...For technical reasons, you could actually argue the traditional vaccines pose more of a threat for individuals due to the possibility of preexisting immune responses to the host vector.
...
Echoing thanks to the scientists willing to help understand what's up with vaccines.
Are you speaking here of ADE? I've been reading up on this a bit, but the biology and scientific terms I'd have to learn to understand what I'm reading are significant! Does mRNA method decrease chances of this? I had read that it was less likely because of this particular virus using ACE2 receptors rather than Fc?
This is the one with too much science for me to follow well:
https://www.nature.com/articles/s41564-020-00789-5
This was better (for me to understand more):
https://www.the-scientist.com/news-opinion/covid-19-vaccine-researchers-mindful-of-immune-enhancement-67576
Some good laymen's overview articles in The Atlantic recently:
https://www.theatlantic.com/health/archive/2020/11/vaccines-end-covid-19-pandemic-sight/617141/
Background on complexity of immune system:
https://www.theatlantic.com/health/archive/2020/08/covid-19-immunity-is-the-pandemics-central-mystery/614956/
I'm a lowly retired neurobiologist, so take everything I say about immunology with a small grain of salt.
ADE refers to antibody-dependent enhancement, which basically means that the antibodies being produced make the situation worse instead of better. This generally happens in one of two ways:
(1) A vaccine can over-juice the immune system's response. Stimulating the immune system is good... to a point. A severe allergic reaction is a very bad thing, as is a situation where the immune system gets confused and starts attacking the wrong thing (Type 1 diabetes, or Multiple Sclerosis come to mind, although here they're talking about acute responses. I think "cytokine storm" is the cook-kids term in the press).
(2) Alternatively (or at the same time, if your luck is really horrible), the antibodies produced by vaccination can actually enhance the infectivity of the target virus. This sounds paradoxical, but I'll try and explain it simply: at the microscopic level, binding between proteins isn't all that different from clicking together legos - complimentary pieces tend to fit together nicely. It's a bit more complicated than this, but work with me. Sometimes the fit between a virus's docking protein and a host's surface receptor isn't perfect, and binding only occurs 50% of the time. But now there's an antibody that comes along that sticks to the side of the viral docking protein. Not enough to block its function or in a way that the body can recognize or destroy the virus, but enough to squeeze the docking protein into a shape that fits into the cell's receptor a little better, so that the infection rate goes from 50% to 80%. Bam, your close-but-not-quite antibody cure made the virus worse.
That said, these aren't big concerns for me, as safety data would have ferreted these issues out. My main concern about non-mRNA vaccines is an existing immune response. Conventional vaccines show some form of virus to the immune system. But remember that the immune system "remembers" what it sees, and this includes viruses. It's an issue in gene therapy, for example; if you receive virus X to treat disease Y, your body will remember virus X and attack the next time it sees it. For vaccines, it means it's very important to use a virus that's vaccine friendly (i.e., makes for good antibody response) and also unlikely to trigger repeat-administration immune reactions in people who have already been exposed. This is the reason Janssen is using Adenovirus 26, which is a crazy obscure virus that few people have ever been exposed to... we think.
While I'm typing, I'll add this:
Comparing any part of the coronavirus to influenza (either viral biology or vaccine development) usually isn't a good idea unless you know a great deal about both viruses and know what you're talking about. There are massive differences in the virus's genetic materials, their target cell populations, their reservoirs (the animal species they live in before jumping into people). But the most common misunderstanding these days is (not) understanding how vaccine development differs for the influenza and coronavirus.
Vaccines are developed, not against the entire virus, but rather against specific proteins. Usually, these are the proteins that sit on the outside of the virus particles, which allow the virus to stick to and enter specific host cells. Influenzavirus infects cells using a combination of two proteins that have been modified with various sugars, which are referred to as glycoproteins. These two glycoproteins are called hemagglutinin and neuraminidase. There are many different variants of each of these, and influenzas are generally categorized by the combination of hemagglutinin/neuraminidase the strain has. You may have heard of H1N1 flu, and now you know where that comes from.
Point is, every year influenza retreats into cormorants and recombines into a new form that infects slightly differently. People who make the flu virus make educated guesses about what H(X)N(X) versions are likely to be this year and make a vaccine targeted at those proteins. It's essentially a yearly game of bop-a-mole.
Depressed? Well, here's the good news: Coronaviruses are much simpler. The protein used to dock the virus is called a spike protein, and it's very, very conserved (meaning it tends to stay the same over time). No seasonal change problem, no moving target. It also reduces/avoids some of the ADE problems mentioned above.
The methods of making the vaccines are also very different, but you get the idea. Point is, the comparison is apples to oranges unless you really know your stuff.
For those interested, I've posted off an on about Covid and vaccine development stuff on my blog, including my experiences participating in the Moderna trial as a volunteer.
Lastly:
I think we'll look back on this period of history as one of our greatest human triumphs. I only wish we applied half this amount of effort to curing other infectious diseases. I have a degree in microbiology and used to work in biotech. However, I left the industry early in my career because I couldn't handle how it focuses only on the money, almost never on the public good. If the industry applied it's considerable resources towards curing malaria or HIV or any of the other awful diseases that affect poor people around the world I'd be happy to work for free. However, what do we get? Fucking Viagra. Only when rich people are in danger do we make these big leaps forward.
The drug that became Viagra was serendipitously discovered. Originally, it was a vasodilator intended to alleviate chest pain by relaxing blood vessels around the heart. Long story short, it didn't work and the trial failed, but when the investigators started asking their heart patients - many of whom were older men - to return their unused pills, they discovered that many of them were reticent to do so. Someone asked why, and they discovered that the drug did relax certain blood vessels, just not the ones they'd originally intended. A happy accident.
