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Influenza is not regular virus, so some new vaccines technology may be needed to be universal-effective?
Yes, INO is doing it as well.
Influenza is (now) not as hot as COVID,...can change in few months.
London-based company PepTcell, universal flu vaccine from P2b:
https://www.clinicaltrials.gov/ct2/show/NCT02962908?term=FLU-v&draw=2&rank=2
https://www.niaid.nih.gov/news-events/promising-results-trial-universal-flu-vaccine-candidate
I am not sure that it is price which will dictate useg of the vaccines. It is effectiveness. I would pay $100 and more, just to have some relief.
Awards are uncontrolled, more like social help that GOV is doing right thing.
IMO, IF challenge study generate +80% infection rate, effective vaccine should reduce that to <25%. Which is 70% relative benefit rate improvement.
50% (and probably it may come that 40%) improvement looks a loot, but actually it is not.
If Eylea can make 3 inj/Y (every 4 months, 16w) PDS is dead.
16 w is feasible, based on current data.
Disclosure: I am in BVXV big time!
For now, allocation (by US) is about $10B (initially, first vaccination round), which is LESS than 0.1% of the economic impact (projected).
My concern is that GOV *focus* is OFF!
For instance...Novavax deal?
GOV need to SUPPORT (with $$$$) scientific efforts toward solutions, multiple approaches. And, so far they are short on it, IMO.
COVID & FLU
In coming winter *season* (viral infections), FLU is due to some improvement (amplified) strength. My prediction is that good flu vaccine may be as important (if not more important) that COVID vaccines (where we will have multiple nAbs to help control pandemic severity).
So, comps that are working on improved *UNIVERSAL* flu vaccines may benefit next year.
Any idea?
I was under the impression that Governments around the world are only buying an option to get first choice
The companies currently expect to manufacture globally up to 100 million doses by the end of 2020 and potentially more than 1.3 billion doses by the end of 2021, subject to final dose selection from their clinical trial.
Taken all together (and not expecting miracle from J&J and Sanofi, as well as Merck), and what is presented so far.....there may be much room for some smaller player (with additional new technologies) that may make bigger difference and impact on vaccines effectiveness.
World needs something that will work for this sucker, CoV2!
I am not putting two compm against each other, comparing two platform that will shape future of the CoV2. Two technology platform:
mRNA.... unproven but sound, and
Adenovirus vector...MERS and SARS demonstrate limited ability.
However, a boost in cellular responses was not
observed following the second ChAdOx1 nCoV-19 dose.
This is consistent with previous findings on viral vectored
vaccines given as part of a homologous prime-boost
regimen.12
It seems to me that they should be testing the 30,000 for the presence of virus rather than only looking for symptoms.
I think most of the warp-speed money has gone to RNA and DNA vaccine candidates.
I am not putting two compm against each other, comparing two platform that will shape future of the CoV2. Two technology platform:
mRNA.... unproven but sound, and
Adenovirus vector...MERS and SARS demonstrate limited ability.
It may be that (each) vaccine works/efficacy is limited....society may need bit more than simple 50% benefit.
Also, as we put *pressure* on virus, it will mutate-evolve.
The society, to return close to normal, need reassurance that vaccine is there to change spread. And help those at high risk.
Ebola was/is *blood* virus, the pharma find the way to treat/deal with it. The same we need for CoV2!
mRNA v Oxford (Ad)
Some compare today Oxford CoV2 vaccine to MERS-one (in rhesus macaques, as failed), and to current CoV2 animal data:
https://pubmed.ncbi.nlm.nih.gov/28579232/ (mice)
https://pubmed.ncbi.nlm.nih.gov/29739720/ (mice)
https://pubmed.ncbi.nlm.nih.gov/32577525/
And, new article on T-cells response in CoV2 infected:
https://science.sciencemag.org/content/early/2020/07/15/science.abc8511
So, it is way too complex to extrapolate animal data to predict effectiveness of the particular vaccine, as well as any early P1 healthy volunteer data (elder population may be more helpful) from nAbs & T-cells response.
Monday Oxford data may just be another point of conflict?
My another thought about sizable side-effects of mRNA vaccines: it appears to me that mRNA vaccinated patients will have severe adverse reactions after being exposed to the virus.
Any comments?
Thanks Doc.
I may need some time (learning, actually I am too old to start learning molecular biology, but I may try...) to digest what you wrote.
My idea was to understand why Oxford vaccines (whole spike, with adjuvant, viral vector) would generate stronger cellular response than mRNA based vaccines? Also, which may be better, modified S1 (MRNA) or S-RBD (PFE)? I do not easily buy simple PR from each company, as well *selective* publication material that may mislead true story.
Anyway, wish that all vaccine candidate works, and that World may come out (quickly) of today misery.
Doc,
A key is T cell help. Some of the activated T cells that can help induce B cells to make IgG will become memory T cells.
The occurrence of measurable SARS-CoV-2 infection is one of the secondary endpoints.
Another puzzle for me, primary:
<Number of Participants with a First Occurrence of COVID-19 Starting 14 Days after Second Dose of mRNA-1273>
So, they will continuously (Q2W) do RT-PCR test on all subjects to confirm infections, or first symptoms???
MRNA phase-3—>interim looks @56, 106 events—final analysis @151 events, according to a Needham analyst.
Nothing in the NEJM article is a deal-breaker, and that’s all the market needed to be contented—for now.
Does AB vaccine need to elicit a T-cell response for it to be effective? If so, has there been exceptions in the past? TIA.
Mandatory N95 + face shield in US for a few months will be far superior solution than any vaccine.
Indeed, no logical explanation to that enrolment criteria (actually excluded criteria).
NIH/MRNA are politically pressured to move fast forward, generating environment where vaccine candidate may have reduced chances. PFE/BNTX may have better chance for effective vaccine. And Oxford is also pressured by UK GOV.
<CONCLUSIONS
The mRNA-1273 vaccine induced anti–SARS-CoV-2 immune responses [very questionable statement] in all participants,,...>
Because *standard* convalescent plasma have very limited positive effects on severity of the infections, 2-5X nAbs level may not be sufficient to *treat*...but who knows for *prevention*?
Unfortunately +CD4 and +CD8 (more pronounced) T-cells level was low and generate serious doubt that vaccine will be broad effective (older population will have worse results).
Mr. Market got results wrong, and Fauci should not comment as he did (covering his ASS, as usual)...very promising results...???!!!
Trial very complex, as third component CDX-1401 effect may be masked,...regardless that as vaccines can enhance immune response of CK-inhibitors. Atezo may not be the best choice.
True.
< Researchers found that two factors—a specific pattern of gene mutations in the tumor cells, and evidence of a vigorous immune response to the cancer—are markers of whether patients will respond to the combination. >
https://www.ascopost.com/news/march-2020/predicting-which-patients-with-ovarian-cancer-may-respond-to-combination-parp-and-pd-1-inhibition/
Is there any advantage of the Fc-nanobody relative to regular nAb? So far show lower affinity/binding strain toward RBD!
This is disappointment, because both target should be complementary/synergistic in ovarian cancer.
Yup, everyone see viruses everywhere...give me a brake!
RE:REGN-CoV2
Failure of the convalescent plasma
https://www.medrxiv.org/content/10.1101/2020.07.01.20139857v1
to make any impact on advance COVID infections leave me with vorry what can specific nAbs ( I would guess at much higher titer level than in recovered subjects) can do for infected population?
For prevention...it may have real chance (if dosed at higher level)!
Can anyone *swallow* significant histological improvements after 16w regardless how big is fat reduction?
Steatosis/fibrosis does not develop overnight!
Oh yes, put older (>65) in *concentration camps*, and let younger enjoy good life!
I am bit sceptical that nucleoside analogue will be able to demonstrate needed level of efficacy in halting viral replications! As science is moving toward more specific inhibitor viral escape will develop as well!
RE: MRNA
It is bit early/premature to declare 100 µg dose (2X) safe based on +50 subjects (from single dose). They do not have choice...Needs overpowered any safety concern!
China data is of no use to anyone!
Regards the modeling, I will left that to *statistic* expert! I am just applying common sense (if applicable).
<COVID-19 who never develop symptoms are not a major source of infection spread,>
Only IF their viral titer is LOW at all time. And for that we do not have real data???
Very impressive results for Ozempic!
It has nothing to do with *warp speed*, it is ASSHOL (CBO) that fauck-up *perspective*!
https://secfilings.nasdaq.com/filingFrameset.asp?FilingID=14196283&RcvdDate=6/2/2020&CoName=VIR%20BIOTECHNOLOGY%2C%20INC.&FormType=4&View=html
Disclosure: At this tine I am looking for exit-point!