Member Info for inanaco

well spotted chap .. really does mess with the immune system ..this Virus can fight back ..

https://www.nanocotechnologies.com/products-applications/vivodots-tm-nanoparticles/

take a look at nano ..

face facts you have about 90% of journalists siding with 15% of the population in regards to the EU .. of which this woman https://twitter.com/carolecadwalla/status/1265068870089551872 behaved like a demon ...

chief in all this was the Guardian and the Mirror ...........

whats interesting the Mirror story on Scancell was OTT ....

atb

Brexit: The Uncivil War ......

Crumbs he mentions a report coming out on the 15th ......... can we find that .. i have been looking .. but nothing coming up

yes the Fox missed a family funeral .. because he followed the law .. even the BBC this morning accepted he followed the law .. but apparently not the spirit ... what does that mean ?
How is all this political ........... ? apart from the London bubble i don't think any really cares

only the press are allowed to break the 2 meter rule ......... they all had a great weekend Fox Hunting outside the Den .... but the Fox out smarted them ... leaving 4 or 5 reporters asking the same question expecting a different answer .... stupidity

not the antigen .............

In conclusion, our data demonstrate that unlike other poxviral vectors rFPV is able to induce favorable antigen -specific CD8+ T cell immunity by modulating the lung derived DCs. Similarly, priming vaccination cell milieu plays a critical role in determining the """"efficacy/avidity of a vaccine.""" Specifically our current findings indicate that (i) i.n delivery of FPV-HIV-IL-13Ra2 and/or IL-4Ra antagonist adjuvanted vaccines recruit elevated percentages of CD11b+ CD103- cDCs to the vaccination site suggesting that the STAT6 pathway and /or IL-13 signaling via the IL-13Ra2 membrane-bound receptor most likely play an important role in the DC recruitment to the vaccination site, (ii) i.n. delivery of rMVA and rVV enhances CD11b- CD103+ DCs compared to rFPV delivery and (iii) this CD11b- CD103+ DCs plays a critical role in dampening the HIV-specific CD8+ T cell avidity. Collectively, the findings highlight the importance of understanding the fundamental mechanisms by which inherent properties of different vaccine vectors and adjuvants modulate antigen-specific immunity at the vaccination site prior to clinical evaluation of these vector-based vaccines.

they even put """"efficacy/avidity of a vaccine.""" together ...

""" Vaccine vectors and priming cell milieu determines the recruitment of DCs and avidity of CD8+ T cells.""""

https://www.sciencedirect.com/science/article/pii/S0042682214004152

So if you start with a platform that delivers "high Avidity" = immunobody

you don't spend years trying to doing work rounds ....

intrigued ........ already mentioned that ...

inanaco

Posted in: SCLP

Posts: 31,264

Price: 6.45

No Opinion

last explanation for now anyway20 May 2020 21:26
this current crop of vaccines target B cell memory ... because the spike protein is only on the virus .. a T cell is blind to the virus ... because its searching for cells infected with the virus , exactly the same as cancer a protein on a cell will identify itself to the immune system "i am in trouble"

so to knock out the virus you neutralize it , but that does not stop an infected cell shedding 1000's ... which have to be neutralized

so that is the job of t cells and NKT cells they will clear infected self cells ... and destroy them

the virus cannot hide unless it can mask itself ... but it can do that as well .........

when a virus cause chronic infection ....... our good friend interferon ............ becomes a problem

https://www.sciencedaily.com/releases/2013/04/130411142815.htm

"And get" .............

not may get

further ahead ?

Definite research of the research

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC387705/

Yes I know this group. We target by a different route and get high avidity T cells. We are incorporating both the receptor biding domain of the spike protein as this is the only antigen that stimulates neutralising mabs and the N protein for additional T cell responses.
lind

so they are running it in Brazil

at least the oxford is being discussed on Marr

SARS was not as contagious like Covid ...

follow the outbreaks ie ... switch to Brazil

Vaccitech’s Chimpanzee Adenovirus Oxford 1 vector (PRIME) encoding the oncofetal antigen 5T4 (ChAdOx.5T4), followed by a Modified Vaccinia Ankara vector

they have to change the vector

i know bermuda ... but then you can only give the vaccine once ...

the important bit ........

baseline of efficacy ......... nobody knows

Currently, correlates of protection for a vaccine against COVID-19 are unknown, and the roles of the specific antibodies or T cells in building effective protection are not yet defined. Therefore, we are unable to predict the protection of the Ad5 vectored COVID-19 vaccine on the basis of the vaccine-elicited immune responses in this study.

However, previous studies investigating SARS and Middle East respiratory syndrome (MERS) found that the increases in specific antibodies were temporary, and declined quickly in patients after recovery, whereas the specific CD4+ and CD8+ T-cell responses played an essential role in immunity.

The researchers started screening healthy volunteers (aged 18-55) in March for their upcoming ChAdOx1 nCoV-19 vaccine trial in the Thames Valley Region. The vaccine is based on an adenovirus vaccine vector and the SARS-CoV-2 spike protein, and has been produced in Oxford.

a Good vaccine should get you 6 years ......

ELISPOT data of the 16 SARS individuals after in vitro expansion of the PBMC. The data showed that 9 of the 16 SARS individuals displayed high frequencies of SFU against the NP protein, the 3a protein, or both proteins. Three individuals had a single response, and others showed multiple responses. These results showed that SARS-specific memory T cells are present in SARS-recovered individuals 6 years after infection, even though the frequency of these cells is low. Interestingly, in contrast to our study, T cell responses can be observed directly in the ex vivo ELISPOT assay conducted in a study by Li et al. (11) in which PBMC were obtained from patients 1 year postinfection. Such comparison suggests that the frequency of SARS-specific memory T cells progressively declines with time. This hypothesis is also supported by another study that monitored immune response in SARS individuals over a 2-year period and showed that CTL responses decline over time at 3, 6, and 18 months postinfection