health

Study suggests dengue may provide some immunity against COVID-19

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By Pedro Fonseca

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© Thomson Reuters 2020.

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Hard to believe that an Infection caused by Flavivirus can confer immunity to infection caused by Coronavirus. If true, cases in the Caribbean such as PR should decrease....it is occurring the opposite with cases increasing to over a thousand for the past several days.

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This finding raises some serious questions. If there is immunological similarity between Dengue and SARS-CoV-2, we must examine the results of a Dengue vaccination campaign in the Philippines which went horribly wrong. The report in Scientific American, April2019, and absent from every other media outlet, explained that if a person had already had Dengue, the immunization would prime them for death if they ever had Dengue again. Not the hoped for result. A vaccine for SARS-CoV-2, if it cross reacted with a pre-existent Dengue infection, could create the same situation. The two viruses do not appear to infect the same kinds of cells but, if there are similarities, could they exchange genetic information and enhance one or both of their genepools, for example, a mosquito transmissible SARS-CoV-2? Lots going on in this article and how much of it is good remains to be seen.

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Another study which uses the word “may.” There is another expression with identical meaning to “may,” and that is “may not.”

Most people seem to think that “may” suggests a large possibility that something will happen, but that is silly. “May” suggests a 50% possibility at best. It may snow on January 1st, but it may not.

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Hard to believe that an Infection caused by Flavivirus can confer immunity to infection caused by Coronavirus.

It is not so rare, some viral antigens are simmilar and confer incomplete protection against other viruses.

. If true, cases in the Caribbean such as PR should decrease...

Decrease compared to what? the same country with less seropositive people? because one limited immunity advantage is not the only thing that influences the number of cases. If you want to say a country has more cases or more complications you need a very detailed analysis including dozens and dozens of variable.

If there is immunological similarity between Dengue and SARS-CoV-2, we must examine the results of a Dengue vaccination campaign in the Philippines which went horribly wrong. The report in Scientific American, April2019, and absent from every other media outlet, explained that if a person had already had Dengue, the immunization would prime them for death if they ever had Dengue again

When it happened it was everywhere, for literally months to no end with politicians blaming the company and viceversa while the people in charge of the safety protocol blaming both for not respecting the accorded limited number of vaccinations first and going directly with vaccinating as much people as they could.

The result is not "prime them for death" the vaccine is effective for 3 or the 4 serotypes of the disease, but increases the rates of complications when infected with the fourth one. In countries like the Philippines where all 4 types co-circulate constantly this is dangerous, but even so it is still LESS dangerous that getting infected consecutively with each serotype because the rate of complications is much worse and begins since the second infection (and increases even more with the third and the fourth). The vaccine still means less overall risk, but ethically it is not justified to use as long as is theoretically possible the person will not get infected more than once. Additionally the immune response to the vaccine is not yet as well understood as the response to natural infection, so it would give much less information for COVID-19 immunity.

A vaccine for SARS-CoV-2, if it cross reacted with a pre-existent Dengue infection, could create the same situation.

Up to this point there has been no report of antigen dependent enhancement, which is the problem with Dengue. Much less increased vascular permeability (the most common complication of hemorrhagic Dengue) if the same situation was possible these both complications should be common in every country where dengue is endemic, but they are not.

The two viruses do not appear to infect the same kinds of cells but, if there are similarities, could they exchange genetic information and enhance one or both of their genepools, for example, a mosquito transmissible SARS-CoV-2?

Not possible, the simmilarities are most likely on antigenic epitopes of the virus, a few amino acids in length. For homologous recombination it is required for the viruses to be similar genetically, and flavi and corona are completely different. If that was a real possibility it would have already happened during the thousands and thousands of years where both families f viruses have existed in the same territory around the world.

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@virusrex ...and flavi and corona are completely different...

Oh King of Viriae, thank you for your detailed analysis but, as a companion to the analysis of "may" and "may not" seen above, I would offer that, at this point even the Big Pharma people who work with these things under threat of great liability are messing up bigly as seen in the Philippine debacle. Any thing we now "know" must be viewed with skepticism. And the take home is that, regardless of any minimal benefit, the risk potential of the vaccination was completely unexpected and unappreciated by the people who KNEW the vaccination was safe based on their own self-images, evidently, and not on physical reality.

Regarding genetic exchange, the major difference in viral structure between flavi and corona are in the capsid and docking mechanism, plus maybe some NSPs, but both viruses are positive-sense single-stranded RNA viruses which, if both were to enter the same cell, they would have much in common. That we have not yet observed such a recombination in these two viruses means very little, and as these two viruses spend more and more time together in an ever increasing number of hosts, no one would be surprised to find a 'novel' flavlvirus or novel 'novel Corona' virus to arise out of that. 'Horizontal transfer' of biological information is hardly a 'new' idea or observed event. Also, "homologous recombination" is different from the 'heterologous recombination' suggested here.

The bottom line is we simply don't know enough, either as individuals or whole pharmaceutical research labs. We are still in the 'first wave' of our 'sense of understanding' being trashed and our resistance to that, something we saw when HIV was first being revealed. We just don't know, and Nature is way more complex than we are and has way more tricks than we have imagination to foresee so we bumble through as best we can until we know more. But this kind of discussion is good exactly for that reason. Thank you, virusrex, and I hope you have more to add to this.

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the risk potential of the vaccination was completely unexpected and unappreciated by the people who KNEW the vaccination was safe based on their own self-images, evidently, and not on physical reality.

Except that is was still a completely possible scenario because that is what makes the Dengue vaccination something not achieved until now. The complication was much less important than what the safety officials feared, but it was still inside what they were actively looking for, precisely because of this was why even after a phase 3 was finished it was agreed that introduction would be slow and limited, something that was not respected. It was not unexpected, it was actively searched for, which is why it was found so quickly.

, but both viruses are positive-sense single-stranded RNA viruses which, if both were to enter the same cell, they would have much in common.

In a viral sense, they have as much in common as humans and octopuses. Which mean very little. Genome structure is completely different, with flaviviruses having 6 clearly delimited non-structural neatly ordered proteins of around the same size coming at the end of the genome after the envelope and capsids protein sequences that come first. Coronaviruses instead have first 16 non-structural proteins that are all wildly different in size, are all necessary and require a "frame shift" phenomenon to be expressed, and after that 12 proteins to make the capsid that now require a "leaky scanning". Just search for "genome structure" of both and the huge differences will become obvious.

Its like saying that since you are making a 3D puzzle of the Tokyo Tower and a normal 2D puzzle of the Eiffel Tower in the same table you may switch pieces and end up with two new and complete puzzles at the end. Not possible.

That we have not yet observed such a recombination in these two viruses means very little, and as these two viruses spend more and more time together in an ever increasing number of hosts,

No, that is not true, there are dozens of species of coronavirus, and dozens of species of flavivirus, and they have been in the same area infecting the same hosts for likely millions of years without any recombination. You are confused between human interaction and natural interaction, the first is increasing, the second has been terribly common from the beginning.

no one would be surprised to find a 'novel' flavlvirus or novel 'novel Corona' virus to arise out of that.

Everybody would be, specially the experts, because homologous recombination requires the same genomic structure to be realistically possible (and even with a shared structure it is still very rare). To be more clear, even between flaviviruses, that share hosts (both hot blooded and mosquitoes) there is no evidence of recombination ever happening. That is between viruses sharing 99% of the genome, much less with a completely unrelated group of viruses with homology below 20%

'Horizontal transfer' of biological information is hardly a 'new' idea or observed event.

In the context of a natural happening between viruses of extremely different genome structures? yes it is. It would be a huge discovery, on the scale of finding out there is actually another star just behind the sun that for some reason wen undetected until now.

Also, "homologous recombination" is different from the 'heterologous recombination' suggested here.

If homologous recombination is practically impossible, heterologous recombination is simply not even worth considering. That means that the extremely rare occurrence of subgenomic RNAs being produced becomes necessary, and that coincidentally it is happening at the same time for 2 viruses at the same cell, and then that the random fragments are compatible, and then that somehow they recombine without help of any natural facilitaion mechanism, and then that every function of the virus is conserved and then that this new virus is not on an adaptive disadvantage compared with both the parental strains so it can survive.

To make it more clear, if homologous recombination means confusing pieces of two very different puzzles, heterologous recombination would mean ordering at random pieces of two random laptops from two makers, putting them in a bag and shaking them until a new model of laptop comes out and it is a better one than the two original ones. Not possible (specially because since you are ordering at random you may end up with several displays and not a single hard disk for example).

The bottom line is we simply don't know enough, either as individuals or whole pharmaceutical research labs.

No, it is clear that YOU don't know enough, but science is way more advanced than what you are apparently imagining. You are talking about things that are not realistically possible to happen, we as humans know this because of literally centuries of scientific advancement that tell us how things happen and what kind of requisites have to be fulfilled for them to happen.

We are still in the 'first wave' of our 'sense of understanding' being trashed and our resistance to that, something we saw when HIV was first being revealed.

That is irrelevant, HIV did what retroviruses do, and infection was a process already described. Specialists know this is possible just by the amount of transposons of retroviral origin. The challenge was never to understand how HIV could infect humans or produce disease, but how to defeat a mechanism we knew was bout to be difficult for the immune system to completely defeat by itself. For this pandemic is the same, nothing we did not understand happened, on the contrary it was predicted to happen (again) if we did not take proper measures. Our understanding is fine, the ability of politicians to actually listen to the experts is what is lacking.

We just don't know, and Nature is way more complex than we are and has way more tricks than we have imagination to foresee so we bumble through as best we can until we know more. But this kind of discussion is good exactly for that reason. Thank you, virusrex, and I hope you have more to add to this.

"we don't know" is a terrible argument to say that something "may" happen. Specially when you personally don't know what we do know. We don't know how a new virus could give the infected the ability to fly or shoot lasers from the eyes, it "may" theoretically happen (by several unknown mechanisms) but considering the possibility does not have any practical usefulness, it is just science-fiction. The real progress come from dedicating effort to study and comprehend what actually have a chance to happen, so we can prevent it if is negative

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