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COVID (nCoV) - Preliminary thoughts. JJackson personal opinion.

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  • COVID (nCoV) - Preliminary thoughts. JJackson personal opinion.


    I have been trying to understand this zoonotic outbreak and have noticed some discussion which, in my opinion, is based on a misinterpretation of the available data and this post is aimed at trying to give a more comprehensive overview of that data, and implications, than I have managed in short posts elsewhere on the site. I have posted in my workshop because it is just my understanding and does not reflect the view of FluTrackers also, as I hope to add additional posts as things progress, I wanted it not to get lost in a fast moving discussion thread.


    Testing.

    To understand the data being released you also need to understand the method and limitations of testing. Once a new pathogen is identified and sequenced a RT PCR primer can be generated. The primers will be a short length of the pathogens DNA/RNA chosen from a conserved (slowly changing) part of the genome which can be matched to pathogen samples. The sequence needs to be long enough not to keep finding matching sequences in the hosts DNA but not so long that random variations in the genome start causing false negatives. Now we have a primer we need to distribute it to as many labs as possible that have RT PCR capacity and can safely handle the pathogen. These are limited and while not a problem outside China, at present due to few cases, in China the situation is different.

    Labs are testing as many samples as they can but there is a backlog collected prior to the primers being available and many more suspect cases being generated so only a sub set of these can be tested. So who to test, there is a rush on to find the animal host so very early suspect cases, even before the fish market cluster, become a priority along with the more severe cases. The implication being that mild cases, or ones with atypical symptoms, will have to wait their turn giving a heavily skewed sample towards severe cases the implications of which I will look at in the section on epidemiology. All of this is normal. In H1N1(2009) before primers were widely distributed the CDC was testing about 100 samples per day with a backlog in the 10s of thousands, in the West African Ebola outbreak the case counts broke down due to ETCs (Ebola Treatment Centres) being full and closed to new patients who consequently could not be counted.

    While it is only beginning to be possible to do serological testing, due to the time lag between infection and antibody build up, this should soon begin to provide useful data. Serological tests will put pressure on different lab equipment and personnel so should be able to run in parallel to RT PCR. Here blood is tested for the presence of antibodies, with antisera, a positive reaction showing the patient had been challenged by the virus in the past and overcame it. What this should tell us is how many cases there have been who did not show symptoms – or at least not to the point of warranting hospitalisation and virus testing. These people should now have a reasonable level of protection making them not part of the ‘susceptible population’, see epidemiology, and add to herd immunity. If there are large numbers of infections that are self-limiting and mild it radically changes the outbreak’s sustainability and impact.


    Contacts.

    It is normal to expect a disease to increase in transmissibility as the patients symptoms get worse due to high viral titres. Exactly how this happens is not constant SARS did not become infectious until there were very high viral loads late in the disease, flu – and apparently nCoV – are infectious prior to symptom onset but there is an infectivity curve over time where and how this peaks is disease dependent but will show some correlation to viral load. ‘Close contacts’ refers to the unprotected contacts in a family or healthcare setting where protracted intimate contact can be expected as opposed to ‘contacts’ which are what you get if you meet someone while walking or shopping. These are very different in terms of the probability in catching the pathogen.


    Symptoms, treatment and capacities.

    The symptom set is quite wide but from early data high temp, cough and breathing difficulty top the list. For a respiratory pathogen it has a high incidence of digestive tract symptoms. Some form of oxygen treatment is used in most cases but not that many end up with invasive mechanical oxygenation or ECMO, in fact one paper shows more patients were on Liver function treatment. The key indicators from blood testing is low lymphocyte and platelet counts. Wuhan is having hospital capacity problems which they are working hard to overcome but as spread continues nationally and internationally this is likely to become a problem for us all. At present we are able to help out the epicentre by bringing in extra capacity from outside but as it spreads first to other Chinese cities and then globally this option will dry up. Treatment is just alleviation of symptoms as there is nothing specific. Vaccine and antivirals specific to this disease will not be available, probably for years, so various off label drugs are being tried with some anecdotal evidence of limited success – early days. One study showed human and horse serum could be useful for treatment.
    Links:
    https://reader.elsevier.com/reader/s...B848F5AD13AA87
    While not the paper I took the data in the text from (which I can't now find) it does cover the same ground. One point of interest is in Table 3 which shows 3 patients (n=41) on continuous renal replacement therapy. I have been keeping an eye open for this as the kidney are rich in ACE2 receptors and so kidney damage in later disease may indicate both increased tissue tropism and that ACE2 is the being used.
    The second link is to a US case history following a single patient's treatment. It informative as it gives significant detail on the procedures used and is an example of idealised treatment in an unstressed health system with vast resources. If I get it I very much doubt I would get the same. https://www.nejm.org/doi/full/10.105...jmO7T4.twitter

    Virology.

    wCov is a positive sense single stranded RNA virus (+ssRNA) with one very long (30,000 nucleotide) segment. As most readers are going to be more familiar with Flu I will try and show how and where they are different. Flu is –ssRNA with 8 segments of about 12k bases in total and half of this is used to make its RNP complex which is only needed for negative sense viruses. Both are encapsulated viruses with prominent surface spike proteins, for flu theses are HA and NA in nCoV it is the S protein. The S protein contains the primary antigenic site and the RBD (Receptor Binding Domain) while HA does the same for flu. Flu uses host proteases to cleave HA for cell endocytosis but nCoV needs to supply its own RdRp (RNA dependent RNA protease) which it cannot replicate without. RdRp and S’s RBD are probably the most likely candidates for a specific nCoV small molecule pharmaceutical. S’s RBD probably binds to the host ACE2 receptor (as HA does to sialic acid residues). SARS uses ACE2 and nCoV has been shown to bind to HeLa cells genetically engineered to express various types of ACE2 receptor including human, bat and pig but not mouse. This does not necessarily mean it is the only cell it can bind to but is an obvious place to start.

    Genetically there are not many samples from the virus’ natural genetic reservoir in bats which is not due to a lack of effort, one team literally spent years netting caves across China looking for the SARS reservoir before they found their first match. CoVs are divided into groups and SARS and nCoV are part of the b (beta) branch. The related bat sequences are grouped into two some of which are referred to as SARS like (SL betaCoVs) while the others generally get listed as bat betaCoVs. Most of both these groups have a very short sequence in the Spike RBD but SARS, MERS and nCoV all have a massive insertion making a long appendage which, while attached through the amino acid's backbone covalent bond, is otherwise largely unlinked to the rest of the protein either by covalent or hydrogen bonding. These inserts are not common across those that have them with very different structures in SARS, MERS and nCoV. The sequences we are getting now for nCoV are showing a lot of sequencing errors which is making it very difficult to say if the minor deviations from the consensus strand are due to lab error or real genetic change, of which there has been little. All the new sequences are basically identical and a number of estimates for the date of convergence are all pointing towards late Nov/ early Dec 2019 implying the all stem from a single introduction. Testing may yet find other independent introductions, either form the same host animal or others, which may be significantly different but they do not seem to have been involved in the general expansion of cases found to date.
    Click image for larger version  Name:	nCoV tree.JPG Views:	147 Size:	54.4 KB ID:	826925
    Links
    The graphic above is taken from https://www.bilibili.com/read/cv4457676/ it is in Chinese but this worked for me https://translate.google.com/transla...2Fcv4457676%2F . From top to bottom the first line (0 - 30k) shows the nucleotide sequence position, below it the open reading frames (ORF1, S, N) then we have the data plot showing how well SARS & various bat SL CoVs match nCoV. RaTG13 being much closer than any other sequences particularly across the spike (S gene covering nucleotides 22 to 25k), CZ45 is close across ORF1a but reverts to SL CoV consensus homology on S. (more detail can be found in the nCoV-genetics thread).

    The second link is to https://www.thelancet.com/journals/l...251-8/fulltext
    (again I can not find the paper I originally read that had clearer protein models but will update if I do) the first graphic shows the protein model with their host binding protein, the point to note is the non purple sections on the CoV proteins, these are insertions mentioned in the text, in the second graphic the table shows which sequences have them, the big white block showing most SL CoV just don't have them. Note also that while MERS does it uses CD26 not ACE2 to bind to.
    As scientists begin to work on the problem towards peer reviewed publication they have been using virological.org to clarify their thoughts and then biorxiv.org before the paper is available for pre-review publication on the journals site - all of these are open access and are goto sites for early information.
    Click image for larger version  Name:	cov protien binding.JPG Views:	129 Size:	140.5 KB ID:	826926

    Click image for larger version  Name:	ncov spike insertions.JPG Views:	130 Size:	461.6 KB ID:	826933
    This link is to the article pathfinder translated and posted re. finding the bat samples. It is quite long but I include it as it shows firstly how much effort goes in to getting samples from wild animals which is why the sequence databases have so few of them. The second point is (from memory) for all their years of work they got 3 live virus samples and 14(?) sequences and all from one cave. The table above holds most of the relevant sequences that exist and if 14 of them came from one cave over a short period how confident should we be they are a realistic representative gene pool. Within these 14 sequences they had all the genes needed to make SARS - with a bit of cut'n'paste. This a problem I have found in flu, lots of one sub-type in a waterfowl only to find all but a couple were netted by one team at one spot over 2 days.

    Epidemiology.

    The pattern of introductions has been exactly what you would expect for a respiratory disease with a single introduction. Clustering about case zero with spread to other areas with high traffic to the epicentre which is creating new geographically and temporally independent clusters. This pattern should become more confused as cross seeding between the new clusters – rather than all coming from a common point source (Wuhan) – starts making the origins of new clusters harder to locate. ‘Self-sustaining clusters’ are those where you consider only locally generated extended transmission chains and not those patients, or their close contacts, who came (or are still coming in) from another area. We are seeing this in other areas in China and early signs in other countries. Unless these other countries can catch every incubating carrier at the boarder – which seems highly unlikely - I see no reason this pattern should not be repeated everywhere else. When modelling the spread and impact of a disease other metrics come into play.

    R0(R naught) is how many new hosts each current host infects directly. It is not a fixed number for a given disease but will vary both by location, and over time, and can be depressed deliberately by our attempts at quarantine, hand hygiene, masks, social distancing etc. A R0 above 1 implies continued spread below 1 and the outbreak peters out, numbers a little above 1 are amenable to wrestling below 1 with interventions but 2 or above is going to merely slow not stop the spread as the necessary interventions would be impractical. To get a decent estimate of R0 we need accurate numbers of infected and new infections but until testing capacity gets close to matching everyone we would like to test this can only be a rough estimate with a large margin of error. It is however very important in calculating treatment capacity, as each city cluster grows and wains it puts terrible strain on medical surge capacity. Once capacity is exceeded treatment of even severe cases becomes impossible and the fatality rate will rise, regardless of how good/advanced a nation’s health care facilities are, as anyone above the capacity limit will not benefit from them. If you cannot stop spread then slowing becomes the priority so, while the total patient load may be the same, distributing them over a long time means few patients above the surge limit and better treatment for more people.

    CAR (clinical attack rate) how many patients catch a disease divided by the susceptible population. Who is susceptible? Homo sapiens would not have been very successful, and may not have survived as a species, without significant diversity in immunity. While you or I may die it is the variation across all of us that stop us from getting wiped out. For all the diseases I know of at least some of us have a natural immunity and we all handle infections differently. Even if everybody is challenged by the virus some will not get infected, some will get infected and recover (with or without symptoms) while developing antibodies others will die – which ever route they take all of these are no longer part of the susceptible population and increase the herd immunity while depressing the R0. The elephant in the room is the first of these for which we have no way of deriving a reliable estimate for at this stage, the others are insignificant at the moment but will grow over time.

    CFR (Case Fatality Rate) number who die/number of infected. Used as a proxy for disease severity it is again dependent on the true number of infections (including mild & subclinical) which again we do not know due to lack of testing across all of the clinical severity spectrum.


    Notes on disease progression.

    There is some evidence that patients can be infectious almost immediately and asymptomatically but I expect them to be much more infectious if they become severely clinically ill. They seem to become symptomatic after ~6 days, if ill enough to warrant testing and found positive they will be treated but not ‘cured’ until virus free for 2 weeks (estimated time before deemed safe from starting further spread), so there is going to be a time lag between those who died and those declared virus free who came into the system on the same day. To compare the two for CFR estimates you would need to be taking the numbers of survivors coming out of the system a couple of weeks after the death figures, with an adjustment for outbreak growth, and that still does not allow for those infected but never tested.

    Conclusion

    Much of the above is an explanation of my reasoning in posting that I was expecting this to most closely resemble H1N1(2009), in terms of impact and spread, which seemed at odds with the discussion consensus of a CFR of 2%+. This would be similar or worse than H1N1(1918) - assuming a similar 'susceptible population' size - leading to over 100 million deaths (allowing for global population growth). 1918 saw 25 million dead in the first 25 weeks (according to wikipedia) which feels wrong for this outbreak. I may be way off the mark - time will tell.
    Attached Files
    Last edited by JJackson; February 2nd, 2020, 10:56 PM.

  • #2
    JJackson - thank you for a most excellent post and summary of the current position on all the various elements you have covered here. I greatly value your expertise and knowledge. Thanks again for putting some perspective on all these elements.

    Comment


    • kiwibird
      kiwibird commented
      Editing a comment
      JJackson thank you. I look forward to reading further thoughts and updates from you.

  • #3
    Thank you, JJackson! I appreciate your time to give us some background. I know I still know little, but it is a lot more than I knew before.
    “‘i love myself.’ the quietest. simplest. most powerful. revolution ever.” ---- nayyirah waheed
    Avatar: Franz Marc, Liegender Hund im Schnee 1911 (My posts are not intended as advice or professional assessments of any kind.)

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    • #4
      Thank you for that thoughtful work. I changed the title to reflect the temporary name for this disease so that the thread will google better.

      Comment


      • #5
        Thank'you JJackson, very interesting. Are you a virologist or an epidemiologist?

        Comment


        • #6
          Thanks all. As promised - if a little late - I have made some updates.
          Sharon - thanks for doing the formatting, I was getting tired and not thinking clearly, so opted to just dump the draft text and fix it later.
          tetano - no academic qualifications. What I know is all based on reading at FluTrackers (albeit for a very long time) and links. It is good here all these nice people keep finding interesting things for me to read. Much of any credit should go to you as I am a primary recipient of your postings to the Scientific library most of what I know came from there and I am deeply in your dept.
          Last edited by JJackson; February 2nd, 2020, 02:58 PM.

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          • #7
            Thank you JJackson for taking the time to write this up for us all.

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            • #8
              Having written the opening post I have now found a truly excellent overview thanks to the author linking it at virological.org . This guy does have credentials, bucket loads of them, having been on the cutting edge of SARS, MERS, Ebola and H1N1(2009). It is written specifically for a general audience, not his peers, but the hard science is there in abundance if you want it. The bad news - it is 80 pages long plus references, I am on page 33 and have already doubled my knowledge on the protein structures and functions. The good news is I have not read anything, yet, which causes me to change my thinking in the first post.
              http://virological.org/uploads/short...Yw2rfJASAS.pdf
              Last edited by JJackson; February 3rd, 2020, 03:56 AM.

              Comment


              • #9
                yes, I had seen that. Linked to it in other posts ... but didn't read it .. only "flying" over it. Mostly text, you can't skip things.
                I'm interested in expert panflu damage estimates
                my current links: [url]http://bit.ly/hFI7H[/url] ILI-charts: [url]http://bit.ly/CcRgT[/url]

                Comment


                • #10
                  Preliminary Thoughts update.
                  It is 6 weeks since I wrote the first post and not a lot has changed. There are more cases and some more spread but we have not advanced a great deal in terms of our understanding of the disease. In 2009 I started a thread for new visitors in anticipation of the confusion the numbers, and case definitions, which were beginning to come out in the MSM, were going to cause. The first post in this thread aimed to do the same but was a little more technical as the target audience was more FT's regular posters.

                  The numbers & case definitions are again causing problems for the same reasons. Test capacity is slowly closing the gap on the numbers the CCDC would like tested in the epicentre. In the UK, where there is ample capacity at present, to get 9 positive tests they tested 2500 people. Each person is likely to need multiple tests, early testing often fails as viral load does not reach the test's diagnostic sensitivity threshold, once confirmed, tests may be taken to check on viral load progression under different treatment regimes and the patient will need two clear test prior to release. Currently the false negatives are as high as 50% and the US CDC is still the only test facility in the US, as the reagents package they shipped turned out not to work adequately across the range of RT PCR labs slated for testing. Sally started an excellent thread covering in more detail where problems can/are occurring, there are many steps and small errors at any point all end up aggregating and reducing the test's reliability. As a new disease sample collection, reagents, procedures, primers and probes all need fine tuning which should increase sensitivity and reduce errors.

                  The combination of a shortage of tests and the reliability problem addressed above have caused a change in case definitions so CT scans that show marked similarity to typical confirmed cases are being accepted as confirmed. While PCR is normally deemed the gold standard for disease confirmation here there are still problems and scan data is probably as reliable. The increased test capacity is allowing for more contacts testing amongst mild cases which is finding asymptomatic infections. The data collected from this group should help to shed light on how much undetected spread is likely to be going on. Serological testing should give much better data but is normally not taken until a month post infection. The candidates for testing here should be the first cured cases, to get a baseline on antibody development and concentrations, followed by a wider examination of the regular visitors to the fish and game market.
                  For all the reasons outline in the first post calculation of epidemiological numbers like CFR and Ro are still dodgy. Based more on overall observation of the outbreak than on calculation I will stick my neck out and suggest a Ro of 2 to 3 and a CFR of 0.5 to 1 – as I say a guess. The apparent stagnation in the increase in numbers is, I think, real and a reflection of the massive and unprecedented actions taken by China to slow/stop spread. The question is ‘how long can they keep this level of containment up?’ The economic and social consequences are enormous. I still do not think it will be enough, while spread outside China may be contained for the moment, in China there is still too much spread between areas. International land boarders are going to be much more difficult to quarantine than ports and airports and, while the creeping spread on land may be much slower than by air, it is going to get into regions without the resources or central control China can bring to bear.
                  The sequence data continues to increase with plenty of random nucleotide mutations but few are resulting in AA changes and, where they have occurred, there is no obvious pattern that can be attributed to host adaption. I have provide links below to a site that is updated regularly with new GISAID sequences where hovering over nodes in the phylogenic tree show the base and AA changes, I have also link to Sally’s thread on the problems encountered in getting clean tests.

                  https://nextstrain.org/ncov?branchLabel=aa&m=num_date set the tree options to 'rectangular' and the 'branch labels' to AA.
                  https://flutrackers.com/forum/forum/...eumonia-caused

                  Comment


                  • #11
                    Things are moving rapidly now and the situation is very different. China has done a phenomenal job in containment but now S. Korea, Italy & Iran are all now reprising the experience of Wuhan at the outset. Again the numbers are causing a problem.
                    Firstly it is important to understand the size of China, which is better thought of as a continent than a country. The world has a population about 7.8 billion and 60% of them are Asians. China’s 1.4 billion is larger than any continent, accept its own, and greater than Europe and N. America combined. It is divided into 31 provinces the largest being Guangdong which, if it was a country, would replace the Philippines as the 13th largest. Hubei is much smaller and is only slightly smaller than the combined size of Texas & California and about the same as the 4 countries that constitute the UK.

                    Now for some key dates. 31st Dec China reports its first Pneumonia of unknown cause, it took them 3 days to find the original cluster of 44 cases and on 7th Jan. they reported the causative agent, on the 11th the epidemiological team found the fish market source and on the 12th they released the first sequence. The first two cases outside China were reported on the 13th and 14th. So to recap China managed to pick up the first case, against a background of about 150 community acquired pneumonia cases a day in Wuhan, find the clusters source, identify it as COV, sequence it & report all of this to the world via the WHO in two weeks and before any cases had shown up outside China. Nothing like this has ever been done before and if you look back at the H1N1(2009) outbreak the US and Mexico were far slower at getting a handle on what was going on, and with a much better understood disease and massive flu surveillance network.

                    Now if we look at S. Korea, Italy & Iran they have populations of 50, 60 & 84 million respectively putting them in the same ball park, population wise, as Hubei. Iran is a special case as it is suffering from an economic war which will have hampered its ability to cope and now has a per capita GDP slightly lower than China where as S. Korea and Italy, GDP per cap, are twice as rich as China. So how well are they responding?

                    S. Korea reported its first case on Jan. 20th today they reported 813 new cases bringing the total 3150 confirmed cases and 17 deaths (only China seems to be submitting suspected case numbers despite repeated requests from WHO for this important data). If we look at Henan, which is a neighbouring province to Hubei and has twice S Korea’s population, they currently have 20 deaths and 1272 confirmed cases with no deaths or confirmed case and one suspect case today. Outside of Hubei China’s 1.4 billion reported 23 confirmed cases, 120 suspect cases and 3 deaths. China is not the problem anymore. The graphs below show the epi curves for Wuhan and China (from the WHO China fact finding mission report).

                    Click image for larger version  Name:	wuhan.JPG Views:	0 Size:	56.8 KB ID:	832507

                    Click image for larger version  Name:	china.JPG Views:	0 Size:	47.4 KB ID:	832506
                    There are two possible explanations either China is giving the rest of the world an object lesson in how to handle a zoonotic outbreak or it is somehow managing to hide a massive uncontrolled outbreak. The English language MSM (and sadly too many FT posters) seem to believe the later I and the WHO believe the former. If I am right I fear for the rest of us. As I pointed out in the first post in this thread neither the R0 nor CFR are fixed numbers for a disease and will reflect the containment and treatment measures taken. I also posted a guestimate for the R0 of 2 to 3 and CFR of 1% but these were based on data coming out of China which I now think has handled its problem far better than any other country is likely to do and expect much worse elsewhere. The CFR age distribution is very worrying with a 10%+ CFR for the over 80’s that’s 17 million (twice the population of New York) US seniors and both my parents.
                    Attached Files

                    Comment


                    • #12
                      JJackson - If these countries were to work to contain, how would they do so and at what point?
                      In California would that be now? And what part? The Bay Area? The State? In Italy? Should the whole country be locked down? Or just the regions affected? I am asking sincerely because a realistic strategy eludes common people like me.

                      One thing China does have that most the other countries do not is human resources. Same disease, same attack rate, same amplification of illness ... but the number of people to help contain is NOT the same.

                      I have seen few updates on the type of quarantine measures still in place in China and other countries. Did Italy stop trains to Northern Sections? Japan closed schools, but have they shut down businesses and transportation?

                      Comment


                      • #13
                        Curiosity the lesson learnt from China regarding containment I would summarise as 1] If you are not clear what is going on but there is evidence of transmission in a geographic area shut things down massively until you do understand. 2] Support anyone caught in the shut down with information, practical and psychological help. 3] Get your population to understand it is everyone's responsibility to do what they can to help. 4] One size does not fit all and local authorities need flexibility to tailor measures to local circumstances but within, and understanding, the bigger plan. 5] Be flexible if things are not working change them. (the clinical guidance has been changed 6 times already). 6] If you are in a low impact area send your medical staff and all their equipment and PPE to the hot spots, do not stock pile it in anticipation of a wave in your area.

                        China is beginning a phased return to work in selected areas but it will be high priority products (PPE & drug chemical precursors etc) and in areas with little or no transmission, which is now most of China. This will increase transmission but, if done slowly while monitoring the effects, it should not overload the system, if they begin to loose control they will re-apply them.
                        The Chinese culture is very different to the US where the curtailing of freedom of movement or anything else viewed as infringement of civil liberties or the ability to earn money are likely to meet resistance. Additionally State and local authorities value their independence from central government and may set their own rules leading to very different spread in different areas (as happened in 1918). Healthcare provision is a commercial operation with many independent companies who are likely to be less amenable to sending their staff or PPE to areas that need them.
                        These are observation of an outsider so I don't really understand what may be workable in a US context but I do worry about some of the US reports giving the impression that China is a lower income country without our advanced health system and that the US would handle it better. Time will tell but I agree with the UN's head of COVID response (Mike Ryan) if I catch this I would want to be treated in China.
                        Yes China has the numbers, but that cuts both ways, big population means more potential patients as well as more people to help them. I don't think scale matters much and any country or area can use its unaffected population to support its clusters as long as they do not let growth overwhelm capacity, through adequate containment, and the unaffected are willing to go into the epicentre.
                        I have not been following the containment measures outside China in any detail so can not comment, beyond saying that it is too early to judge their efficacy anyway which is why I have not taken the time to look at these actions.

                        Comment


                        • #14
                          Originally posted by JJackson View Post
                          Curiosity the lesson learnt from China regarding containment I would summarise as 1] If you are not clear what is going on but there is evidence of transmission in a geographic area shut things down massively until you do understand. 2] Support anyone caught in the shut down with information, practical and psychological help. 3] Get your population to understand it is everyone's responsibility to do what they can to help. 4] One size does not fit all and local authorities need flexibility to tailor measures to local circumstances but within, and understanding, the bigger plan. 5] Be flexible if things are not working change them. (the clinical guidance has been changed 6 times already). 6] If you are in a low impact area send your medical staff and all their equipment and PPE to the hot spots, do not stock pile it in anticipation of a wave in your area.
                          .
                          Clear lessons. I will cite in other settings.
                          Thought has a dual purpose in ethics: to affirm life, and to lead from ethical impulses to a rational course of action - Teaching Reverence for Life -Albert Schweitzer. JT

                          Comment


                          • JJackson
                            JJackson commented
                            Editing a comment
                            There is one more point and it probably should have been the first. Speed!
                            The main enemy on a battle field is a lack of information and China has put together a command center that is using 5G coms to each contact trace team so they can ask for expertise and feed data into the system as it is being collected. Ditto for labs, hospitals and researcher.
                            The Ebola outbreak taught us that bringing help into an area experiencing exponential growth too slowly is hopeless. If you have a doubling time of 10 days and need a 1000 beds you actually need 8000 if it is going to take you a month to get them built, staffed and fully operational. China seems to have absorbed this and applied it, they converted a stadium into a 1000 bed hospital fully staffed (all of whom had had PPE training) complete with CT scanners etc. in 24hrs.
                            They have sent in an additional 40,000 medical staff but what I loved was that anyone entering in these teams had to come with all the equipment and PPE they would need and be full trained in their use and know what they were going to do. They would be kept as a team and given a unit to run. All other logistics (food, accommodation, transportation) are handled by non medical teams.
                            Last edited by JJackson; March 8th, 2020, 08:51 AM.

                        • #15
                          wikipedia has a good summary about the measures :https://en.wikipedia.org/wiki/2019%E...Mainland_China
                          more detailed in the WHO-China-Mission report , with a nice summary from @kaka , I wrote about it here:
                          https://thisbluemarble.com/showthread.php?t=79399
                          Note also their sophisticated case tracking with AI,apps, lots of teams.
                          As I understood in most parts of China there were almost no measures, except prolonged holiday. In come cities outside
                          Hubei i.e. Zhejiang they allowed only 1 person per household to shop every 2 days
                          I'm interested in expert panflu damage estimates
                          my current links: [url]http://bit.ly/hFI7H[/url] ILI-charts: [url]http://bit.ly/CcRgT[/url]

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