Covid Vaccines Reducing Infections

[OmCheeto]

Sure. Worked. But, sadly, that won't have much prediction power regarding the future.

Those lines are converging back to the baseline there: some assessment will be needed to check if it's a general trend, or just the relevance of the available boosters gone as new strains emerged: whether we could get back that 'work' with updated boosters...

With the best available one here is 'up to date' () against Omicron only, what do you think about the efficiency I can expect?

How is Covid the same and different than the flu?
Are there different strains? Yes.
Are some strains worse than others? Yes
Are new strains expected to emerge? Yes

So in response to your comments and question, I would say it's not much different than the flu, other than it's a lot deadlier. Correct me if I'm wrong, but it sounds like you expect the Covid vaccines to work like the Polio or Small Pox vaccines, where they seem to provide decades long immunity. (This article in Scientific American seems to imply that we have no idea how long a Small Pox vaccine is good for.)

I would be interested to see what other similarities and dissimilarities there are between the various bugs and our vaccines to combat them. Does anyone know how long an H1N1 vaccine lasts for the average person?

 

[Rive]

How is Covid the same and different than the flu?

Compared to Covid, flu seems to work on a steady, slow, clockwork schedule, so we can casually pick a strain at spring to roll out a vaccine against it at autumn.

For Covid, we already know that the strain picked might be even extinct by the time the vaccine will be available and we can only hope for cross-immunity for its descendants to remain adequate/useful.
Though we also know, that one of the key points for a descendant strain to grow prevalent is to be able to at least partially bypass the immunity present in the population...

Correct me if I'm wrong, but it sounds like you expect

You are wrong. I do know for a long time that it won't be like that.

Also, what I expect is questions to be raised and answers sought instead of (false) confidence. See:

Regarding boosters, at this point I think we need to wait for some comprehensive studies adjusted for new strains versus multivalent boosters.

With the actual who-knows-how-many re- and re-reinfections and types of available vaccines adjusted for various strains it's just a big mess now.

 

[Laroxe]

I tend to agree that it is highly unlikely that recent vaccination will have no effect on transmission, but we need to revisit what we know about infectious diseases. The presence of antibodies in the blood is a considerable barrier to infection, the antibodies will bind to the virus, reducing the number of viable virus particles, while the immune system starts to ramp up production. The "little bundle of joy" that causes COVID-19, is of course an RNA virus and the reproduction of RNA viruses is inefficient to say the least, the virus compensates for this by a massive increase in its reproduction rate. This does mean that pre-existing antibodies can be quickly depleted as they bind to the new virus particles then if the number of viruses reach the level needed to cause symptoms occurs very rapidly, the immune system simply can't keep up. COVID-19 appears to have evolved in ways to ensure a very short incubation time, Omicron variants may become symptomatic within 1 or 2 days of infection.

As we appear to be almost totally dependent on pre-existing antibodies to prevent infection and the antibodies will be the ones that prevent cell entry, the first idea was to create a vaccine that would boost the antibodies to the ancestral strain and also promote antibodies to one of the newer variants. It was suggested that this would not only increase the range of the antibodies but would also boost the production of antibodies specific to the later strains, to a much higher level, the so-called bivalent vaccines. Initial studies did suggest that the levels achieved were much higher, but over time it became clear that this wasn't translating into significantly increased resistance to infection.
The latest idea is that the so-called "original antigenic sin" may mean that if a person is exposed to the original strain, as was used in the 1st vaccines, following a bivalent vaccine the immune system would preferentially produce antibodies to the original strain, effectively reducing the production of antibodies to the more recent strain. The new vaccine which should be available within a week or so is a monovalent vaccine targeting one of the Omicron variants. The hope is that this will stimulate much higher levels of more specific antibodies which should be more protective, the trouble is that this is "a hope", we will only know if this actually works after its introduction.
The approval of the monovalent vaccines has been based on the known safety profile of the mRNA vaccines, not evidence of its ability to induce the specific effects wanted. Of course, the effectiveness against severe disease should remain the same.

 

[pinball1970]

I got this alert today

https://medicalxpress.com/news/2023-09-moderna-reveals-highly-covid-vaccine.html

These plus points:

• Improved antigen expression: mRNA-1283 demonstrated improved antigen expression compared to the clinically available mRNA-1273, which encodes the full-length spike protein. This suggests that mRNA-1283 can produce higher levels of the target antigens.

• Enhanced antibody responses: When administered as a primary series, booster, or variant-specific booster, mRNA-1283 elicited similar or greater immune responses than the original mRNA-1273.
• Greater stability: mRNA-1283 showed greater stability at refrigerated temperatures (2° to 8°C). Specifically, mRNA-1283 reached 62% of its initial integrity at 12 months when stored at 2° to 8°C, while the original version reached 63% integrity after only six months under the same conditions, effectively doubling the shelf life.
• Dose-sparing: mRNA-1283 demonstrated the ability to elicit effective immunogenic responses even at lower doses, suggesting the possibility of dose-sparing, which could reduce potential reactogenicity.
• Protection against variants: mRNA-1283, including variant-specific versions, produced more significant neutralizing antibody (nAb) responses against variants such as B.1.351 and B.1.617.2 compared to mRNA-1273, indicating its effectiveness against emerging variants.

Abstract to a paper here. https://www.science.org/doi/10.1126/scitranslmed.adf4100

 

[morrobay]

As we appear to be almost totally dependent on pre-existing antibodies to prevent infection and the antibodies will be the ones that prevent cell entry,

Not quite: The ubiquitous first line defense by T cells that target non mutating viral proteins and up to 30 epitopes on virus most likely account for exposures by infected family members that do not result in seroconversion/antibodies. Or mild/asymptomatic infections , with antibodies. I am unvaccinated for SARS-CoV-2. However Im sure have been exposed many times especially in these crowded wet markets. https://www.science.org/doi/10.1126/science.abh1823

 

[pinball1970]

Already a lot of threads on Covid so I will put this here if that is ok.

This article in phys.org today describes a study based on (ACE2) protein acting as a decoy for the virus. https://medicalxpress.com/news/2023-11-long-acting-biologic-transmucosal-properties-sars-cov-.html

There is a link to the paper in the article.

From the discussion in terms of the need for new treatments in addition to the vaccines.

“The low effectiveness of COVID-19 vaccines in specific patient groups, such as immunocompromised patients, along with the emergence of SARS-CoV-2 variants capable of evading vaccine-induced immunity, underlines the need for novel treatment approaches.”

 

[Nik_2213]

Upside, caution, masking and vaccinations mean I've had neither Covid nor 'Flu during the pandemic.
Downside, this Autumn's UK Covid and Flu' boosters totally 'lit off' my immune system, gave me what felt like '3-day flu' then a week of severely streaming head-cold. (Generic anti-histamines mitigated the misery...)
I reckon I'd had enough residual immunity to the boosters' content to send my immune system on a rampage.

But, hey, a zillion times better than 'Blues & Twos', or being stuck 'Home Alone' with full-on fever and a clan of puzzled cats...

 

[Laroxe]

Not quite: The ubiquitous first line defense by T cells that target non mutating viral proteins and up to 30 epitopes on virus most likely account for exposures by infected family members that do not result in seroconversion/antibodies. Or mild/asymptomatic infections , with antibodies. I am unvaccinated for SARS-CoV-2. However Im sure have been exposed many times especially in these crowded wet markets. https://www.science.org/doi/10.1126/science.abh1823

You are of course right, our immune system targets a wide range of viral proteins which influence our responses to future exposures. Some of these viral proteins can indeed be shared with other virus's, particularly those closely related to the SARS-Cov2, and these include several coronaviruses that cause cold like symptoms. It's interesting that the huge research effort that COVID-19 stimulated even identified parts of the immune responses that had previously unrecognised, and we know that any recent viral infection can activate a general immune response that increases resistance. We have also become increasingly aware of the way in which different antibodies can interact and effect the functioning of others, in some cases adversely, as happens in what is called, the original antigenic sin. I will however stick with my statement, it was confirmed in early research that it was the antibodies that targeted the spike protein, used to gain cell entry, that had the most important effect on preventing disease progression. It was this finding that was used in the development of all the vaccines, if the virus can't gain entry to the cells, it can't reproduce and cause disease. While with Covid the initial viral load seems able to overwhelm this protection, it does seem that a wider range of antibodies with different targets increases protection, often acting during different stages of the infection.

I am aware of the way in which people try to use the raw data available to draw conclusions about prevention and disease severity / mortality, often comparing COVID-19 with influenza. I think that both of these infections are seasonal, respiratory infections, this means that the numbers of cases vary dramatically depending on the time of year and the presence of other seasonal virus's. Viruses appear to be rather well-mannered, they, for whatever reason, appear to take turns causing infections in the population. Being respiratory virus's it does make sense that masks will affect transmission, though Covid does appear to be far more transmissible, this means that the effectiveness is much more dependent on the type of mask and how it's worn. The raw data on the risk of serious disease or death is much more misleading, while it clearly shows that Covid presents a greater risk, flu like many other infections has its greatest effect on the very young and the very old. In the case of Covid, the very young appear to have some inherent resistance to the disease, so mortality for example is concentrated in the elderly, using the raw data from population studies significantly underestimates the risk to the elderly. I am aware of the very real issues that people have with mandated vaccination and personal autonomy, few people appear to address this issue in relation to health care staff who work with vulnerable populations. In the UK it is already the case that vaccination against specific diseases is required to work in a clinical setting, depending on risk, this includes having had the routine vaccines given in childhood, the Hep.B vaccination, Chickenpox, possibly BCG for TB is there is a risk of exposure and of course COVID-19.