Covid-19 Cepiva
- Ustvarjalec teme AndY1
- Začetni datum
Glede na to da si preštudiral zadevo, ti verjetno ne bo težko izpostaviti par ključnih poudarkov (executive summary) in seveda v obliki trditev v jasni slovenski povedi (osebek, povedek, predmet). Če je trditev, seveda brez veleumnih facebook dikcij, "a se samo men zdi čudno", "sam povem", itd.
Vse je zadnje čase v glavnem samo PR ... za manipulacijo fin.trgov ... "poštenega" cepiva še nekaj časa za mase ne bo, pri nas IMHO ne pred poletjem. Vmes pa tragedija, ekonomska in drugačna ... Vzbujanje upanja, pa pomaga pri depresijah. Luč na koncu tunela bodo pa najprej zagledali Turki ... oni ki vrtajo tunel skozi Karavanke ... pa ne da vas strašim ... Kmalu ne bo več toliko pomembno, kateri 60 inč TV za kupit, amprak za večino, ali si lahko privoščim šop banan ali ne ...
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" ... " I See Dead People..." - The 6th Sense ! ..."
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" ... " I See Dead People..." - The 6th Sense ! ..."
Nehaj no. Takšne poslušamo od bademajstra ..eeee..khm ..Kacina vsaki dan.Vse je zadnje čase v glavnem samo PR ... za manipulacijo fin.trgov ... "poštenega" cepiva še nekaj časa za mase ne bo, pri nas IMHO ne pred poletjem. Vmes pa tragedija, ekonomska in drugačna ... Vzbujanje upanja, pa pomaga pri depresijah. Luč na koncu tunela bodo pa najprej zagledali Turki ... oni ki vrtajo tunel skozi Karavanke ... pa ne da vas strašim ... Kmalu ne bo več toliko pomembno, kateri 60 inč TV za kupit, amprak za večino, ali si lahko privoščim šop banan ali ne ...
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" ... " I See Dead People..." - The 6th Sense ! ..."
Žal ima prav; če malo spremljate napovedane količine, ki jih lahko izdela vseh 5, 6, 7, trenutnih proizvajalcev, je vse skupaj "Blažev žegn"! Resno cepljenje se začne pred poletjem, ali celo pred naslednjo zimo - takrat pa tega sploh ne bomo rabili več - glavno, da se bo masa denarja preselila v žepe "izumiteljev" in proizvajalcev. Pa da se razumemo, onima dvema turkoma iz D nisem nič fauš, saj sta do sedaj "kamne žrla" z raziskavami zdravil za raka.
Resno vprašanje, zakaj meniš, da cepiva pred naslednjo zimo pravzaprav niti rabili ne bomo.
PS: Ja, od vsega začetka je bilo jasno da bo sama proizvodnja ozko grlo (in logistika je tudi hud zalogaj, sploh Pfizer in suhi led).
Vsi spremljajo za kakšne odmerke se bodo odločili, če bodo na koncu šli z višjimi odmerki, bo matematika enostavna, samo polovico načrtovanih ljudi bodo uspeli cepiti.
Za Regeneron in njihova protitelesa je pa še toliko bolj težavno, kar se tiče kapacitet proizvodnje.
Kot zanimivost, lansko poletje je zmankalo suhega ledu v UK in so nekatere stvari so enostavno obstale, npr. pivovarne ter tudi transporti snovi, kjer potrebuješ -80 °C
To je pa zato, ker se hoče precepiti vse. Stalno govorimo, potrebno je zaščititi ranljive, da se jih ne okuži, da ne umrejo. In za te delamo vse tole.
Torej naj se cepi ranljive skupine, pa je. Ostale pa naj se pusti, da se prekuži in dobijo naravno imunost. Že če odštejemo tiste, ki so že preboleli virus, jih bo ogromno manj za cepiti, koliko jih bo še, dokler cepiva ne pridejo.
Kako je lahko naravna imunost preko prebolenja virusa slabša kot cepljenje?
Pa sej je tolk simpl. Virusa ne bomo izkoreninili. Zakaj bi se moralo cepiti vse?
Torej naj se cepi ranljive skupine, pa je. Ostale pa naj se pusti, da se prekuži in dobijo naravno imunost. Že če odštejemo tiste, ki so že preboleli virus, jih bo ogromno manj za cepiti, koliko jih bo še, dokler cepiva ne pridejo.
Kako je lahko naravna imunost preko prebolenja virusa slabša kot cepljenje?
Pa sej je tolk simpl. Virusa ne bomo izkoreninili. Zakaj bi se moralo cepiti vse?
Resno vprašanje: težave z razumevanjem ali samo šlampasto branje?
PS: po sedanjih ugotovitvah (ker raziskave temu ne moremo reči) je virus PRVIČ zaznan lani pomladi v kanalizaciji Barcelone - torej je skrajni čas, da se nehamo sprenevedat.
PS2: upoštevam ukaze vlade, nosim masko kjer je to smiselno in potrebno, se čuvam v mejah normalnega človeka, VSEENO, ali pa PRAV ZARADI TEGA, pa se vedno bolj sprašujem KDO NAS TU FIJU-FIJU!?
Pa saj je tolk simpl. Zakaj cepimo vse proti davici, tetanusu, oslovskem kašlju, otroški paralizi, ospicam, mumpsu. Zako ker smo z faking precepljenostjo prakticno izkoreninli te bolezni. Dokler niste vi teoretiki pogruntali, da je cepjenje itak brezveze in so se bolezni spet zacele pojavljat. Ker vam osnove cepljenja niso jasne. Če bi vam ble bi vedeli zakaj cepit vse. Tak da bejži nazaj na yt (al pa v osnovno šolo), da se se to naučiš.
Milanski Tumor inštitut je testiral zamrznjene vzorce tkiv ... našli so korona protitelesa iz vzorcev z začetka septembra lani ... torej je bil v obtoku že konec avgusta lani !!! ... sem že enkrat napisal ta teden ...
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" ... The Truth Is Out There ..."
No ja od tvojih naštetih bolezni je par takih ki so vezane na človeka, so nalezljive in dejansko s cepljenjem nadziraš stanje virusa v populaciji oz. ga lahko izkoreniniš. Imaš pa na seznamu tudi take kjer cepljenje nima efekta na pojavnost bolezni, recimo tetanus. Tetanus obstaja in bo obstajal pa če smo vsi precepljeni, cepiš se zato da ne zboliš oz. da ne dobiš hujših posledic.
Koronavirusi in gripa spadajo čisto izven zgornjega seznama, ker gre za viruse s hitrimi mutacijami za katere ni enotnega cepiva in razvite življenske imunosti. Tako da cepljenje nas lahko reši covid19a, ne bo nas pa rešilo covid19b in še manj covid20, covid21 itd.
Sem že enkrat to omenjal ampak še 1x, cepljenje recimo proti gripi dokazano povečuje mutacije virusa. Če bi cepili v nekem trenutku 100% populacije za vse znane variacije virusa gripe, bi takoj naslednji dan prišla na "trg" nova proti kateri nebi bili imuni. Problem je da je taka "umetno" ustvarjena variacija lahko precej bolj "patogena" oz. ima nepredvidljive učinke na telo. Za to razumet je potrebno malo poznat virologijo, specifičnost mutacij in pa predvsem vplive okolja na te mutacije.
Na srečo je cepljenje proti gripi svetovno gledano minimalno in ne vpliva veliko na razvoj virusa .. zna pa bit pri covid19 drugače, in zna se zgodit da bomo "umetno" naredili precej bolj smrtonosen covid21 sev, kot bi stvar naredila narava sama.
Sem šel pogledat originalni članek:Milanski Tumor inštitut je testiral zamrznjene vzorce tkiv ... našli so korona protitelesa iz vzorcev z začetka septembra lani ... torej je bil v obtoku že konec avgusta lani !!! ... sem že enkrat napisal ta teden ...
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" ... The Truth Is Out There ..."
Unexpected detection of SARS-CoV-2 antibodies in the prepandemic period in Italy
Tumori, 2020
Giovanni Apolone*, Emanuele Montomoli*, Alessandro Manenti, ...
First Published November 11, 2020 Research Article
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journals.sagepub.com
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Subscription and open access journals from SAGE Publishing, the world's leading independent academic publisher.
journals.sagepub.com
Ključna je tabela
V vseh testiranih mesecih so bili pozitivni rezultati (in to ranga 1 - 2 % pozitivnih, kar mi na prvi pogled deluje kot probem specifičnosti testa). Če bi bili v tej tabeli še rezultati za julij, avgust in za julij in avgust bi bili rezultati 0, bi še smatral analizo za relevantno. Glede na podane rezulate bi se upal trditi, da je članek metodološko neustrezen.
Jaz si na podlagi teh podatkov nikakor ne bi upal podati trditve, da je bilo z veliko verjetnostjo potrjeno, da je bil SARS-COV-2 prisoten v teh mesecih.
To je prazaprav vprašanje za delodajalce (Fondazione IRCCS Istituto Nazionale Tumori, Milan, Italy) kej je s tem.
Lani POMLADI je prej kot lani Avgusta.Milanski Tumor inštitut je testiral zamrznjene vzorce tkiv ... našli so korona protitelesa iz vzorcev z začetka septembra lani ... torej je bil v obtoku že konec avgusta lani !!! ... sem že enkrat napisal ta teden ...
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" ... The Truth Is Out There ..."
Sem kje napisal, da se anti vaxxer na splosno? Nisem. Zakaj me tega obtozujes.
Se za klopni meningoencefalitis sem cepljen, ravno spomladi smo sli na osvezitveno cepljenje.
Kar pravim je, da je prvotno potrebno cepiti ranljive na virus, ostali pa po zelji. Naj se sami odlocijo, ali se zelijo prekuziti na naraven nacin ali pa s cepljenjem.
Sicer pa, zakaj bi cepil nekoga, ki je ze prekuzen?
Virusa se pa ne bomo znebili, ce to mislis. Ti je ze Utisevalec napisal, zakaj ne.
Glej nobeno cepivo ni 100%, nikoli ne se smejo cepit vsi (zaradi takšnih ali drugačnih razlogov). Torej bojo v ranljivih skupinah ljudje, ki so nezaščiteni. Zaradi takih stvari se cepijo vsi. In mi na alterju definitivno nimamo znanja, (čeprav eni ste prepričani, da ga imate), da odločamo koga cepit koga ne.
Za klopnega si pa cepljen, ker gledaš na svojo rit, ker to cepljenje pa res nima vpliva na širšo populacijo. Ampak samo na tisti osebek, ki je cepljen.
Za klopnega si pa cepljen, ker gledaš na svojo rit, ker to cepljenje pa res nima vpliva na širšo populacijo. Ampak samo na tisti osebek, ki je cepljen.
How long will the vaccine protection last?
This one can’t be answered with total confidence by any other way than just waiting and watching. But we will be able to give a meaningful answer well before that, fortunately. Here, just out in the last couple of days, is the most long-term and comprehensive look at the duration of immunity in recovered coronavirus patients. In fact, it appears to be the largest and most detailed study of post-viral-infection immunity in the entire medical literature (!) It’s from a multi-center team at the La Jolla Institute for Immunology, UCSD, and Mt. Sinai, and it looks at 185 patients who had a range of infection experiences, from asymptomatic to severe. 38 of the subjects provided longitudinal blood samples across six months.
We’ve already seen from the convalescent plasma comparison samples in the various vaccine Phase I trials that the antibody response to coronavirus infection can be quite variable, and that was the case in this study as well. That gives you wide error bars when you try. to calculate half-lives, and it’s not even clear what kind of decay curve the antibody levels will best fit to (it might well be different in different patients). But one figure to take home is that 90% of the subjects were still seropositive for neutralizing antibodies at the 6 to 8 month time points. The authors point out that in primate studies, even low titers (>1:20) of such neutralizing antibodies were still largely protective, so if humans work similarly, that’s a good sign. An even better sign, though, are the numbers for memory B cells, which are the long-term antibody producers that help to provide immunological memory. B-cells specific to the Spike and to the nucleocapsid coronavirus proteins actually increased over a five-month period post-symptom-onset, thus with no apparent half-life at all. These had interesting variations in antibody type (by the end of the period, they were strongly IgG, the others having dropped off), but as the paper notes, we really don’t have many viral infection profiles in humans to compare these results to. B-cell memory overall, though, looks to be long-lasting, and is expected by these results to stretch into years. For what it’s worth, there are patients who survived the 1918 influenza pandemic who had B cells that still responded with fresh neutralizing antibodies after over 90 years, so they can be rather hardy.
What about the other immune (and immune memory) component, T cells? The news there is good as well. CD4+ and CD8+ memory T cells appear to have half-lives of at least five or six months in these patients, and helper T cells (crucial for those memory B cells to respond later on) were completely stable over the entire period studied. Again, there are very few viral infection studies to compare this one to, but these numbers look consistent with long-term protection via reactivated immune memory.
Looking over the whole set of patients, it was clear that the immune system’s famously individual character was on full display here. That heterogeneity could well be the reason that there are real cases of re-infection, although it still seems to be rare. Different components of the immune response (both in antibodies and T cells) varied widely among patients, and these differences only became more pronounced over time. Nevertheless, at the five-month time point in a measure of five components of immune response and memory, 96% of patients were still positive on at least three of them (the categories were IgG antibodies against the Spike receptor-binding domain (RBD), IgA antibodies against the same Spike RBD, memory B cells aimed at the RBD, total SARS-CoV-2-specific CD8+ T cells, and total SARS-CoV-2-specific CD4+ T cells).
Bottom line: Taken together, this study, several others over the past few months, and this recent work all paint a consistent picture of a strong, normal, lasting immune response in the great majority of patients. Add in the results we’re seeing from the two vaccines that have reported interim data so far, and I think that the prospects for lasting immunity from vaccination are also very good. Remember, the early vaccine data suggested antibody responses at least as strong as those found in naturally infected cases. There seems (so far) every reason to think that vaccine-based immunity will be as good or better than that conferred by actual coronavirus infection. I very much look forward to more data to shore up this conclusion, but that’s how it looks to me at the moment.
This one can’t be answered with total confidence by any other way than just waiting and watching. But we will be able to give a meaningful answer well before that, fortunately. Here, just out in the last couple of days, is the most long-term and comprehensive look at the duration of immunity in recovered coronavirus patients. In fact, it appears to be the largest and most detailed study of post-viral-infection immunity in the entire medical literature (!) It’s from a multi-center team at the La Jolla Institute for Immunology, UCSD, and Mt. Sinai, and it looks at 185 patients who had a range of infection experiences, from asymptomatic to severe. 38 of the subjects provided longitudinal blood samples across six months.
We’ve already seen from the convalescent plasma comparison samples in the various vaccine Phase I trials that the antibody response to coronavirus infection can be quite variable, and that was the case in this study as well. That gives you wide error bars when you try. to calculate half-lives, and it’s not even clear what kind of decay curve the antibody levels will best fit to (it might well be different in different patients). But one figure to take home is that 90% of the subjects were still seropositive for neutralizing antibodies at the 6 to 8 month time points. The authors point out that in primate studies, even low titers (>1:20) of such neutralizing antibodies were still largely protective, so if humans work similarly, that’s a good sign. An even better sign, though, are the numbers for memory B cells, which are the long-term antibody producers that help to provide immunological memory. B-cells specific to the Spike and to the nucleocapsid coronavirus proteins actually increased over a five-month period post-symptom-onset, thus with no apparent half-life at all. These had interesting variations in antibody type (by the end of the period, they were strongly IgG, the others having dropped off), but as the paper notes, we really don’t have many viral infection profiles in humans to compare these results to. B-cell memory overall, though, looks to be long-lasting, and is expected by these results to stretch into years. For what it’s worth, there are patients who survived the 1918 influenza pandemic who had B cells that still responded with fresh neutralizing antibodies after over 90 years, so they can be rather hardy.
What about the other immune (and immune memory) component, T cells? The news there is good as well. CD4+ and CD8+ memory T cells appear to have half-lives of at least five or six months in these patients, and helper T cells (crucial for those memory B cells to respond later on) were completely stable over the entire period studied. Again, there are very few viral infection studies to compare this one to, but these numbers look consistent with long-term protection via reactivated immune memory.
Looking over the whole set of patients, it was clear that the immune system’s famously individual character was on full display here. That heterogeneity could well be the reason that there are real cases of re-infection, although it still seems to be rare. Different components of the immune response (both in antibodies and T cells) varied widely among patients, and these differences only became more pronounced over time. Nevertheless, at the five-month time point in a measure of five components of immune response and memory, 96% of patients were still positive on at least three of them (the categories were IgG antibodies against the Spike receptor-binding domain (RBD), IgA antibodies against the same Spike RBD, memory B cells aimed at the RBD, total SARS-CoV-2-specific CD8+ T cells, and total SARS-CoV-2-specific CD4+ T cells).
Bottom line: Taken together, this study, several others over the past few months, and this recent work all paint a consistent picture of a strong, normal, lasting immune response in the great majority of patients. Add in the results we’re seeing from the two vaccines that have reported interim data so far, and I think that the prospects for lasting immunity from vaccination are also very good. Remember, the early vaccine data suggested antibody responses at least as strong as those found in naturally infected cases. There seems (so far) every reason to think that vaccine-based immunity will be as good or better than that conferred by actual coronavirus infection. I very much look forward to more data to shore up this conclusion, but that’s how it looks to me at the moment.
How effective are these vaccines? Will they provide total protection or not?
We’re just starting to get numbers on this, and we are definitely going to know more as the various trials read out interim data and then reach their conclusions. So far, though, the efficacies we’re seeing have been more than I had really hoped for. I thought that they would work, and I didn’t think that meant just the FDA’s floor of 50% efficacy, but I sure didn’t have the nerve to predict that the first two readouts would be 95% (Pfizer just reported their final readout this morning). I can’t overemphasize how good that news is, especially when you compare it to some earlier worries that a useful coronavirus vaccine might not even be possible at all. Cross that one off the list!
Those efficacy numbers, though, are measured for symptomatic coronavirus cases. The vaccine trial participants are not being pulled in at regular intervals for testing to see if they’ve gone positive-though-asymptomatic. We may get controlled data of that sort eventually, but for now, we know from the Moderna trial that the few people who came down with symptoms at all had very mild cases. The antibody levels that we’re seeing would argue for a low probability of having a significant number of vaccinated people walking around asymptomatically shedding coronavirus, and for anyone who does to be shedding a lot less of it for a shorter period of time.
From a public health standpoint, that’s what you need. Epidemics are a matter of probabilities, and you can lower the chances of spread for a virus like this in any number of ways. They surely vary in efficacy, but include keeping distant from other people and avoiding any crowding in general, wearing masks, avoiding indoor situations with people that you haven’t been exposed to (such as going to the grocery store when it’s not so crowded), minimizing the time you spend in any higher-risk situation in general (getting those groceries in an organized fashion and getting back outside), and more. The fewer people there are around shedding infectious particles, the better (obviously), but the worst case for a weakly effective vaccine might be that it could actually raise that number for a while by creating more asymptomatic cases rather than having the infection make people aware that they need to stay the hell inside. But I don’t think we’re going to see that. I think that the efficacy levels we’re seeing are indeed going to be epidemic-breaking if we can get sufficient numbers of people vaccinated. Right now we’re up around the efficacy of the measles vaccine, which is very effective against a virus that is far more infectious than SARS-Cov-2. . .if enough people take it. (Believe it, if the current coronavirus were as infectious as measles is, we would be hosed).
Bottom line: the results we have so far indicate that these vaccines will indeed provide strong protection in the great majority of patients. The number of asymptomatic cases among the vaccinated population will be a harder number to pin down, but I believe that we should be in good enough shape there as well, based on antibody levels in the primate studies and what we’re seeing in humans.
We’re just starting to get numbers on this, and we are definitely going to know more as the various trials read out interim data and then reach their conclusions. So far, though, the efficacies we’re seeing have been more than I had really hoped for. I thought that they would work, and I didn’t think that meant just the FDA’s floor of 50% efficacy, but I sure didn’t have the nerve to predict that the first two readouts would be 95% (Pfizer just reported their final readout this morning). I can’t overemphasize how good that news is, especially when you compare it to some earlier worries that a useful coronavirus vaccine might not even be possible at all. Cross that one off the list!
Those efficacy numbers, though, are measured for symptomatic coronavirus cases. The vaccine trial participants are not being pulled in at regular intervals for testing to see if they’ve gone positive-though-asymptomatic. We may get controlled data of that sort eventually, but for now, we know from the Moderna trial that the few people who came down with symptoms at all had very mild cases. The antibody levels that we’re seeing would argue for a low probability of having a significant number of vaccinated people walking around asymptomatically shedding coronavirus, and for anyone who does to be shedding a lot less of it for a shorter period of time.
From a public health standpoint, that’s what you need. Epidemics are a matter of probabilities, and you can lower the chances of spread for a virus like this in any number of ways. They surely vary in efficacy, but include keeping distant from other people and avoiding any crowding in general, wearing masks, avoiding indoor situations with people that you haven’t been exposed to (such as going to the grocery store when it’s not so crowded), minimizing the time you spend in any higher-risk situation in general (getting those groceries in an organized fashion and getting back outside), and more. The fewer people there are around shedding infectious particles, the better (obviously), but the worst case for a weakly effective vaccine might be that it could actually raise that number for a while by creating more asymptomatic cases rather than having the infection make people aware that they need to stay the hell inside. But I don’t think we’re going to see that. I think that the efficacy levels we’re seeing are indeed going to be epidemic-breaking if we can get sufficient numbers of people vaccinated. Right now we’re up around the efficacy of the measles vaccine, which is very effective against a virus that is far more infectious than SARS-Cov-2. . .if enough people take it. (Believe it, if the current coronavirus were as infectious as measles is, we would be hosed).
Bottom line: the results we have so far indicate that these vaccines will indeed provide strong protection in the great majority of patients. The number of asymptomatic cases among the vaccinated population will be a harder number to pin down, but I believe that we should be in good enough shape there as well, based on antibody levels in the primate studies and what we’re seeing in humans.
