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UK-CIC1422 karma

Hello, I can understand the concerns but be rest assured that none of the vaccines were rushed and safety was never compromised.

In fact in this study published in 2018 they very clearly talk about the mRNA technology and some studies where it had been used in and plans for future studies https://www.nature.com/articles/nrd.2017.243 . The reason we saw it used for COVID-19 first is because everything else stopped because of the pandemic. There are currently plans to use the technology for Flu and HIV vaccine clinical trials. The adenovirus vectored vaccines have been in development of several years for Flu, MERS, EBOLA, Malaria and has we had a chance to optimised it from what we learnt in those trials. I worked on one of such studies in 2016.

The success of the covid-19 vaccines is a true testament to the hard work of lots of researchers who have been working through the years on this from Barney Graham, Jason Maclellan, Katalin Kariko, Drew Weissmann, Sarah Gilbert and Tess Lambe to all other scientists all over the world. not only have we been working for years on these technologies, but we also dropped everything else and all hands focused on getting COVID-19 vaccines out. Labs were running 24 hours a day and 7 days a week for months. This all facilitated the world.

Finally, because of the large scale devastation the pandemic was causing, we had an injection of funds like no other from the government and funding organisations. we had great collaboration between the government, industry partners, funding bodies and academics. and we were allowed to run our clinical trials in parallel to each other rather than sequentially. The regulators also worked tirelessly to remove red tapes to get the vaccine to the world

Your friend can be rest assured that in all this, safety and having an efficient vaccine was our top priority. We did not compromise on this


UK-CIC294 karma

Very interesting question Ms-Piggy. There are a few studies that have looked at how long our immune response to COVID-19 lasts. I would like to answer your question in 2 parts

Natural infection - One study looked at people who were naturally infected with COVID-19 and found that they could still find immune cells that can fight COVID-19 8 months after infection. This would suggest that we are protected at least up to 8 months after infection. Other studies are following these recovered COVID-19 patients for a much longer time and we expect the results from these studies soon.

Vaccine responses - The clinical trials for the vaccines release interim data which showed efficacy of the vaccines within a time period. There are plans to follow these volunteers on for a while to answer the questions you have raised regarding how durable the immune response is. In the real-world setting with vaccination, we only started vaccination in December 2020 and so its too soon to tell, however we expect that vaccine induced responses should last for as long, if not longer than those from natural infection.

Regarding re-infection - This is hard to say at the moment and would depend on how well a person mounts an immune response after infection or vaccination, the ability of the antibodies to disarm (neutralise) the new variant and how long our immune responses after infection or vaccination lasts. The easiest way we can prevent re-infections is by stopping transmission and thus preventing viral mutation. The most certain way to do that at the moment is by getting vaccinated


UK-CIC259 karma

Hi Knute, this is a great questions so all 3 researchers are going to have a go I think.

For me the biggest unknown is what is the immune correlate of protection against SARS-CoV-2 infection. What we mean by correlate of protection is the one (or several) parameters we can measure to say 'yes that person has an immune response which is highly likely to stop them from getting infected and getting ill even if they were exposed to sars-cov-2'. For instance, for hepatitis B, my other area of interest, when you're vaccinated we can measure the antibodies in your blood and say yes this person is likely to be protected. We don't yet know what that is for SARS-CoV-2. So we know vaccinated people are less likely to get infected and we can measure their antibodies and other immune parameters but we can't put a number on what is enough yet. So we can't identify who is still vunerable etc, who needs a boost vaccine, we can't optimise vaccines as easily. It could tell us also how long vaccine protection last etc. It is often the immune system as a whole that helps protect but sometimes its possible to identify a correlate of protection and thats what we need now I think. - Leo

UK-CIC183 karma

Hey Knute5,

We thought it would be fun for each of us to answer and see how (dis)similar our answers are!

For me there are two big questions:

1) Will the virus evolve to evade the vaccines? - Unfortunately only time will give us the answer to that one.

2) What causes some people to have life-threatening disease and others to have asymptomatic infection? Can we suppress severe disease? - Some big strides have already been made in preventing fatal disease, and case-fatalities have fallen quite a bit as we learn which drugs work. However, I think we'll see our understanding of this disease improve to the extent that we can target even better drugs to limit disease severity.

- Ryan

UK-CIC177 karma

Hey! Firstly, thank you for the work you do - as Immunologists we work closely with all sorts of clinical staff and know what a hectic/intense/crazy year you have all experienced.

In Immunology we often talk about 'mechanisms', meaning the immune reaction that triggers a response. The mechanism(s) behind multi-organ failure in respiratory infections (including and beyond Covid) aren't completely understood. Certainly hypoxia can cause tissue damage to non-respiratory organs and this presents one likely mechanism, but the immune response itself might be at least as important in causing organ damage. We know that in patients with severe disease the immune response goes beyond it's helpful role in clearing the virus and actually starts driving some of the symptoms and progression of the disease. This has been termed a 'cytokine storm' by some, but (in my opinion) that's a bit of an exaggeration. It seems that some aspects of the immune response are over active, or don't switch off properly when they've done their job in tackling the virus. This causes inflammatory responses that perpetuate themselves and start damaging the organs. To tackle that, some anti-inflammatory therapies have been shown to limit disease severity/prevent mortality e.g. the steroid Dexamethasone and an anti-inflammatory antibody therapy called Tocilizumab - both suppress different bits of the immune response, and this seems to benefit the patients, supporting the idea that the immune response itself at least partially causes the disease. - Ryan