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intrigued

"An ultraspecific anti-SSEA-4 monoclonal antibody recognizes stem memory T cells" by Scancell, Nottingham University and Josep Carreras Leukaemia Research Institute

this is Mab 2811

so i then looked at SAR which is a chronovirus as well .. which also appears to lock onto the ACE2 receptor

""ACE2 acts as the host cell receptor for SARS-CoV, by binding to the spike protein on the viral capsid."""

ACE2 was identified as the receptor for SARS virus in vitro [77, 78] and also acts as receptor for the NL63 virus. Soon after, studies confirmed that ACE2 was essential for SARS infection in vivo using ACE2-knockout mice [79]. Concurrently it was discovered that ACE2 protects murine lungs from severe acute injury [80] and subsequently that SARS-CoV infections and the SARS spike protein itself downregulate ACE2 expression

appreciate this Virus is only a few months old ...... so little data is known , what this highlights is a possible link to Total organ failure ..

Therefore, once exposed to the coronavirus (e.g. through the blood or other body fluid), these organs may also get affected especially for those the receptor has the direct-acting control. This paper aims to analyze the possibility of the association between 2019-nCoV infection and the multiple organ failure (MOF) other than pneumonia.

ACE2 also links to SARS

Outside the cardiovascular system another noncatalytic function of ACE2 had previously been shown. In 2003 a new disease termed “severe acute respiratory syndrome (SARS)” caused by a novel coronavirus (SARS-CoV) spread quickly around the world, causing more than 800 deaths. ACE2 was identified as the receptor for SARS virus in vitro [77, 78] and also acts as receptor for the NL63 virus. Soon after, studies confirmed that ACE2 was essential for SARS infection in vivo using ACE2-knockout mice [79]. Concurrently it was discovered that ACE2 protects murine lungs from severe acute injury [80] and subsequently that SARS-CoV infections and the SARS spike protein itself downregulate ACE2 expression (Figure 3) [81].

https://www.hindawi.com/journals/ijhy/2012/307315/

As previously mentioned SARS virus downregulates cellular expression of ACE2 [102]. Binding of the SARS spike protein induced ADAM-17-dependent shedding of ACE2 N-terminal domain [103] (Figure 3). This shedding has been reported by different groups to be both essential for viral replication [104] and unnecessary [97]. The SARS virus undergoes clathrin-dependent endocytosis upon receptor binding; this process internalises both the SARS virus and its receptor further clearing ACE2 from the cell membrane (Figure 3) and hence allowing enhanced (and damaging) reactivity towards circulating Ang II. In contrast to ectodomain shedding, the cytoplasmic domain of ACE2 appears to play no role in the regulation of internalisation [105].

Abstract
Angiotensin converting enzyme 2 (ACE2) in the lung has been recognized as the key receptor of the 2019 novel coronavirus (2019-nCoV) as people may get infected through the respiratory tract. However, the clinical features of other systems have not been addressed yet. More than the respiratory system, ACE2 also extensively expressed in the vascular endothelial cells of the heart, kidney, liver, intestine, and testis, etc. In other words, the new coronavirus may probably intrude on any tissues or organs as long as the needed number of ACE2 is available. Therefore, once exposed to the coronavirus (e.g. through the blood or other body fluid), these organs may also get affected especially for those the receptor has the direct-acting control. This paper aims to analyze the possibility of the association between 2019-nCoV infection and the multiple organ failure (MOF) other than pneumonia.

https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3532272

Keywords: Angiotensin converting enzyme 2 (ACE2), 2019 novel coronavirus (2019-nCoV), blood-air barrier, multiple organ failure(MOF)

Suggested Citation:

Kiss the sky goodbye ...

LOL

I think i have put it into perspective. "Main Transmission" ATB

the issue with coughing seems at odds with the way the virus is spreading .. ie the cough is late stage and most would be in bed, which does not explain the explosive growth in transmission ..

so the best advice is Stay clear of crowds and no touchy ...

face mask is a waste of time, however wearing surgical cloves and regular disposal may be more beneficial between washing hands

Loz will be pickled in alcohol by now ...

safe

main transmission is hand to mouth ........

wash

ps.

Bleach mixed 10% with water will destroy DNA

cheap ...

How many people shake your throat ? stick fingers up your nose or poke you in the eye ........

simple solution

Use Rusty metal .. coat hands in the "Red Stuff" ... the iron content is so high the virus cannot survive

1. you will not lick your fingers ...
2. nobody will shake your hand

sorted

https://www.reuters.com/article/us-health-coronavirus-china-toll/wuhan-closes-makeshift-hospital-as-new-coronavirus-cases-in-china-drop-sharply-idUSKBN20P01K

one other point ..........

Remember there are four coronaviruses that already circulate in human beings. They cause the common cold and we don't have vaccines for any of them.

Viruses

Coronaviruses are a group of viruses known for causing the common cold. They have a halo or crown-like (corona) appearance when viewed under an electron microscope.
The common cold is a viral infection of the upper respiratory tract. The most commonly implicated virus is a rhinovirus (30–80%), a type of picornavirus with 99 known serotypes.[29][30] Other commonly implicated viruses include human coronavirus (˜ 15%),[31][32] influenza viruses (10–15%),[33] adenoviruses (5%),[33] human respiratory syncytial virus (orthopneumovirus), enteroviruses other than rhinoviruses, human parainfluenza viruses, and human metapneumovirus.[34] Frequently more than one virus is present.[35] In total over 200 viral types are associated with colds.[3]

following on .......... Immunobody and Avidity ....

In contrast to the physical parameters affinity and avidity, the functional avidity describes how well a T-cell responds to antigens. Though all of the three parameters correlate in most cases, that is, high-affinity T cells often have a high functional avidity, this does not need to be the case. There are several factors besides the antigen recognition ability of the TCR that can impact the T-cell response. In principle, T cells could express a high-affinity TCR, but due to other factors, for example, inhibitory molecules, it might show a very weak response to antigen stimulation. Thus, determining the functional avidity is not only often more practical, but is also the only one out of the three parameters that actually describes the functional outcome of the stimulation.

Notably, the level of TCR expression impacts the functional avidity. Even though T cells are functional when they express very little TCR, it has been shown that reduced expression levels go along with decreased ability to respond to antigen [54]. T cells with reduced TCR expression levels are impaired in their proliferative capacity and in their ability to secrete IL-2 and IFN-?

This also highlights just how much work needs to be done to "SELECT" the appropriate TCR to clone and to build into a lentivirus to infect a patients t cells to make an effective and potent response for patients that may need BioNtech moditope

as i have explained before , its very easy to "Rush" ..... example Inovio ... but just look how many programs big pharma signed up to that have failed with Inovio.

https://www.hindawi.com/journals/jir/2012/153863/

so this is what many investors don't see or don't understand ...

the Key to success against cancer is the word "potent"

SCIB1 has it proven ...

Lindy even understands it with the MAB's ...... they have to be High Avidity ... = Avidmab

so as i posted last year ...... Scancell is skilled in the art of Binding ...

zapping patients and effective .........

1/ electropolation and nano delivery create damage , this damage is equivalent to an adjuvant ... ie it stimulates the immune response to the vaccine by cytokines released to repair the damage.

2. by firing into different cells Ie Dendritic cells and muscle cells a dual mode of action is developed called Cross presentation .... ie The dendritic cells take up the DNA directly and the muscle cells release SCIB1 MABs that then lock onto the Dendritic cells that already have the antigen giving you this dual activation ...... this is then giving you a "High Avidity T cells" which is far more potent that a peptide vaccine which tends to give you low affinity which may be good enough against a virus but not good enough against cancer

This cross presentation overcomes the bodies natural instinct to produce low affinity which is less reactive to self
so you can see Immunobody is still state of the art even after 10 years

https://www.frontiersin.org/articles/10.3389/fimmu.2018.02874/full

that is why Scancell headlines "cross presentation" as a milestone

now in the recent links from crumbs you will see

adjuvant gave you a "strong response"

Immunobody gave you a "potent response"

Moditope is different, it is so immunogenic it drives a "differential" event .... ie creates a cytotoxic Cd4 . which can be differentiated again by the ISA Pharma adjuvant conjugate .... to generate CD4 Th1 pro inflammatory

hope that helps ... IMHO .. of course

Ruck

Not Yours

ATB

Inan,
If you didn’t mean both, which one were you referring to as “Good sensible post”
Just for the avoidance of doubt.

or perhaps he didn't ....

you still selling Bonds knowlesi ...

Good sensible post ....

another new word

Biolistics