendants in sister clades with and without a specific allele. We apply this index to a curated set of recurrent mutations identified within a dataset of 46,723 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent mutations currently in circulation appear to be evolutionary neutral and primarily induced by the human immune system via RNA editing, rather than being signatures of adaptation. At this stage we find no evidence for significantly more transmissible lineages of SARS-CoV-2 due to recurrent mutations.
We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent mutations currently in circulation appear to be evolutionary neutral and primarily induced by the human immune system via RNA editing, rather than being signatures of adaptation. At this stage we find no evidence for significantly more transmissible lineages of SARS-CoV-2 due to recurrent mutations.
While the testing data are so opaque, using them to direct local lockdowns is unhelpful, argues Heneghan. “The testing is there to drive the test and trace strategy,” he says. “But what seems to be happening is that, as soon as we see an outbreak, there tends to be panic and over-reacting. This is a huge problem because politicians are operating in a non-evidence-based way when it comes to non-drug interventions.”