Science journals have encouraged and enforced a false Covid narrative
Bear in mind that in the heat of this pandemic, papers printed in important journals were peer-reviewed within 10 weeks; one rattled through the process in just nine days for Nature. But, like Petrovsky, I have heard similar stories from many other frustrated experts who confronted the conventional wisdom that this lethal virus was a natural spillover event. Some could not even get letters published, let alone challenge those key papers promoting the Chinese perspective which have since turned out to be flawed or wrong.
Only now is acceptance emerging that the science establishment colluded to dismiss the lab leak hypothesis as a conspiracy theory, assisted by prominent experts with clear conflicts of interest, patsy politicians and a pathetic media that mostly failed to do its job. And yet, at the heart of this scandal lie some of the world’s most influential science journals. These should provide a forum for pulsating debate as experts explore and test theories, especially on something as contentious and fascinating as the possible origins of a global pandemic. Instead, some have played a central role in shutting down discussion and discrediting alternative views on the origins, with disastrous consequences for our understanding of events.
The scientific literature and publishing scientists have been rapidly and massively infected by COVID-19 creating opportunities and challenges. There is evidence for hyper-prolific productivity.
“[R]oughly twice as many people have developed T-cell immunity compared with those who we can detect antibodies in.“
SARS-CoV-2-specific memory T cells will likely prove critical for long-term immune protection against COVID-19. We systematically mapped the functional and phenotypic landscape of SARS-CoV-2-specific T cell responses in a large cohort of unexposed individuals as well as exposed family members and individuals with acute or convalescent COVID-19. Acute phase SARS-CoV-2-specific T cells displayed a highly activated cytotoxic phenotype that correlated with various clinical markers of disease severity, whereas convalescent phase SARS-CoV-2-specific T cells were polyfunctional and displayed a stem-like memory phenotype. Importantly, SARS-CoV-2-specific T cells were detectable in antibody-seronegative family members and individuals with a history of asymptomatic or mild COVID-19. Our collective dataset shows that SARS-CoV-2 elicits robust memory T cell responses akin to those observed in the context of successful vaccines, suggesting that natural exposure or infection may prevent recurrent episodes of severe COVID-19 also in seronegative individuals.