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originally posted by: ketsuko
a reply to: Adphil28
Oh, on the flu testing, I meant that if someone presents to the doctor with flu-like symptoms such that they test them for the flu and that test comes back negative (and it's a very fast test; they did one on my kiddo last year when he had flu A), they will automatically test for corona virus to screen for it.
originally posted by: ketsuko
a reply to: liejunkie01
I'm going to guess the massive damage to the lungs was seen in patients who had died.
originally posted by: TheIrvy2
a reply to: tanstaafl
Except that those figures you're basing everything on are widely considered to be propaganda
... covering up the true extent of a disease that may have an undetectable first stage and may have been brewing in the population for much longer than we're being told.
originally posted by: confiden
a reply to: tanstaafl
Those are only the cases we have found. Surely you understand that we cannot test everyone in the world every day to know the exact numbers. You have to use your judgement if that many were found in the population of X million, how many were asymptomatic never tested, had a false-positive result and not retested or misdiagnosed as flu.
Estimates of the timing of the most recent common ancestor (tMRCA) of SARS-CoV-2 using currently available genome sequence data point to virus emergence in late November to early December 201920,21, compatible with the earliest retrospectively confirmed cases22. Hence, this scenario presumes a period of unrecognised transmission in humans between the initial zoonotic transfer event and the acquisition of the polybasic cleavage site. Sufficient opportunity could occur if there had been many prior zoonotic events producing short chains of human-to-human transmission (so-called ‘stuttering chains’) over an extended period. This is essentially the situation for MERS-CoV in the Arabian Peninsula where all the human cases are the result of repeated jumps of the virus from dromedary camels, producing single infections or short chains of transmission that eventually resolve. To date, after 2,499 cases over 8 years, no human adaptation has emerged that has allowed MERS-CoV to take hold in the human population.
originally posted by: RamsesOzymandias
"originally posted by: tanstaafl
Are there any indications that this thing can/will kill those that are otherwise healthy with reasonably strong immune systems?"
HIVCOVID-20 sounds good.
originally posted by: Alien Abduct
a reply to: tanstaafl
"If only those who have compromised immune systems and/or are otherwise at risk (elderly, infants, etc) - which appears to be the case -"
Can you cite your source for this?
originally posted by: Oppenheimer67
"originally posted by: tanstaafl
... if your argument is that there are lots of cases not yet confirmed - where are the huge spikes in numbers of reported serious illnesses from 'flu' or pneumonia or anything related?"
For that you will want to watch data for Flu-Like Illnesses.
Here's data for Illinois.
That's IF they were to go down as flu-like rather than something else.
source:
dph.illinois.gov...
originally posted by: ketsuko
a reply to: St Udio
nCoV19 = the virus
Covid19 = the disease caused by the virus
It's like HIV and AIDS. HIV is the virus, and AIDS is the disease.
originally posted by: checkmeout
Just posting this which is a weekly tracker of UK flu like illnesses. Interestingly it is a weekly tracker but I can't see that it's been updated since end of Jan. Up to that point GP consultations were falling for such illnesses. For non UK readers, a GP would generally not test for flu. Just give you general advice. It is only those with more severe illness who would go to hospital and then be tested (my experience anyway). I was interested to know if there had been a spike of flu (which might not have been actual flu) but there are no figures for last 2 weeks. Unless I'm being dim
www.gov.uk...
originally posted by: ketsuko
SARS-CoV-2 *NOT* genetically engineered. This paper was popped up about three hours ago, and argues through genetic analysis that wherever this thing came from, it was not created intentionally, but occurred naturally.
They conclude that the binder specific to ACE2 may be efficient to human and human-like ACE2, but it would also target several other species like cats and pigs among others.
They say that the virus does not show the hallmarks of what a predicted engineered virus of that type would have. The processes available to reverse engineer it have not been used. It doesn't have the viral backbone of an engineered virus of that type.
One of the possible theories they explore is that this thing did jump out of animals but did so over time and no one noticed. Basically, it jumped out an animal to person here or there, possibly that person passed it on to another one or two people, and over time it acquired mutations through all those previous short chains.
Estimates of the timing of the most recent common ancestor (tMRCA) of SARS-CoV-2 using currently available genome sequence data point to virus emergence in late November to early December 201920,21, compatible with the earliest retrospectively confirmed cases22. Hence, this scenario presumes a period of unrecognised transmission in humans between the initial zoonotic transfer event and the acquisition of the polybasic cleavage site. Sufficient opportunity could occur if there had been many prior zoonotic events producing short chains of human-to-human transmission (so-called ‘stuttering chains’) over an extended period. This is essentially the situation for MERS-CoV in the Arabian Peninsula where all the human cases are the result of repeated jumps of the virus from dromedary camels, producing single infections or short chains of transmission that eventually resolve. To date, after 2,499 cases over 8 years, no human adaptation has emerged that has allowed MERS-CoV to take hold in the human population.
Apparently, this is something we may need to watch for with MERS.
In other words, it's possible this thing had been there for some time at very low levels but only recently finally got its missing genetic ducks in a row so to speak. They call that cryptic spread.
They also do not rule out selection during passage which does bring the laboratory back into focus, but not as an engineered virus, merely as a studied strain of disease. However, they say that one of the features of the disease argues against this scenario because that feature has only arisen in a passage event once in an avian virus, and in order to see this in this virus, it would have had to have been an intensive, long-term program of passage through animal culture with the right kind of ACE2 (like cats or ferrets, not bats). Not to mention, they say the receptor in question has to involve a living immune system, not just cell culture.
So there we are ... this paper argues against genetic engineering although not conclusively against a lab escape.