Coronavirus entry point[edit]
As a transmembrane protein, ACE2 serves as the main entry point into cells for some coronaviruses, including HCoV-NL63,[5] SARS-CoV (the virus that causes SARS),[23][24][25] and SARS-CoV-2[26] (the virus that causes COVID-19).[27][28][29] More specifically, the binding of the spike S1 protein of SARS-CoV and SARS-CoV2 to the enzymatic domain of ACE2 on the surface of cells results in endocytosis and translocation of both the virus and the enzyme into endosomes located within cells.[30][31] This entry process also requires priming of the S protein by the host serine protease TMPRSS2, the inhibition of which is under current investigation as a potential therapeutic.[32]
This has led some to hypothesize that decreasing the levels of ACE2, in cells, might help in fighting the infection. On the other hand, ACE2 has been shown to have a protective effect against virus-induced lung injury by increasing the production of the vasodilator angiotensin 1–7.[33] Furthermore, according to studies conducted on mice, the interaction of the spike protein of the coronavirus with ACE2 induces a drop in the levels of ACE2 in cells through internalization and degradation of the protein and hence may contribute to lung damage.[33][34]
https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2
By replying threads other more often sometimes.How there is no activity on forum since many days?
Key Proteins and Their Roles in Viral Infection
Identification of targets is important for identifying drugs with high target specificity and/or uncovering existing drugs that could be repurposed to treat SARS-CoV-2 infection. Table2 lists potential targets, their roles in viral infection, and representative existing drugs or drug candidates that reportedly act on the corresponding targets in similar viruses and thus are to be assessed for their effects on SARS-CoV-2 infection...
Conceivably, the interaction of viral S protein with its receptor ACE2 on host cells, and subsequent viral endocytosis into the cells, may also be a viable drug target. For example, the broad-spectrum antiviral drug Arbidol, which functions as a virus-host cell fusion inhibitor to prevent viral entry into host cells against influenza virus,(20) has entered into a clinical trial for treatment of SARS-CoV-2.(21,22) The protease TMPRSS2 produced by the host cells plays an important role in proteolytic processing of S protein priming to the receptor ACE2 binding in human cells.(11) It has been shown that camostat mesylate, a clinically approved TMPRSS2 inhibitor, was able to block SARS-CoV-2 entry to human cells, indicating its potential as a drug for COVID-19
https://pubs.acs.org/doi/10.1021/acscentsci.0c00272
Some new body areas defined.
Best wishes.
immunological memory
growing reports of the virus being detected in CSF
that sure would take a nasty turn for pregnant people(& children at the potential long term growth mutations & defects)
anyone potentially
despite the 'best wishes' of many
it appears the immune response to produce anti bodies "appears" to stop at around 3 months
"if" this is true
then best wish is about all you can have
defining the difference between immune systems in people that do not contract a virus
equally to those whom contract it but appear some what a-symptomatic
is not a clear water and oil situation to define.
the immune system is over activated by covid 19 and goes on full throttle until it kills the host
soo
you mean memory to memories an immune response to not produce an allergic response ?
if you see my point
there is no public media i have seen so far that comes from "actual Doctors" that says they have found out why some peoples immune system triggers to over load(the effective fatal part of covid to the majority not counting co-morbidity)
Why, at first, host body cells allow this virus to infect them?
Corona-viruses have three main activities: to deliver genetic instructions in the form of RNA across the membrane of uninfected human cells, to allow newly-made RNA to escape from an infected cell, and to protect the RNA during its journey to discover new, uninfected cells. The RNA of the new coronavirus SARS-CoV-2 is contained within an envelope – an outer fatty membrane. Three viral proteins, called spike, membrane, and envelope are embedded in this outer membrane, and give the virus its distinctive shape and structure. Inside the virus particle the RNA is tightly coiled and coated by a fourth, nucleocapsid protein.
Does this virus present friendly entity to cells or do fatty envelop or protein cuspid of this virus
is somewhat like a nutrient for host cells who therefore allow or welcome it?
Okay, look at these;you appear to be using a text translator to read & write with
this changes the meaning of some technical words and makes discussion more difficult
https://coronavirusexplained.ukri.org/en/article/cad0010/
translation of words that mean
attach to
comes from
changes from
changes to
can be lost in text translators
when technical words are added and common language is used inside that
you easily get 3 layers of wrong/bad text
this makes discussion very difficult
this information is freely and widely available on the internet
you appear to be attempting to discuss things that are news web site head lines
and then argue if they are scientifically correct
that is called
Gossip
Urban myths
miss information
conspiracy theories
These links seem to be advertising puffery, for the makers of a supercomputer, which tell us nothing about the virus.Okay, look at these;
https://insidehpc.com/2020/06/front...ecular-sugar-coating-for-spreading-infection/
[17/07, 5:31 am] A virus uses camouflage to trick the cell. Its capsid or receptor proteins look like nutrients the cell needs. When the virus receptor binds to the cell receptor, the cell thinks the virus is a nutrient, and pulls it in. Now the cell is infected!
https://askabiologist.asu.edu/virus#:~:text=A virus uses camouflage to,Now the cell is infected!
[17/07, 6:17 am] https://insidehpc.com/2020/06/front...ecular-sugar-coating-for-spreading-infection/
Instead on trying to control the behavior of viruses which readily mutate anyway, why not trick the cell to NOT allow the virus to bind to the cell?A virus uses camouflage to trick the cell. Its capsid or receptor proteins look like nutrients the cell needs. When the virus receptor binds to the cell receptor, the cell thinks the virus is a nutrient, and pulls it in. Now the cell is infected!
Please refer my previous posts for it.Instead on trying to control the behavior of viruses which readily mutate anyway, why not trick the cell to NOT allow the virus to bind to the cell?
The virus triggers cell division via the mitotic mechanism. The mitotic mechanism makes a copy of the original cell including the virus. If we destroy the cells mitotic (MTOC) centers, the cell cannot divide and dies, killing the virus in the process.
An option might be to make the cell "deaf" to the virus' attemps to bind and the virus will just die without doing any harm.
Any knowledgeable comments?