Archiv: ACE2 (enzym)

20.02.2021 - 04:50 [ ]

Studie zum Ursprung der Coronavirus-Pandemie

Zusammenfassend kann festgehalten werden, dass es sehr viele Indizien gibt, die einen Laborunfall im „Wuhan Institute of Virology“ als die mit Abstand wahrscheinlichste Ursache für die Corona-Pandemie erscheinen lassen. In diesem Fall würde es sich nicht um eine „Naturkatastrophe“ handeln, sondern um eine von Menschen selbst herbeigeführte Tragödie. Es besteht eine sehr große Gefahr darin, die Frage nach der Ursache für die gegenwärtige Pandemie „als geklärt“ zu deklarieren, wie etwa in dem Statement [III.4] einiger Virologen. Für politische Entscheidungsträger macht es unbestreitbar einen Unterschied, ob sie Wildtiermärkte oder Hochrisikoforschung mit gentechnisch manipulierten Viren weltweit verbieten sollen. Diese Frage muss verstärkt in den Vordergrund rücken, ansonsten könnten Corona- und andere Virenarten noch ein viel größeres Gefahrenpotential entwickeln, nicht nur in der Gegenwart, sondern auch in der Zukunft.


Auffallend bei der gegenwärtigen Pandemie im Vergleich zu früheren Ausbrüchen von Coronavirus-bedingten Erkrankungen ist:
1) Wir haben es in der gegenwärtigen Pandemie mit einem Erreger zu tun, der mit einer bislang nicht bekannten Effizienz menschliche Zellen angreift.
2) Dabei werden nicht nur die (oberen) Atemwege, sondern auch innere Organe angegriffen und in ihrer Funktion teilweise schwer geschädigt.
Man muss sich daher notwendigerweise die Frage stellen, wie eine solche nahezu perfekte Adaption von Coronaviren an menschliche Zellrezeptoren zustande kommen konnte, um zukünftige Pandemie-Gefahrenpotentiale identifizieren zu können.

11.01.2021 - 20:39 [ University of Cambridge / ]

Study identifies genetic changes likely to have enabled SARS-CoV-2 to jump from bats to humans

A new study, involving the University of Cambridge and led by the Pirbright Institute, has identified key genetic changes in SARS-CoV-2—the virus that causes COVID-19—that may be responsible for the jump from bats to humans, and established which animals have cellular receptors that allow the virus to enter their cells most effectively.

The genetic adaptions identified were similar to those made by SARS-CoV—which caused the 2002-2003 SARS epidemic—when it adapted from bats to infect humans.

04.01.2021 - 11:08 [ Rubikon ]

Die Vertuschungsaktion


Laut Alina Chan, Molekularbiologin am Broad Institute of Harvard und am MIT, kann man die Evolution von SARS-CoV-2 nicht mit der These eines zoonotischen Ursprungs in Einklang bringen, denn das Virus war bereits vollständig für die Mensch-zu-Mensch-Übertragung angepasst, als es zum ersten Mal auftrat.

Die renommierte medizinische Fachzeitschrift „Nature“ erlaubte anscheinend einigen Autoren, ihre Daten heimlich zu ändern, ohne auf diese Korrekturen in den Artikeln hinzuweisen.

Chans Untersuchungen zeigen, dass die Autoren ihre Proben umbenannt, falsch zugeordnet und ein Genomprofil generiert haben, das mit keiner ihrer Proben übereinstimmt. In anderen Papers fehlen Daten.

Das Coronavirus RaTG13, zu 96 Prozent mit SARS-CoV-2 identisch und somit der engste Verwandte, ist in Wirklichkeit btCoV-4991. Dieses Genom wurde schon 2013 in Proben nachgewiesen und 2016 veröffentlicht.

03.01.2021 - 18:07 [ ]

Did Top Medical Journal Help Cover Up Origins of SARS-CoV-2?


– According to Alina Chan, a molecular biologist at the Broad Institute of Harvard and MIT, SARS-CoV-2 did not evolve in a manner you’d expect, had it jumped from an animal to a human. It sprang into action fully evolved for human transmission
– It appears Nature, a top medical journal, has allowed authors to secretly alter data sets in their papers without publishing notices of correction
– Chan’s investigation reveals authors have renamed samples, failed to attribute them properly, and produced a genomic profile that doesn’t match the samples in their paper. Others are missing data
– RaTG13 — the coronavirus that most resembles SARS-CoV-2, being 96% identical — is actually btCoV-4991, a virus found in samples collected in 2013 and published in 2016
– If SARS-CoV-2, the virus responsible for COVID-19 and the subsequent response to it, came from a lab, then we need to reassess the future of gain-of-function research that allows for the weaponization of viruses

03.01.2021 - 17:53 [ Alina Chan / Twitter / ]

Get ready. This is going to be an important thread. Election season will be over soon and hopefully more people will devote some attention to this… I’m going to walk through a timeline of SARS2-related virus data published in the months after the outbreak. (1/30)

(25 Oct 20)

Since the outbreak in late 2019, events have been unfolding at such a fast pace that it is difficult to keep track of what happened and in what order.

I use visualizations of the timeline to follow key events relating to the search for the animal host of SARS2. (2/30)

Even today, I still hear people saying that SARS-CoV-2 came from pangolins and a Seafood market in Wuhan. I hope this analysis will help to clear things up. It will refresh us on significant early pandemic events and major publications discussing the origins of the virus (3/30).

03.01.2021 - 16:55 [ Dr. Jurgen Mayer / ]

Scientific history of RaTG13

(Jul 07, 2020)

In early February 2019, Dr. Shi’s team suddenly tossed a brand new genome online and published a paper, citing that hCoV-2019 must come from (horseshoe) Bats because it is so similar to this other sample obtained from Bats in July 2013.

*If an existing genome was already in the system and the new data was uploaded we would expect to see reference notes and that the previous listing had been removed or updated.

*The scientists were forcing an argument that this newly published genome (RaTG13) came from a Bat and is the closest relative to hCoV-2019, therefore our pandemic virus more than likely came from a bat.

At the time of this publication, there is quite literally zero record or publication referencing this sudden new virus that they designated as Bat SL-CoV RaTG13 (Ra being Rhinolophus affinis, 13 being sampling year). How could this new virus have been just ABSENT from the scientific community for SEVEN YEARS?!

In fact, there are (comparatively) barely any Rhinolophus Affinis Samples in our databases. Meaning there is a small pool or Bat viruses from this specific species. The team simply renamed the sample and maybe forgot that 4991 was already in GenBank?! Because 4991 is actually RaTG13, yet this super important publication which was read by all of the top scientists in the world makes zero mention of this important fact.

03.01.2021 - 16:33 [ Shing Hei Zhan, Benjamin E. Deverman, Yujia Alina Chan / ]

SARS-CoV-2 is well adapted for humans. What does this mean for re-emergence?

(May 02, 2020)

Abstract: In a side-by-side comparison of evolutionary dynamics between the 2019/2020 SARS-CoV-2 and the 2003 SARS-CoV, we were surprised to find that SARS-CoV-2 resembles SARS-CoV in the late phase of the 2003 epidemic after SARS-CoV had developed several advantageous adaptations for human transmission. Our observations suggest that by the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV. However, no precursors or branches of evolution stemming from a less human-adapted SARS-CoV-2-like virus have been detected. The sudden appearance of a highly infectious SARS-CoV-2 presents a major cause for concern that should motivate stronger international efforts to identify the source and prevent near future re-emergence.

14.12.2020 - 23:20 [ ]

What is ‚VUI – 202012/01‘? Matt Hancock reveals new fast-spreading strain of coronavirus could be behind surging cases in London and the South East – but it has ‚only been found in 1,000 people and isn’t more deadly‘

However, there have been three that have caught scientists‘ attention:


D614G is by far the most common strain of coronavirus affecting humans worldwide and first appeared in February in Germany.

It is thought to account for 85 per cent of global cases.

The D614G mutation sprung up at one specific location, position 614, on the spike protein of the virus, in a European patient.

This viral spike hijacks the human receptor ACE2 and this is how it infects human cells.

16.04.2020 - 13:41 [ Washington Post ]

State Department cables warned of safety issues at Wuhan lab studying bat coronaviruses

“The idea that it was just a totally natural occurrence is circumstantial. The evidence it leaked from the lab is circumstantial. Right now, the ledger on the side of it leaking from the lab is packed with bullet points and there’s almost nothing on the other side,” the official said.

As my colleague David Ignatius noted, the Chinese government’s original story — that the virus emerged from a seafood market in Wuhan — is shaky. Research by Chinese experts published in the Lancet in January showed the first known patient, identified on Dec. 1, had no connection to the market, nor did more than one-third of the cases in the first large cluster. Also, the market didn’t sell bats.

03.04.2020 - 10:35 [ Kai Kupferschmidt / ]

My good news contribution for today: Researchers in Denmark are starting to test a promising drug in #covid19 patients, barely a month after research appeared showing the drug could stop the virus in cell culture.

KroganLab Camostat mesylate binds to a protein on human cells called TMPRSS2. And SARS-CoV-2 needs this protein to efficiently enter human cells: The spike protein on top of the virus attaches to the ACE2 receptor on human cells. And then TMPRSS2 needs to make a cut in the spike.

26.03.2020 - 09:25 [ Forbes ]

There Is A Drug Already Used In Japan Which May Treat COVID-19, Says New Study


“We knew from our previous work that camostat mesylate was active against other coronaviruses, including SARS-CoV. Therefore, we tested whether it is also active against SARS-CoV-2,” said Stefan Pöhlmann, PhD, Professor in the same institute in Göttingen. “Our study shows that camostat mesylate blocks infection of cells with SARS-CoV-2-like particles and with authentic, patient-derived SARS-CoV-2. Moreover, camostat mesylate inhibited infection of important target cells – human lung epithelial cells,” he added.

26.03.2020 - 08:47 [ Markus Hoffmann, Hannah Kleine-Weber, Nadine Krüger, Marcel Müller, Christian Drosten, Stefan Pöhlmann / ]

The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells


Here, we demonstrate that 2019-nCoV-S uses the SARS-coronavirus receptor, ACE2, for entry and the cellular protease TMPRSS2 for 2019-nCoV-S priming. A TMPRSS2 inhibitor blocked entry and might constitute a treatment option. Finally, we show that the serum form a convalescent SARS patient neutralized 2019-nCoV-S-driven entry. Our results reveal important commonalities between 2019-nCoV and SARS-coronavirus infection, which might translate into similar transmissibility and disease pathogenesis. Moreover, they identify a target for antiviral intervention.


The present study suggests that 2019-nCoV spread might also depend on TMPRSS2 activity and it is noteworthy that the serine protease inhibitor camostat mesylate blocks TMPRSS2 activity (24, 26) and has been approved in Japan for human use, although for an unrelated indication. This compound or related ones should be considered for treatment of 2019-nCoV infected patients.

26.03.2020 - 08:29 [ ]

New Israeli research says COVID-19 is here to stay


The researchers claim that this new virus strain, named COVID-19, bears a striking 72.8% resemblance in structure to the SARS strain, and so the researchers tested the way in which COVID-19 attaches itself to the ACE2 enzyme, which is part of almost every cell in the human body and is known to serve as an entry point for the SARS virus.

According to the research, SARS attaches itself to human cells in such a way that researchers found easy to break using medicine.

Unlike SARS, the COVID-19 strain attaches itself to human cells in a much more aggressive manner, meaning that its removal from a cell is much harder when compared to SARS.

09.03.2020 - 05:40 [ Deutsches Primatenzentrum - Leibniz-Institut für Primatenforschung ]

Die Vermehrung von SARS-Coronavirus-2 im Menschen verhindern: Göttinger Infektionsforscher identifizieren potentielles Medikament

Um eine Krankheit auszulösen, müssen Viren in Körperzellen eindringen. Dazu heften sie sich an geeignete Zellen an und schleusen ihre Erbinformation in diese Zellen ein. Infektionsforscher vom Deutschen Primatenzentrum – Leibniz-Institut für Primatenforschung in Göttingen haben zusammen mit Kollegen an der Charité – Universitätsmedizin Berlin untersucht, wie das neuartige Coronavirus SARS-CoV-2 in Zellen eindringt. Sie haben ein zelluläres Enzym identifiziert, das für den Eintritt des Virus in Lungenzellen unverzichtbar ist: die Protease TMPRSS2. Ein bereits existierendes Medikament, das diese Protease hemmt, könnte daher eine erfolgversprechende Behandlungsmöglichkeit darstellen (Cell).