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At this time any hypothesis regarding the parosmia seems to be untested. Speculative sentences in lay and technical sources point toward the olfactory bulb. (I have seen indications regarding the cilia of the olfactory neurons, the bulb itself, and the blood supply, but this seems to stray from our topic) When we look in more detail, the olfactory bulb ...


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This is not completely clear to say the least, but there are some hints. Please keep in mind that there was not much time for extensive research, since this disease is still quite new. What seems clear (at least at the moment) is that most like the nerve cells (in the olfactory bulb as well as in the taste bud) are not directly affected, since they do not ...


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The mRNA won't be entirely perfect, but the imperfections will not matter. The spike protein is big, encoded by thousands of base pairs in the virus. In the virus itself, it's not entirely homogeneous: there are always going to be small mutations that cause different variants to be produced, but nearly all of those are nearly identical. The mRNA in a vaccine ...


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Saying that a vaccine is $95\%$ efficacious is neither claiming that it works $95\%$ of the time nor that it protects $95\%$ of its recipients.† Rather, a $95\%$ efficacy means that—during the clinical trial in which half the subjects had been vaccinated and half hadn't—among those who eventually developed the disease, the ratio of those who had been ...


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You are the victim of the "post hoc ergo propter hoc" fallacy: just because event B follows event A doesn't mean that B is caused by A. The probability of a mutation to occur depends on the number of virions out there multiplied with some constant that models the faithfulness of the virus reproduction machinery. The lock-down was instituted because ...


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Current Biology 30, R841–R870, August 3, 2020 R857, does support some of your theory. The paper summarizes the scientific basis of their statements: Even though the adaptive significance of genetic variants remains to be established, we can use evolutionary theory to gain insights about how natural selection might act on disease characteristics. The ...


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The question asks about some advantage of a "fast" spreading virus. By intuition a population of not infected individuals spared out by lock-downs seems like some "open field" a fast virus might run through unhindered, then impeding other strains by some kind of pre-established dominance. However trivial that may appear, the allegory of ...


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Not necessarily. Sensitivity and specificity are decision criterion-based measures. They are not actually separable from another, they are a consequence of choosing a threshold at which to say "the test reports positive" or "the test reports negative", a consequence of this binary result. As such they are weighed against each other. You ...


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I'm going to answer this one with a No. Outside of a simple simulation with very unrealistic constraints, we can't know the basic parameters to generate such a number. From an omniscient point of view there would be some number where this becomes inevitable, but from that point of view we could say it is inevitable or impossible right now. Some aspects to ...


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Epidemiological modeling If a virus is able to change so that it renders previous vaccination inefficient, reinfecting those who were previously vaccinated, one could describe this process using epidemiological SIS model (Susceptible-Infected-Susceptible) or its modification that includes a vaccinated group (like SISV model), and indeed estimate how quick ...


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First of all, there is a question on stackexchange that is not only related but to be considered similar, if your explanatory text, last paragraph may be ignored Why cytotoxic T cells don't kill dendritic cells when they present antigen? Your question refers to "some cells" (explanatory text) and "transfected cells" (wording of your ...


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No, on cannot say it this way, since further expose always carries a risk of getting infected. However, one could argue that after certain time of exposure one is nearly certainly infected, so being exposed longer doesn't really change the result. This statement could be formulated more rigorously in terms of compartamental epidemiological models. If we take ...


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To judge about this assay, it is important to see how they worked. They used different sets of primers to analyze for SARS-CoV-2. Namely targets IP2 und IP4 from Institute Pasteur in Paris (see reference 1) and to validate results also primers targeting the "E" sequence (reference 2) and two against the nucleoproteins N1 and N2 (reference 3). Then ...


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As was observed (by others) under related q's here on material from that site, it seems Pfzier/BioNTech has done a global optimization to increase CG contents in the sequence, generally thought to be beneficial to mRNA expression (in addition to all the other things they've done, like U -> m1Ψ global substitution, specific to mRNA therapeutics). That (...


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The other answer is a bit convoluted IMHO. First note that as the article cited notes, that's not actually CCA -> CCU but CCA -> CCΨ; they only used ASCII for convenience. Furthermore, these three all code for proline as the article also notes. Second, Ψ stands for pseudouridine and it's the golden discovery of Kariko and colleagues (which made mRNA ...


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The two stop codons are obviously to prevent read-through of the termination codon. Why this should be necessary is not clear to me, but the following may be relevant: The synthetic mRNA differs from the natural mRNA in a particular respect that is easier to explain with reference to the transcript map of the virus, below. The two ORFs 1a and 1b are ...


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