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#ace2

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Lorraine

Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link

mdpi.com/2076-0817/13/12/1070

my new edited🧵listing all the important papers that have come out over the past 4 years

actually understood >90% of this thanks to a couple books & lectures prior to reading

every abstract starts the same.. in 2019 SARSCov2 first appeared…
you do not want cancer in any form, yet so many pathways via Covid #ace2 #CovidPapers published December 6, 2024

MDPIEquivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a LinkThe COVID-19 infection caused by SARS-CoV-2 in late 2019 posed unprecedented global health challenges of massive proportions. The persistent effects of COVID-19 have become a subject of significant concern amongst the medical and scientific community. This article aims to explore the probability of a link between the COVID-19 infection and the risk of lung cancer development. First, this article reports that SARS-CoV-2 induces severe inflammatory response and cellular stress, potentially leading to tumorigenesis through common pathways between SARS-CoV-2 infection and cancer. These pathways include the JAK/STAT3 pathway which is activated after the initiation of cytokine storm following SARS-CoV-2 infection. This pathway is involved in cellular proliferation, differentiation, and immune homeostasis. The JAK/STAT3 pathway is also hyperactivated in lung cancer which serves as a link thereof. It predisposes patients to lung cancer through myriad molecular mechanisms such as DNA damage, genomic instability, and cell cycle dysregulation. Another probable pathway to tumorigenesis is based on the possibility of an oncogenic nature of SARS-CoV-2 through hijacking the p53 protein, leading to cell oxidative stress and interfering with the DNA repair mechanisms. Finally, this article highlights the overexpression of the SLC22A18 gene in lung cancer. This gene can be overexpressed by the ZEB1 transcription factor, which was found to be highly expressed during COVID-19 infection.
Public
datum (n=1)

Reminder: a housecat that can bite through your skin is unlike a tiger that can puncture any organ!

SARS-CoV-2 is unlike all common colds, because it can infect almost every organ in the body (through ACE2 and synctia) unlike every common cold.

"Vaccines have not turned covid into a common cold."

"Multiple infections will not turn covid into a common cold."

donotpanic.news/p/why-covid-ca

¡Do Not Panic! · Why Covid Can Never Be 'Just A Cold'By Nate Bear
#ACE2#SARS2#COVID
Public
datum (n=1)

I can see why donotpanic.news/p/why-covid-ca is rising on the #zeroes list.

Accessible and packing citations, it might help people who are on the fence to understand and risk model.

Takeaways:

"Vaccines have not turned covid into a common cold."

"Multiple infections will not turn covid into a common cold."

SARS-CoV-2 is unlike all common colds, because it can effectively infect almost every organ in the body (through ACE2) unlike every common cold.

But like SARS1.

¡Do Not Panic! · Why Covid Can Never Be 'Just A Cold'By Nate Bear
#ACE2#SARS2#COVID
Public
Auscandoc

#StanfordMedicine study flags unexpected cells in lung as suspected source of severe #COVID | med.stanford.edu/news/all-news “Important covid clues! Researchers find that #macrophages - the cells that usually scavenge and destroy viruses - are the cells most susceptible to being infected/hijacked by #SARSCoV2. To enter macrophages, SARS-CoV-2 uses #CD209 receptors (not #ACE2). Interfering with SARS-CoV-2/CD209 binding could be a promising target for new and better prevention and/or treatment!”

News CenterStanford Medicine study flags unexpected cells in lung as suspected source of severe COVIDA previously overlooked type of immune cell allows SARS-CoV-2 to proliferate, Stanford Medicine scientists have found. The discovery has important implications for preventing severe COVID-19.
Public
Aho

in they have developed a new virus which was 100% lethal for with

This project seems to not have had any scientific meaning, more a test to a that could be a new and ultra deadly

Souce: dimsumdaily.hk/chinese-develop

Dimsum Daily · Chinese development of new coronavirus with 100% mouse fatality rate draws criticism from British and American academic circles - Dimsum Daily23rd January 2024 – (Beijing) A research team composed of academic and medical institutions in China announced the development of a new strain of coronavirus with a 100% fatality rate in laboratory mice. The virus was derived from a strain previously discovered in pangolins, a type of scaly anteater, prior to the outbreak of the […]
Public
Giuseppe Michieli

Convergent #evolution of #SARS-CoV-2 #XBB #lineages on #RBD 455–456 synergistically enhances #antibody #evasion and #ACE2 binding journals.plos.org/plospathogen

journals.plos.orgConvergent evolution of SARS-CoV-2 XBB lineages on receptor-binding domain 455–456 synergistically enhances antibody evasion and ACE2 bindingAuthor summary The continuous evolution of SARS-CoV-2 presents a challenge to global public health and the development of vaccines and treatments against COVID-19. Recently, an adjacent residue alteration, L455F+F456L, also known as “FLip”, on the receptor-binding domain of the virus, which has been identified in multiple strains of the virus, alters how the virus interacts with human cells and immune response. We show that the combination of these mutations synergistically increases the virus’s ability to bind to ACE2, the primary receptor on cell surfaces, enabling it to specifically escape a public type of neutralizing antibodies elicited by vaccination and infection, and the molecular mechanisms are explained by structural analyses. The enhancement of receptor binding increases the potential of the virus to further accumulate immune evasive mutations. These findings broaden our understanding of SARS-CoV-2 evolution and highlight the importance of paying attention to these ongoing antigenic drifts in the virus as we continue to develop and evaluate current antibody therapeutics and vaccines.
Public
Giuseppe Michieli

Regulatory T cell-like response to #SARS-CoV-2 in Jamaican fruit #bats (Artibeus jamaicensis) transduced with #human #ACE2 journals.plos.org/plospathogen

journals.plos.orgRegulatory T cell-like response to SARS-CoV-2 in Jamaican fruit bats (Artibeus jamaicensis) transduced with human ACE2Author summary Bats are reservoir hosts of many viruses that infect humans, yet little is known about how they host these viruses, principally because of a lack of relevant and susceptible bat experimental infection models. Although SARS-CoV-2 originated in bats, no robust infection models of bats have been established. We determined that Jamaican fruit bats are poorly susceptible to SARS-CoV-2; however, their lungs can be transduced with human ACE2, which renders them susceptible to the virus. Despite robust infection of the lungs and diminishment of pulmonary cellularity, the bats showed no overt signs of disease and cleared the infection after two weeks. Despite clearance of infection, only low-titer antibody responses occurred and only a single bat produced neutralizing antibody, consistent with other experimental infection studies of bats. Assessment of the CD4+ helper T cell response showed that activated cells expressed the regulatory T cell cytokines IL-10 and TGFβ that may have tempered pulmonary inflammation.
Replied in thread
Public
Rev. GothAlice

@croissant If only mutation weren't a thing.

If only.

My work simulating the folding of proteins (e.g. the #ace2 receptor binding surface used for initial infection) from #COVID might never end.

Computational physical simulation of rather absurd chemistry? Absurd because the "folding" process—taking a printed strip of chemicals and forming a functional 3D shape—takes milliseconds to /microseconds/ in reality. Up to three days to accurately simulate.

Better than getting infected, even once.

Public
Zoomers of the Sunshine Coast

Surprise COVID discovery helps
explain how coronaviruses jump species

SARS-CoV-2 can also bind with other proteins, however. Could it use those other proteins to infiltrate cells? ACE-2 was the most efficient route but there were others. And that suggests the virus can bind and infect even cells without ACE-2 receptors.

The ACE2 receptor accelerates but is not biochemically required for SARS-CoV-2 membrane fusion
pubs.rsc.org/en/content/articl

#CellBinding #ACE2

phys.org/news/2023-08-covid-di

Illustration of the virus entering the cell. Protease =/- ACE2
Public
Victoria Stuart 🇨🇦 🏳️‍⚧️

Scientists discover antibodies that neutralize COVID-19 variants
ctvnews.ca/sci-tech/scientists

science.org/doi/10.1126/sciadv

* potent antibodies neutralize virt. all known COVID-19 variants
* antibodies f. recovered SARS patient (vacc. against COVID-19) “exhibited remarkable breadth” against respiratory viruses SARS, COVID-19
* combination of prior coronavirus infection & vaccination gen. “extremely broad & powerful” antibody response capable of stopping nearly all coronaviruses

CTVNews · Scientists discover antibodies that can neutralize COVID-19 variants, potentially prevent future coronavirus outbreaksScientists have discovered antibodies that can neutralize virtually all known variants of the COVID-19 virus, potentially preventing future coronavirus outbreaks.
#COVID19#ACE2#SARSCoV2
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