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About Hannoverover

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    Hannover, Germany

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  1. https://www.medrxiv.org/content/10.1101/2021.04.06.21254882v1 Here's the data you are looking for ;-). It's not peer-reviewed and wasn't designed to test the effectiveness of the Pfizer vaccines against the SA variant. The data suggests that a higher than expected proportion of vaccinated people who were infected had the SA variant. This suggests that the vaccine is less efficient. Similar results were shown for the Oxford-AZ vaccine, however both vaccines will prevent severe illness, hospitalisations and deaths. Further better designed studies are ongoing.
  2. A good read explaining the latest data on the Oxford-AZ vaccine: https://www.nature.com/articles/d41586-021-00785-7?utm&fbclid=IwAR1gPyNNVKFPNtd-xOG8zERmDFpFYFbfRB0c3-ozGXID6wi_PP118AtHrTs I attended an online conference where one of the lead scientists presented their work. Its amazing what they have managed to achieve in such a short space of time.
  3. Yes, it's quite interesting how the effects of non-pharmaceutical measures (mask wearing, social distancing) influence the spread of other respiratory pathogens or pathogens spread via close contact. I'm actually involved in a project studying this in European countries. Here's a nice interactive graph to look at: https://syndromictrends.com/metric/panel/rp/percent_positivity/organism/main You can change between gastrointestinal and respiratory pathogens using the images at the top right of the page.
  4. Yep. risk for placebo group (4 people)- risk for vaccinated group (1 person) รท risk for placebo group (4 people). Meaning you are 4 times more likely to contract the virus if you aren't vaccinated.
  5. 79% reduction in testing positive (being infected) compared to not being vaccinated. So to flip it round, if identical twins were sat next to each other eating lunch opposite an infected person, the non-vaccinated twin would be 5 x more likely to become infected than his vaccinated identical twin. Some people get confused and think that there's a 21% chance of being infected, but that would only be true if the whole population were to be equally exposed. here's a nice video to explain it better than I can:
  6. Update on the rare brain blood clots: 20 cases have been found in 20 million vaccinated people. I'm still waiting to see some proof that the vaccine can cause this, however once detected it can be in theory treated. The theory is an autoimmune response which the vaccine induces, whereby platelets are activated and form a clot in the brain. Similar symptoms and 1 in a million occurance are also seen in the US with Pfizer and moderna vaccines. In summary, a 1 in a million occurance can be treated and this occurance is not statistically increased by having any of the vaccines.
  7. Yes, this is very good news, although not unexpected. Apologies if I misread it,... the 79% vs 21% doesn't actually mean that 21% of the vaccinated group got COVID-19, its just a 79% reduction compared to the non-vaccinated group. E.g. approx 100 vs 20 out of 32000 people enrolled in the study. Other good news is that, as speedie posted above, the peak viral load is lower in the vaccinated patients and is one of the main reasons why the symptoms aren't severe. I've seen the data presented, but not sure if they are published yet. This peak virus load is very important in the outcome of the
  8. Here's a bit more of a scientific perspective of the suspension of the Oxford-AZ vaccine, plus an interesting hypothesis: https://www.sciencemag.org/news/2021/03/it-s-very-special-picture-why-vaccine-safety-experts-put-brakes-astrazeneca-s-covid-19 Personally, I understand why, but I disagree with the suspension as its caused more harm than good. Even if it was statistically proven to cause these special types of blood clots (CVTs), I'm not sure how you would really prevent them. Even so, the benefits far far outweigh the unproven increase in CVT. It would be very hard to prove thi
  9. I'm going to try to watch it. I'm still behind Mowbray, but I've only managed to watch 2 games this season. A one sided victory against PNE and a rather frustrating 1-1 against Sheffield Wednesday. Maybe my view will change after watching a third game...
  10. Here's a summary of the lancet paper detailing the effectiveness of Oxford-AZ vaccine in reducing asymptomatic infections in phase 3 trails: https://www.bmj.com/content/371/bmj.m4777. Yes, this is a key issue, asymptomatic transmission will be reduced, however the extent still needs to be determined and several groups will be studying this for all the vaccines currently available. I would expect data to appear in the near future, especially in the UK due to the high level of testing and vaccination rate. In theory, reduction in asymptomatic infections and transmission should decreas
  11. I think I posted a scientific viewpoint a few pages back but can't quote it. I can understand both sides of the argument. My personal opinion is that the benefits far outweigh the potential risks in the UK due to the relatively high death rate and daily infections. The main risk would be that the person receiving the vaccine with a longer delay may not reach the same level of immunity as someone who received the second dose after 2-4 weeks. I'm sure the 12 week gap will not be the norm though. The longer gap will be investigated but the data won't be known for quite a while. It's nice to
  12. This I can't answer, but when I see some data I will let you know.
  13. As promised I can give a little update on the SARS-CoV-2 variant detected in S.A. and a bit more about the UK variant. Background: Once infected or vaccinated, our immune system produces specific antibodies which bind to a part of the virus, e.g. the spike protein. The viral spike protein binds to cells and helps it to enter and replicate in our cells. However, once these antibodies bind to the spike protein, they cover it and stop it from functioning. A bit like putting a perfectly fitting cover on the end of the a key. Once covered it can't open the lock. This is one mechanism that our
  14. Good question. The vaccines work by producing the whole spike protein of the virus in cells. Our immune system will detect it and create a range of antibodies that bind to different points of this spike protein. This means that a single, or even several mutations won't stop all of these antibodies from binding to the spike protein of the virus, as the majority of the spike remains unchanged. A huge change may make the spike protein work less efficiently too, which would be bad for the virus. I read a report that the mutation detected in S.A. may result in antibodies binding less st
  15. I'm not a politician, but I can imagine it's hard to give a clear constant message during these changing times. From a scientific standpoint the administration strategy is probably the best current option. Of course we can only make educated decisions based on experiments/trials we do. We haven't done the 12 week gap trials, but we can make educated guesses based on what we know on how the immune system works and the effects of similar vaccines.
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