The research team of MIT and Harvard University worked together to identify specific types of cells that appear to be the “target” of the novel coronavirus. Their findings explain the “AI” feature of the virus and back the theory that the virus got out-of-control after the Chinese Communist Party unleashed it.
The scientific evidence to back Miles Guo’s claim of the “Artificial Intelligence” (AI) feature of the virus:
As reported in MIT news, the virus may have evolved to take advantage of host cells’ natural defenses, hijacking some proteins for their own use.
The species-specific role of interferon may explain why the virus got out-of-control for the CCP
Researchers found that interferon in mice does not induce ACE2 as it does in the human bodies. In layman’s terms, the virus is more lethal for humans than for mice, which might explain why the CCP initially thought that the virus was controllable when Wang Qishan told his confidant that the outbreak would be over soon as disclosed by Miles Guo.
On Jan 2, Chinese dissident Miles Guo warned the world that CCP was suspected of using “SARS” to crack down the pro-democracy protests in Hong Kong.
If the CCP scientists only tested the virus on mice in a lab environment, they must have gotten “controllable” results in terms of transmission and lethality. But it got out of hand after it was unleashed to infect humans.
This might also explain the CCP’s intensified hacking of the research information of the CCP virus. The US government recently pointed out that Chinese hackers are rampantly attacking the websites of government agencies and research organizations in the US medical and health field, stealing research information about the novel coronavirus. This series of hacking attacks have been launched since the outbreak of the novel coronavirus and is one of the largest attacks in a few years.
Link to MIT News:
Research Paper Summary and link:
There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2) which causes the disease COVID-19. SARS-CoV- 2 spike (S)-protein binds ACE2, and in concert with host proteases, principally TMPRSS2, promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues, and the factors that regulate ACE2 expression, remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 amongst tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discover that ACE2 is human interferon- stimulated gene (ISG) in vitro using airway epithelial cells, and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.