Covid vaccine

“When experts optimistically say that they expect a Covid-19 vaccine by the end of 2020, they’re talking about an emergency use authorized vaccine, not a fully-approved one,” says Dr. Seema Yasmin, director of the Stanford Health Communication Initiative.

No one can say for sure when a Covid-19 vaccine might arrive, because vaccine development is broken into several stages, each with a highly variable timeline. “But here’s a comparison,” Yasmin says. “The fastest vaccine we previously developed was for mumps, and that took four years to develop. And typically it takes 10 to 15 years to develop a vaccine. So 12 to 18 months would be record-breaking.”

The first is the exploratory phase, in which drug companies tinker with different approaches. With Covid-19, for instance, some drugmakers are trying to develop a nucleotide-based vaccine, which uses the virus’s genetic code instead of its proteins. Typically, the exploratory phase could take two to four years, though new technologies are speeding up the progress. Also, this novel coronavirus is similar to the first SARS virus, so that may give researchers a head start.

Next comes the preclinical stage, in which a vaccine candidate is tested in cell cultures and animals to see if it triggers an immune response. “If there’s no immune response or the vaccine is causing harm to cells, then it’s back to square one, the exploratory stage,” says Yasmin. “The reality is there’s no way to speed up this stage, and it will probably take at least a year.”

But if all goes well, the candidate heads to clinical trials. The experimental vaccine is given to a small group of people, then a bigger group, then an even bigger group, typically in an outbreak area. This series of tests can take years to complete. Some bioethicists have recently proposed that the Covid-19 pandemic is so serious that so-called “challenge trials” should be considered to accelerate the process. In a challenge trial, researchers would intentionally infect the people they vaccinate in a controlled environment to see if the drug is effective. No such studies have been authorized yet.

The next stage is regulatory review, in which the manufacturer submits an application for a license to produce the vaccine. In the US, this typically takes 10 months and is authorized through the Food and Drug Administration, though it’s virtually a given that regulators will speed up the approval of a Covid-19 vaccine.

So who is this person who knows what they are talking about because, with no offence intended, it's not you?

Everything you've posted shows little knowledge of vaccine development

or an understanding of Covid-19, a disease by the way, that even the experts don't fully understand so your comment about mortality rate is moot

It was originally assumed that only those who had previously been infected by the virus and developed an antibody response had any immunity, hence the initial focus on testing for the presence of these antibodies as well as infection. However, studies of antibodies in formerly infected patients demonstrated accuracy issues which subsequently could be explained instead by the antibodies’ rapid decay in recovering patients.The often disappointingly low levels of antibodies in population samples is often used as evidence that herd immunity is not a realistic goal without a vaccine. This is not correct.

At the end of May there was a significant breakthrough in understanding of COVID antibodies which was not widely reported: a Swiss study from Zurich led by Professor Onur Boyman demonstrated that a large proportion of the population had a natural immunity through existing antibodies on the mucous membrane (IgA) or cellular immunity (T cells), likely to have been acquired through previous exposure to coronaviruses such as influenza or the common cold (the absence of exposure to previous coronavirus is now thought to explain the opposite effect in 1918).

The study found that that the presence of (IgG and IgM) antibodies generated on infection which tests had previously focused on, were NOT in fact required to defeat the virus and that existing (IgA and T cell) antibodies that gave a natural immunity. Moreover, the population with this natural immunity was demonstrated to be five times greater than those with the IgG and IgM antibodies on which tests had hitherto focused. If this could be substantiated, then the population already exposed to COVID would also be five times greater than previously assumed. In other words, if a population sample showed 10% had IgG and IgM antibodies (which might be subject to decay) then it was likely that at least half of the population had already been exposed to COVID.
It followed that antibody studies that measured only IgG and IgM that were now predicting population-based mortality risk of 0.1% to 0.5% (lower than the 1% in the elderly population aboard the Diamond Princess) could be even further reduced by a factor of five to 0.02% to 0.1% and the level of symptomatic exposure from 20% to below 5% (consistent with the flu season ironically predicted by Fauci in March). Not only would this mean a further similar reduction in the estimated true mortality rate but it meant that there were far fewer people in the population who had never had exposure to the virus, so a far lower number who could potentially catch the virus in the future. In short, the infamous herd immunity was much closer than previously realised.

This explained why, by July, the virus had all but disappeared in populations like Sweden, New York and Wuhan (which reportedly tested its entire population of 11 million and found only 300 cases, all of which were asymptomatic) which were significantly affected by a “first wave”: if the ratio of those with IgA and T cell antibodies to IgG and IgM antibodies across population was confirmed at a factor of five then if 20% of the population had traditional IgG and IgM antibodies (such as New York with 21% and London with 17%) then the virus died out because there was simply no one left for it to infect. It followed that the virus could only survive in population samples where testing showed the presence of IgG and IgM antibodies was below 20% (and allowing for their decay probably well below).

We should also expect the mortality rate to reduce further as hospital treatment has evolved. We now know that invasive use of ventilators in fact caused COVID deaths which was particularly unfortunate given the initial scandalous news reports on their initial shortage and in the US questionable financial incentives for nursing staff to use ventilators. Doctors have also realised that the specific cause of death in many cases is pulmonary embolism, which can be treated though cheap and well-established blood-thinning medication. Several studies have also shown early intervention with the use of zinc and malaria drug hydroxychloroquine in combination has an immediate significantly reduced hospitalisation rate, of up to 80% and mortality by 50%. There is a great irony that the mortality rate could be reduced to almost zero by proven inexpensive drug combination, though this is not necessarily in the interests of the pharmaceutical industry which would prefer there to be a need for costly new drugs and vaccines.

Yet inexplicably we still hear the daily groupthink catechism that the only “long-term solution” to beating COVID is a vaccine, often without any understanding of the historic limitations of vaccines particularly in the immunisation against coronaviruses (there is still no vaccine against the common cold and vaccines against influenza are patchy in their effectiveness).

A significant obstacle to a successful vaccine is the rapid degradation of IgG and IgM COVID antibodies meaning that even a successful vaccine might not give any benefit for longer than a few weeks. As the CEO of world leading testing company Roche Diagnostics recently commented: “What appears to happen is that people do lose antibodies over time. And that of course poses the question, will vaccines actually work if you lose antibodies”.

Reports of successful antibody responses amongst healthy adults in vaccine trials should be viewed with more scepticism. It is also almost certain that any antibody response would be more difficult in population samples with impaired immune systems that are most at risk from COVID. Even an efficacious vaccine might have to be ramped in dosage that would be intolerable to those most likely to benefit from vaccination. Leading Swiss epidemiologist Pietro Vernazza has demonstrated that the high-risk group is least likely to respond to the vaccine since their immune system is already impaired. Whilst it is possible for vaccine trials to demonstrate antibody responses, whether these will have any practical lasting benefits in reducing COVID mortality risk which are tolerable for the population group most at risk from COVID is unlikely.

Vaccines hastily developed, rushed to market without proper trials by panicked governments ready to throw money at any promising trial candidate, creates a clear moral hazard for pharmaceutical companies and a public healthcare risk which might rival the virus itself. We remain sceptical of biotech companies raising equity on tricked up trials, only never to deliver medication that has any practical application or insiders dumping stock after supposedly promising “game changing” data, or even worse mandatory vaccination of a population on the basis of an erroneous assumption that herd immunity hasn’t already been reached, with the potential for dangerous and unnecessary side-effects in population groups who would otherwise (if they had not already been exposed to COVID) have been asymptomatic.