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18 minutes ago, rh3000 said:

Have a listen to that Chris Smith interview I linked you to - WHO investigates all sorts of shit - doesn't make it so....

I did.  The challenge at the moment is that there is no authority on everything. Indeed there is little certainty and no authority on many, many (most) discrete attributes of this disease currently.  There are threads of this disease being explored and researched and tested and observed and monitored and treated on so many layers and in so many places even while there are some very fundamental questions that are yet to be answered.  And for that, there is a growing body of observance, and a slowly growing body of substantive research that will help to further categorise this virus and its capabilities with a higher degree of certainty, probably over the next 6-12 mths. 

When you have access to the research articles arriving by the hour from academics and researchers and clinicians and virologists and epidemiologists even while the medical response to this disease remains in overdrive, then you may appreciate the potential significance of some of the things you're downplaying - particularly given NZ's response to this pandemic to date.  Yes, the citations I provided are publicly accessible mainstream articles - that is perhaps more appropriate for a forum such as this, largely read by lay people in medico-science. I am not the doom merchant delivering news with a sense of foreboding, merely someone pointing out that this virus may not be ready to be as certainly defeated for now as we may all hope. 

Singapore was regarded as more ready than almost all and the nation state others should aspire to mirror in pandemic management.  Its second wave is already more significant than its first, and it's scarcely begun. We need to give this virus no way out.  It's already shown it needs little assistance to wreak havoc even after it was apparently contained.

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COVID-19 infection: the perspectives on immune responses
Yufang Shi
Ying WangChangshun ShaoJianan HuangJianhe GanXiaoping HuangEnrico BucciMauro PiacentiniGiuseppe Ippolito & Gerry Melino 

Cell Death & Differentiation (2020)Cite this article

More than 100 years since the outbreak of the 1918 influenza pandemic, we now seem to face another pandemic. The outbreak of the new coronavirus (SARS-CoV-2) infection is spreading to every continent, forcing us to live with this virus for perhaps a long time. Scientists and clinicians have learned much of coronavirus disease 2019, COVID-19, and its pathogenesis [1]: not all people exposed to SARS-CoV-2 are infected and not all infected patients develop severe respiratory illness. Accordingly, SARS-CoV-2 infection can be roughly divided into three stages: stage I, an asymptomatic incubation period with or without detectable virus; stage II, non-severe symptomatic period with the presence of virus; stage III, severe respiratory symptomatic stage with high viral load [2]. From the point of view of prevention, individuals at stage I, the stealth carriers, are the least manageable because, at least on some occasions, they spread the virus unknowingly: indeed, the first asymptomatic transmission has been reported in Germany [3]. The role of asymptomatic SARS-CoV-2 infected individuals in disseminating the infection remains to be defined.

Among over 1000 patients analyzed in Wuhan, except occasionally in children and adolescence, it infects all the other age groups evenly. About 15% of the confirmed cases progress to the severe phase, although there is a higher chance for patients over 65 to progress into the severe phase [1]. One of the biggest unanswered questions is why some develop severe disease, whilst others do not. Clearly, the conventional wisdom based on overall immunity of the infected patients cannot explain this broad spectrum in disease presentation.

Two-phase immune responses induced by COVID-19 infection

Clinically, the immune responses induced by SARS-CoV-2 infection are two phased. During the incubation and non-severe stages, a specific adaptive immune response is required to eliminate the virus and to preclude disease progression to severe stages. Therefore, strategies to boost immune responses (anti-sera or pegylated IFNα) at this stage are certainly important. For the development of an endogenous protective immune response at the incubation and non-severe stages, the host should be in good general health and an appropriate genetic background (e.g. HLA) that elicits specific antiviral immunity. Genetic differences are well-known to contribute to individual variations in the immune response to pathogens. However, when a protective immune response is impaired, virus will propagate and massive destruction of the affected tissues will occur, especially in organs that have high ACE2 expression, such as intestine and kidney. The damaged cells induce innate inflammation in the lungs that is largely mediated by pro-inflammatory macrophages and granulocytes. Lung inflammation is the main cause of life-threatening respiratory disorders at the severe stage [4]. Therefore, good general health may not be advantageous for patients who have advanced to the severe stage: once severe lung damage occurs, efforts should be made to suppress inflammation and to manage the symptoms.

Alarmingly, after discharge from hospital, some patients remain/return viral positive and others even relapse. This indicates that a virus-eliminating immune response to SARS-CoV-2 may be difficult to induce at least in some patients and vaccines may not work in these individuals. Those recovered from the non-severe stage should be monitored for the virus together with T/B cell responses. These scenarios should be considered when determining the strategies of vaccine development. In addition, there are many types or subtypes of coronavirus. Thus, if vaccines directly targeting SARS-CoV-2 prove to be difficult to develop, the Edward Jenner approach should be considered.

Cytokine storm and lung damage

The cytokine release syndrome (CRS) seems to affect patients with severe conditions. Since lymphocytopenia is often seen in severe COVID-19 patients, the CRS caused by SARS-CoV-2 virus has to be mediated by leukocytes other than T cells, as in patients receiving CAR-T therapy; a high WBC-count is common, suggesting it, in association with lymphocytopenia, as a differential diagnostic criterion for COVID-19. In any case, blocking IL-6 may be effective. Blocking IL-1 and TNF may also benefit patients. Although various clinical sites in China have announced the use of mesenchymal stromal/stem cells (MSCs) in severe cases with COVID-19 infection, solid results have yet to be seen. One caveat is that MSCs need to be activated by IFNγ to exert their anti-inflammatory effects, which may be absent in severely affected patients as T cells are not well activated by SARS-CoV-2 infection. To enhance effectiveness, one could consider employing the “licensing-approach”: pretreat MSCs with IFNγ with/without TNF or IL-1 [5]. Such cytokine-licensed MSCs could be more effective in the suppression of hyperactive immune response and promotion of tissue repair, as licensed-MSCs are effective in LPS-induced acute lung damage [6].

Lung damage is a major hurdle to recovery in those severe patients. Through producing various growth factors, MSCs may help repair of the damaged lung tissue. It is important to mention that various studies have shown that in animal models with bleomycin-induced lung injury, vitamin B3 (niacin or nicotinamide) is highly effective in preventing lung tissue damage [7]. It might be a wise approach to supply this food supplement to the COVID-19 patients.

HLA haplotypes and SARS-CoV-2 infection

The major-histocompatibility-complex antigen loci (HLA) are the prototypical candidates for genetic susceptibility to infectious diseases [8, 9]. Haplotype HLA-loci variability results from selective pressure during co-evolution with pathogens. Immunologists have found that T-cell antigen receptors, on CD4+ or CD8+ T cells recognize the conformational structure of the antigen-binding-grove together with the associated antigen peptides. Therefore, different HLA haplotypes are associated with distinct disease susceptibilities. The repertoire of the HLA molecules composing a haplotype determines the survival during evolution. Accordingly, it seems advantageous to have HLA molecules with increased binding specificities to the SARS-CoV-2 virus peptides on the cell surface of antigen-presenting cells. Indeed, the susceptibility to various infectious diseases such as tuberculosis, leprosy, HIV, hepatitis B, and influenza is associated with specific HLA haplotypes. Particular murine MHC class II haplotypes are associated with the susceptibility to influenza. In man, HLA class I is also associated with H1N1 infections: HLA-A*11, HLA-B*35, and HLA-DRB1*10 confers susceptibility to influenza A(H1N1)pdm09 infection [10]. Therefore, it is imperative to study whether specific HLA loci are associated with the development of anti-SARS-CoV-2 immunity and, if so, to identify the alleles, either class I or II, that demonstrate induction of protective immunity. Once the dominant alleles are identified, simple detection kits can be developed. Such information is critical for (1) strategic clinical management; (2) evaluation of the efficacy of vaccination in different individuals in the general population; (3) assignment of clinical professional and managerial teams amid interactions with COVID-19 patients.

Hyaluronan: a potential cause of fatalities

The innate immune response to tissue damage caused by the virus could lead to acute respiratory distress syndrome (ARDS), in which respiratory failure is characterized by the rapid onset of widespread inflammation in the lungs and subsequent fatality [4]. The symptoms of ARDS patients include short/rapid breathing, and cyanosis. Severe patients admitted to intensive care units often require mechanical ventilators and those unable to breath have to be connected to extracorporeal membrane oxygenation (ECMO) to support life [11]. CT images revealed that there are characteristic white patches called “ground glass”, containing fluid in the lungs [2]. Recent autopsies have confirmed that the lungs are filled with clear liquid jelly, much resembling the lungs of wet drowning [4]. Although the nature of the clear jelly has yet to be determined, hyaluronan (HA) is associated with ARDS [12]; moreover, during SARS infection, the production and regulation of hyaluronan is defective. The levels of inflammatory cytokines (IL-1, TNF) are high in the lungs of COVID-19 patients and these cytokines are strong inducers of HA-synthase-2 (HAS2) in CD31+ endothelium, EpCAM+ lung alveolar epithelial cells, and fibroblasts [13]. Importantly, HA has the ability to absorb water up to 1000 times its molecular weight. Therefore, reducing the presence or inhibiting the production of HA holds a great promise in helping COVID-19 patients breathe. Doctors can simply provide patients medical grade hyaluronidase to reduce the accumulation of HA and thus to clear the jelly in the lung. In animal models, influenza-induced breathing difficulties can be relieved by intranasal administration of hyaluronidase. Doctors can also use a clinically approved bile therapy drug, Hymecromone (4-Methylumbelliferone, 4-MU), an inhibitor of HAS2 [14]. LPS-induced lung inflammation can be relieved by 4-MU. 4-MU or its chemical derivatives exist widely in various herbs used in traditional Chinese medicine, which may explain the observed effectiveness of combined herbal medicine in some patients.

Overall, this synopsis is based on some clinical common sense. We propose some simple, but largely ignored, approaches to the treatment of COVID-19 patients (Fig. 1). We believe that the two-phase division is very important: the first immune defense-based protective phase and the second inflammation-driven damaging phase. Doctors should try to boost immune responses during the first, while suppressing it in the second phase. Since Vitamin B3 is highly lung protective, it should be used as soon as coughing begins. When breathing difficulty becomes apparent, hyaluronidase can be used intratracheally and at the same time 4-MU can be given to inhibit HAS2. Of course, HLA typing will provide susceptibility information for strategizing prevention, treatment, vaccination, and clinical approaches. We hope that some of the above ideas can be employed to help combat this deadly contagious disease of increasing incidence around the world.

Fig. 1: Schematic representation of the progression of COVID-19 infection and potential adjuvant interventions.
 

figure1

After an incubation period, the invading COVID-19 virus causes non-severe symptoms and elicits protective immune responses. The successful elimination of the infection relies on the health status and the HLA haplotype of the infected individual. In this period, strategies to boost immune response can be applied. If the general health status and the HLA haplotype of the infected individual do not eliminate the virus, the patient then enters the severe stage, when strong damaging inflammatory response occurs, especially in the lungs. At this stage, inhibition of hyaluronan synthase and elimination of hyaluronan can be prescribed. Cytokine activated mesenchymal stem cells can be used to block inflammation and promote tissue reparation. Vitamin B3 can be given to patients starting to have lung CT image abnormalities.

References

  1. Guan WJ, Ni ZY, Hu Y, Liang WH, Ou CQ, He JX, et al. Clinical Characteristics of Coronavirus Disease 2019 in China. The New England journal of medicine. 2020. https://doi.org/10.1056/NEJMoa2002032.

  2. Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. Jama. 2020. https://doi.org/10.1001/jama.2020.1585.

  3. Rothe C, Schunk M, Sothmann P, Bretzel G, Froeschl G, Wallrauch C, et al. Transmission of 2019-nCoV Infection from an Asymptomatic Contact in Germany. The New England journal of medicine. 2020;382:970-1. https://doi.org/10.1056/NEJMc2001468

  4. Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. The Lancet Respiratory medicine. 2020. https://doi.org/10.1016/S2213-2600(20)30076-X.

  5. Wang Y, Chen X, Cao W, Shi Y. Plasticity of mesenchymal stem cells in immunomodulation: pathological and therapeutic implications. Nat Immunol. 2014;15:1009–16. https://doi.org/10.1038/ni.3002

  6. Wang G, Cao K, Liu K, Xue Y, Roberts AI, Li F, et al. Kynurenic acid, an IDO metabolite, controls TSG-6-mediated immunosuppression of human mesenchymal stem cells. Cell death and differentiation. 2018;25:1209-23. https://doi.org/10.1038/s41418-017-0006-2

  7. Nagai A, Matsumiya H, Hayashi M, Yasui S, Okamoto H, Konno K. Effects of nicotinamide and niacin on bleomycin-induced acute injury and subsequent fibrosis in hamster lungs. Experimental lung research. 1994;20:263-81. https://doi.org/10.3109/01902149409064387

  8. Blackwell JM, Jamieson SE, Burgner D. HLA and infectious diseases. Clin Microbiol Rev. 2009;22:370–85. https://doi.org/10.1128/CMR.00048-08

  9. Matzaraki V, Kumar V, Wijmenga C, Zhernakova A. The MHC locus and genetic susceptibility to autoimmune and infectious diseases. Genome Biol. 2017;18:76. https://doi.org/10.1186/s13059-017-1207-1

  10. Dutta M, Dutta P, Medhi S, Borkakoty B, Biswas D. Polymorphism of HLA class I and class II alleles in influenza A(H1N1)pdm09 virus infected population of Assam, Northeast India. J Med Virol. 2018;90:854–60. https://doi.org/10.1002/jmv.25018

  11. MacLaren G, Fisher D, Brodie D. Preparing for the most critically Ill patients with COVID-19: the potential role of extracorporeal membrane oxygenation. JAMA. 2020. https://doi.org/10.1001/jama.2020.2342.

  12. Hallgren R, Samuelsson T, Laurent TC, Modig J. Accumulation of hyaluronan (hyaluronic acid) in the lung in adult respiratory distress syndrome. Am Rev Respir Dis. 1989;139:682–7. https://doi.org/10.1164/ajrccm/139.3.682

  13. Bell TJ, B O, Morgan DJ, Salek-Ardakani S, Jagger C, Fujimori T, et al. Defective lung function following influenza virus is due to prolonged, reversible hyaluronan synthesis. Matrix Biol. 2018;80:14–28

  14. Collum SD, Chen NY, Hernandez AM, Hanmandlu A, Sweeney H, Mertens TCJ, et al. Inhibition of hyaluronan synthesis attenuates pulmonary hypertension associated with lung fibrosis. British journal of pharmacology. 2017;174:3 284–301. https://doi.org/10.1111/bph.13947

 

Acknowledgements

The work has been partially supported by grants from the National Key R&D Program of China (2018YFA0107500), the Scientific Innovation Project of the Chinese Academy of Sciences (XDA16020403), Suzhou 2020 Emergency Innovation Funding on COVID-19 Infection, the National Natural Science Foundation of China (81530043, 81861138015, 31771641 and 81571612), PANDORA-ID-NET (to GI), the European & Developing Countries Clinical Trials Partner-ship, supported under Horizon 2020 to GI), Italian Ministry of Health (RC, 1 to MP and GI).

Author information

Affiliations

  1. The First Affiliated Hospital of Soochow University, State Key Laboratory of Radiation Medicine and Protection, Institutes for Translational Medicine, Soochow University Medical College, Suzhou, China
    • Yufang Shi
    • , Changshun Shao
    • , Jianan Huang
    • , Jianhe Gan
    •  & Xiaoping Huang
  2. Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, China
    • Yufang Shi
    •  & Ying Wang
  3. Sbarro Health Research Organization, Temple University, Philadelphia, PA, 19122, USA
    • Enrico Bucci
  4. Resis Srl, 10010, Samone, TO, Italy
    • Enrico Bucci
  5. National Institute for Infectious Diseases ‘Lazzaro Spallanzani” IRCCS, 00149, Rome, Italy
    • Mauro Piacentini
    •  & Giuseppe Ippolito
  6. Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy
    • Gerry Melino
  7. Medical Research Council (MRC) Toxicology Unit, University of Cambridge, Cambridge, CB2 1QP, UK
    • Gerry Melino

Corresponding author

Correspondence to Yufang Shi.

Ethics declarations

Conflict of interest

The authors declare that they have no relevant conflict of interest.

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Coronavirus: Low antibody levels raise questions about reinfection risk

  • Scientists in Shanghai say some recovered patients show no signs of the neutralising proteins
  • Early-stage findings could have implications for vaccine development and herd immunity

Researchers in Shanghai found low levels of coronavirus antibodies in some people who had recently recovered from Covid-19.

Researchers in Shanghai hope to determine whether some recovered coronavirus patients have a higher risk of reinfection after finding surprisingly low levels of Covid-19 antibodies in a number of people discharged from hospital.

A team from Fudan University analysed blood samples from 175 patients discharged from the Shanghai Public Health Clinical Centre and found that nearly a third had unexpectedly low levels of antibodies.

In some cases, antibodies could not be detected at all.

“Whether these patients were at high risk of rebound or reinfection should be explored in further studies,” the team wrote in preliminary research released on Monday on Medrxiv.org, an online platform for preprint papers.

Although the study was preliminary and not peer-reviewed, it was the world’s first systematic examination of antibody levels in patients who had recovered from Covid-19, the disease caused by the coronavirus, the researchers said.

All of the patients had recently recovered from mild symptoms of the disease and most of those with low antibody levels were young. The researchers excluded patients who had been admitted to intensive care units because many of them already had antibodies from donated blood plasma.

Antibodies are generated by the immune system and have unique chemical structures to inhibit specific pathogens. The coronavirus antibody intercepts the spike protein on the viral envelope to prevent it from binding with human cells.

The researchers said they were surprised to find that the antibody “titer” value in about a third of the patients was less than 500, a level that might be too low to provide protection.

“About 30 per cent of patients failed to develop high titers of neutralising antibodies after Covid-19 infection. However, the disease duration of these patients compared to others was similar," they said.

The team also found that antibody levels rose with age, with people in the 60-85 age group displaying more than three times the amount of antibodies as people in the 15-39 age group.

The low amounts of antibodies could affect herd immunity, resistance to the disease among the general population to stop its spread.

“This is a clinical observation we made at the front line. What this will mean to herd immunity will require more data from other parts of the world,” Professor Huang Jinghe, the leader of the team, said on Tuesday.

Huang said 10 of the patients in the study had an antibody presence so low it could not even be detected in the laboratory.

These patients experienced typical Covid-19 symptoms including fever, chill and a cough, but might have beaten back the virus with other parts of the immune system such as T-cells or cytokines.

How they did this was still unclear.

“Vaccine developers may need to pay particular attention to these patients,” Huang said. If the real virus could not induce antibody response, the weakened version in the vaccine might not work in these patients either.

The researchers also found that the Covid-19 antibody could bind with a distantly related strain that caused an outbreak of severe acute respiratory syndrome (Sars) in 2003.

But the binding could not suppress Sars virus replication in cells, dashing hopes of developing a vaccine for two or even more coronavirus strains at once.

Many questions about the virus remain unanswered, including how the virus made the jump from animal to humans; why some people die from Covid-19 and others are asymptomatic; and why some recovered patients test positive again.

Professor Wang Chen, a senior scientific adviser to the central government, told state media on Monday that it was way too early to declare victory against the disease even in China, where the situation was under control for now.

“Who knows whether this will become something like a seasonal flu, or chronic disease like hepatitis B, or just vanish like Sars?” he was quoted in the official Science and Technology Daily.

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1 hour ago, Skipstone said:

I did.  The challenge at the moment is that there is no authority on everything. Indeed there is little certainty and no authority on many, many (most) discrete attributes of this disease currently.  There are threads of this disease being explored and researched and tested and observed and monitored and treated on so many layers and in so many places even while there are some very fundamental questions that are yet to be answered.  And for that, there is a growing body of observance, and a slowly growing body of substantive research that will help to further categorise this virus and its capabilities with a higher degree of certainty, probably over the next 6-12 mths. 

When you have access to the research articles arriving by the hour from academics and researchers and clinicians and virologists and epidemiologists even while the medical response to this disease remains in overdrive, then you may appreciate the potential significance of some of the things you're downplaying - particularly given NZ's response to this pandemic to date.  Yes, the citations I provided are publicly accessible mainstream articles - that is perhaps more appropriate for a forum such as this, largely read by lay people in medico-science. I am not the doom merchant delivering news with a sense of foreboding, merely someone pointing out that this virus may not be ready to be as certainly defeated for now as we may all hope. 

Singapore was regarded as more ready than almost all and the nation state others should aspire to mirror in pandemic management.  Its second wave is already more significant than its first, and it's scarcely begun. We need to give this virus no way out.  It's already shown it needs little assistance to wreak havoc even after it was apparently contained.

Wasn't aware Singapore's second wave was reinfections... ?

Access to research papers isn't the problem, but pearl clutching at anecdotes is not a particularly valuable contribution for medico-scientists is it?

None is claiming it is defeated - only an idiot would do that but there's at least one of those running the USA.

Despite all the almost 2 million infections, there's still very little to suggest there isn't meaningful immunity upon recovery - for exactly how long of course no one knows until large groups no longer have any antibodies - that hasn't happened yet.

Me arguing with you does not mean I don't take COVID deadly seriously. Indeed NZ has taken it about as seriously as any other nation. When there is good evidence of meaningful rates if reinfection, then it will be a thing, until then it's just aberration or conjecture - which is not valid scientific fact.

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i take a few things from that

main ones being ...

the usefulness of the flattening the curve tactic effectively moves closer to doing nothing in both the long term  survival and financial costs for the epidemic

 

doing everything possible to eradicate the virus becomes a far more efficient action for promoting survival and lowering future health problems and the financial burden

 

this not only holds true for the viral attack/s on the person .. but also the problems that seem to be arising of longer term health effects due to the damage inflicted on the  lungs of some patients .. this damage will likely lower their life expectancy and exacerbate future health problems

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2 hours ago, rh3000 said:

Wasn't aware Singapore's second wave was reinfections... ?

Access to research papers isn't the problem, but pearl clutching at anecdotes is not a particularly valuable contribution for medico-scientists is it?

None is claiming it is defeated - only an idiot would do that but there's at least one of those running the USA.

Despite all the almost 2 million infections, there's still very little to suggest there isn't meaningful immunity upon recovery - for exactly how long of course no one knows until large groups no longer have any antibodies - that hasn't happened yet.

Me arguing with you does not mean I don't take COVID deadly seriously. Indeed NZ has taken it about as seriously as any other nation. When there is good evidence of meaningful rates if reinfection, then it will be a thing, until then it's just aberration or conjecture - which is not valid scientific fact. 

There has been precious little testing of immunity, because there is no simple antibody test yet that is remotely accurate enough for quick and certain mass testing.  So samples in studies such as these are small (typically ranging from a few to a few hundred patients) and research driven.  It's a bit like saying of CoViD-19 several weeks ago, we don't know how large this issue of infection is because we're not testing.  Or we don't know how much community transmission there is because we're not testing widely enough. 

What is already becoming clearer on the immunity front is that the assumed 2-3 year natural immunity post-infection will likely be realized in very few patients, if any.  A one year immunity is increasingly being viewed by researchers as a best case scenario, and for a significant percentage of patients any meaningful immunity at all without vaccination may be wishful.  To date this relative absence of antibodies seems particularly to be the case in the younger and arguably more social age groups making on-going transmission difficult to avoid without on-going distancing provisions.

You can argue all you like, but this research is vital, is a growing area of focus, and is increasingly looking like the next battleground in staving off waves of CoViD-19 until an effective  vaccination or other preventative treatment can be determined, tested, approved and delivered to the global populace.

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Maybe the AC can be raced on schedule but with an NZ-only public  fan presence (plus TV). It was always likely to be NZ that was the biggest ‘market’ by far, anyway.

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3 hours ago, Stingray~ said:

Maybe the AC can be raced on schedule but with an NZ-only public  fan presence (plus TV). It was always likely to be NZ that was the biggest ‘market’ by far, anyway.

Rather than risk our borders with importing the contenders boats gear and personnel there is a competitively active fleet of Mullet boats that could be raced in lieu for the AC.

TNZ would of course race in Orion.

3FCC875C-845C-4BF3-AF2C-0716666DE1CE.thumb.jpeg.b01937ffbb7997a799238be73b1135b0.jpeg

 

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1 hour ago, Priscilla said:

Rather than risk our borders with importing the contenders boats gear and personnel there is a competitively active fleet of Mullet boats that could be raced in lieu for the AC.

TNZ would of course race in Orion.

3FCC875C-845C-4BF3-AF2C-0716666DE1CE.thumb.jpeg.b01937ffbb7997a799238be73b1135b0.jpeg

 

For those interested in a dated sideline read about Auckland's Mullet boats... The Lipton Cup

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OK I have a theory to run by you all......

Tomorrow we're to be told what will and won't be allowed if we go out of full lockdown at the end of next week.

The general opinion seems to be that some of us will be allowed to go back to work, others not.

So the way I see it is, if construction of the bases is allowed to restart and ETNZ to start training and boatbuilding is listed amongst the allowed activities it would be a pretty clear indication that the government at least, is thinking that the cup will go ahead on the planned dates. If they don't allow at least base construction to continue then I suspect that the cup is not likely to go ahead. This needs to be completed before any of the teams can get here, particularly if they want to get here in advance of their original planned arrival as there are no longer events in Europe. I don't see a tweak in the current immigration guidelines to allow overseas teams in provided they're put through quarantine being too much of an issue with most, so getting the teams here shouldn't be too hard.

I can't help thinking the current plan is to go ahead and hope that the current situation changes enough to allow overseas spectators in for the event.

Thoughts anyone?

 

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^ I doubt the AC factors into the media release we are to get this arvo.

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4 hours ago, barfy said:

^ I doubt the AC factors into the media release we are to get this arvo.

Sounds like construction will be allowed.

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2 hours ago, Woolfy said:

Sounds like construction will be allowed.

Bugger I was enjoying my taxpayer funded holiday.

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Posted (edited)
On 4/14/2020 at 8:07 AM, Priscilla said:

Rather than risk our borders with importing the contenders boats gear and personnel there is a competitively active fleet of Mullet boats that could be raced in lieu for the AC.

TNZ would of course race in Orion.

3FCC875C-845C-4BF3-AF2C-0716666DE1CE.thumb.jpeg.b01937ffbb7997a799238be73b1135b0.jpeg

 

That's my dad Reg Haysom on the helm. We owned the Tamariki for many years, he skippered her in all her Lipton wins (I think) I also sailed her many times

Edited by kiwi777
spelling

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10 minutes ago, kiwi777 said:

That's my dad Reg Haysom on the helm. We owned the Tamariki for many years, he skippered her in all her Lipton wins (I think) I also sailed her many times

https://www.pressreader.com/new-zealand/boating-nz/20180901/281578061517704

Getting a birthday.

https://www.facebook.com/pages/category/Sports---Recreation/Mullet-Boat-Tamariki-640175619820814/

post-4983-0-30549500-1474329360.thumb.jpg.be72b1aebdc4e8c886b0701c9709c860.jpg

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wow, is that her? she sat in our back yard in the 70's for about 10 years. sailed her many times. What a treasure. 13 time Lipton cup winning with my old man at the helm

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2 minutes ago, Priscilla said:

Any photos ?

I have some somewhere, ill try and dig them out and post. She looks white in that photo but her main livery was teal green from my memory anyway which was from the mid-'60s to the mid-'80s. always no 11 with the dog

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wasn't Paul Henry on the news yesterday saying the AC had to be postponed ... what a muppet

he somehow becomes an essential service and puts together a tv show in 2 weeks under lockdown and has the audacity to comment on an event he knows nothing about 1 year in the future.

the only factor that is going to stop this AC being completed on time is the NZ govt stopping teams from entering the country

ETNZ have no requirement to take into account what the Italian, UK and USA governments do, if they shut down their borders and are unable to travel here that is not ETNZ's problem

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16 minutes ago, Lickindip said:

wasn't Paul Henry on the news yesterday saying the AC had to be postponed ... what a muppet

he somehow becomes an essential service and puts together a tv show in 2 weeks under lockdown and has the audacity to comment on an event he knows nothing about 1 year in the future.

the only factor that is going to stop this AC being completed on time is the NZ govt stopping teams from entering the country

ETNZ have no requirement to take into account what the Italian, UK and USA governments do, if they shut down their borders and are unable to travel here that is not ETNZ's problem

Ironically I'm not sure there is anything you could define as less essential than that man's opines.

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1 hour ago, rh3000 said:

has the audacity to comment on an event he knows nothing about 

Leopard and spots comes to mind although dog would be more apt in that loudmouths case.

Whats with the absolutely puerile standard of the fourth estate in Aotearoa.

MediaWorks is broke so they would have thankfully paid Paul peanuts for his latest lame effort.

 

 

 

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its all good and well saying "we must rebuild" "we can do it" etc etc etc but don't cut down the tall poppies out there actually trying to doing it

if this country cant look forward 1 year and say we can make this work ... may as well stay in your house and watch the country burn

they are expecting 1/2 a million to go back to some form of work in 6 days time ... stop the negativity for an event planned for 1 year in the future

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Posted (edited)

don't get me wrong, personally I think the govt is allowing too much in the proposed L3

I would have thought online businesses that can prove they can working safely including background warehouse staff would have been a sensible L3 ... sending kids back to school = trouble

only going to take 1-2 clusters to pop up and we might be expected to go back to L4 (although you could do localised L4 if clusters pop up)

 

Edit: i'll just sit at home and do as im told. gives me time to argue with people online

Edited by Lickindip
addition

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We keep switching roles :) In one respect, I’m more “liberal” than you, and that’s sending kids back to school. Not necessarily because I’m evil, but because it’s sort of proven young blighters don’t fall ill. Curious to see if French president Macron follows through with his intention of reopening schools as early as May 11

 

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A 5 year old died in the US today, in Detroit. Her name was Skyler. Not the first.  Can happen. 

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3 hours ago, Priscilla said:

MediaWorks is broke so they would have thankfully paid Paul peanuts for his latest lame effort.

Hopefully so.  But I have this creeping suspicion whatever they paid for it will have come from their NZ On Air pot of public funds...

So you probably paid for it...

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4 hours ago, rh3000 said:

Ironically I'm not sure there is anything you could define as less essential than that man's opines.

Except maybe Mike Hoskings?

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1 hour ago, Skipstone said:

Hopefully so.  But I have this creeping suspicion whatever they paid for it will have come from their NZ On Air pot of public funds...

So you probably paid for it...

Bugger.

Notice his stinkpot is Cook Islands registered.

961280637_OLIVE(1).thumb.jpg.7be4e6f14e25fa6a6943d244e3d62c57.jpg

 

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3 hours ago, Xlot said:

We keep switching roles :) In one respect, I’m more “liberal” than you, and that’s sending kids back to school. Not necessarily because I’m evil, but because it’s sort of proven young blighters don’t fall ill. Curious to see if French president Macron follows through with his intention of reopening schools as early as May 11

 

you must not have kids.  they are always superspreaders.

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8 minutes ago, MR.CLEAN said:

you must not have kids.  they are always superspreaders.

There's two sure ways to get sick - kids & hospitals...

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Seems from some of the feedback around the globe (re how and when a return to pre-CoViD-19 practices might be possible) that negotiating with the NZ government to get a team across the border to participate may only be half the mission.

In the case of Italy the following hypothetical timetable has been produced... notably it doesn't project Italian borders re-opening until at least 1 April 2021.

Now I'm guessing that it won't take too much to convince the Italian government to let Luna Rossa travel (?) if there is a basis for them to make it across the NZ border (?), but even so the timetable at large paints a picture about what life might be like for far longer than some may have expected.

 

Reopening is the buzzword around Europe and something everyone is looking to see applied to lives given the coronavirus pandemic.

The process though will be arduous and apparently long, as it is possible the peak was higher than expected.

All European countries are working to prepare a route so we can get back to normality in the most comfortable way.

In Italy a hypothetical timetable has been produced and shows how a reopening would potentially take place. The plan has three phases.

For example, Serie A would be able to resume from May 31 with matches played behind closed doors, as stadia and nightclubs would not be open to the public until March 2021.

The stages of reopening

End of phase 1

April 14: bookstores and stationery stores open

April 18: The reopening of agricultural and industrial companies begins.

Phase 2

May 4: End of lockdown, but with obligations to wear masks and maintain social distance. Textile, furniture and clothing stores resume their activities, but with staggered openings. Shopping centres remain closed.

May 11: Reopening of courts and professional offices.

May 18: bars, restaurants and other catering activities return to activity. Always respecting the obligation of social distancing between customers.

May 25: Hairdressers reopen. Workers must wear a mask and clients will enter one at a time

May 31: Serie A and the other leagues can resume. Matches will be played behind closed doors.

June 8: Gyms can reopen but only with small groups of people.

Phase 3

September: Schools reopen, but this only affects middle and high school students. There is no news of a possible return for elementary and nursery schools.

December: Cinemas and theatres open

Beyond March 31: The last step will be to reopen the borders and allow travel

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26 minutes ago, MR.CLEAN said:

you must not have kids.  they are always superspreaders.

Agreed.  However the science with CoViD-19 doesn't back this up.  It's currently held that in general infected children experience very mild symptoms and do not transfer the illness at anything like the rate one might ordinarily expect with other respiratory illnesses, to peers, or to adults.

Of course there are outliers and we are all aware there have been child deaths so this is not to say we should let down our guard - but in general CoViD-19 does not affect children as seriously as others and nor are they an effective transmission vector to date.

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its probably more a generational thing

adults look at people as they talk to them and any cough is over that person

kids talk to their phones with a non specific grunt occasionally to any perceived noise around them and just cough over the screens they rarely take their eyes off

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Oktoberfest canceled for 2020. Had already happened in 1854 and 1873, for cholera epidemics

Just sayin’...

 

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Ineos is planning to fly 2 boats over for September.  

Assuming quarantine requirements can be met, you got a race in 2021.

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Trump wants to stop people coming into the US (‘immigration ban’) and while the details are far from clear it makes you wonder if travel out of, and then back into, the USA will be allowed - even by US citizens. 
 

Under current Italian (Schengen?) regulations, can Italians leave and then return?

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Even if not, NZ is good enough for refuge seeking billionaires so why not US AC teams? Or maybe they can protest while Ineos races there. 

Actually I think Dear Leader's ban does not apply to US citizens, green card holders or or migrant ag workers. It's jobs not health really. So maybe he won't let Dean back in because they should have hired an American. But the Amway folks are donors...so no problema. 

 

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4 hours ago, NeedAClew said:

Ineos is planning to fly 2 boats over for September.  

Assuming quarantine requirements can be met, you got a race in 2021.

We have chosen eradication as the objective regarding Covid19 here in Aotearoa.

If say the AC goes ahead and new clusters of Covid19 can be contact traced back to the event requiring a return to lockdown whose going to compensate the locals for further loss of lives and incomes.

A boat race in these times is simply not worth the risk.

 

 

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16 hours ago, Skipstone said:

Agreed.  However the science with CoViD-19 doesn't back this up.  It's currently held that in general infected children...do not transfer the illness at anything like the rate one might ordinarily expect with other respiratory illnesses, to peers, or to adults.

Please share this science.  Should I hold my breath?

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12 minutes ago, Priscilla said:

We have chosen eradication as the objective regarding Covid19 here in Aotearoa.

If say the AC goes ahead and new clusters of Covid19 can be contact traced back to the event requiring a return to lockdown whose going to compensate the locals for further loss of lives and incomes.

A boat race in these times is simply not worth the risk.

 

 

Great objective. You will have done it by then. 

But if there is a long supervised quarantine and accurate frequent testing of the 100 or so team members is done over that long period then clusters are not likely. We are not talking spectators coming in.  You can even keep all the AC participants in a zone. Nobody in and out. 

If you do not have AC races and still let people in and get an outbreak, who compensates you then? Will each person post bond? 

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14 minutes ago, MR.CLEAN said:

Please share this science.  Should I hold my breath?

The science is, "Because Ashley says so".

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3 minutes ago, NeedAClew said:

then clusters are not likely

Sounds to ominously Trumpian for my liking.

 

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10 minutes ago, NeedAClew said:

You can even keep all the AC participants in a zone. Nobody in and out. 

Crikey what a farce or a regatta that scenario would be.

As I said before simply why take the risk.

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36 minutes ago, MR.CLEAN said:

Please share this science.  Should I hold my breath?

Feel free to exhale -  but you’ll have to Gtran it (also see the Virus thread for context)

https://www.oggiscuola.com/web/2020/04/21/scuola-il-virologo-crisanti-i-bambini-non-infettano-il-problema-e-come-portarli-in-classe/

In short, kids are not the problem - it’s the parents that’ll bring them to school

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1 hour ago, Stingray~ said:

Trump wants to stop people coming into the US (‘immigration ban’) and while the details are far from clear it makes you wonder if travel out of, and then back into, the USA will be allowed - even by US citizens. 
 

Under current Italian (Schengen?) regulations, can Italians leave and then return?

A US citizen returning to the US is not "immigrating".  They could in theory enforce a quarantine on return to the US.

Trump's proposal are nominally (I use the term loosely) about preventing furriners from taking 'Merican jobs. The proposal apparently makes exceptions for agricultural jobs , of course, since 'Mericans aren't that keen on that type of labor. Probably will consider golf course workers as "agricultural", since a large percentage of those workers in Florida are Hispanic immigrants. Might get an exemption for housekeepers at clubs and resorts, too.

This is about using the cover of the pandemic to support the anti-immigration agenda. It's pretty transparent.

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26 minutes ago, Priscilla said:

Sounds to ominously Trumpian for my liking.

 

After all, it's only one person from China...

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19 minutes ago, NeedAClew said:

Fine. Don't have it. Your rules. 

Crikey Clew don’t throw your toys out of the cot.

All I am suggesting is having the AC at a later date where it can be held without risk and provide the local economy the possible opportunity to claw back some of $250m invested.

Terry Hutchinson

“You could go out on the water with face masks and other measures that would be steps towards fulfilling health guidelines, and yet, I’m not quite sure you’d ever guarantee anything 100 percent, so it just feels prudent to pull the handbrake and put safety ahead of ambition, so that’s the decision we made.”

 

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1 hour ago, MR.CLEAN said:

Please share this science.  Should I hold my breath?

Among the first 425 corona virus patients studied in Wuhan, China, in December and January, no cases were reported among children under age 15. Later, a study of more than 1,000 patients in China found that kids younger than 15 represented 1% of cases.

Other countries have identified a similar pattern: CDC data suggests that children represent just 2% of cases in the US, and an analysis of 4,700 confirmed cases in Spain came to the same conclusion.

But children’s cases are also tougher to detect – let alone isolate – since many pediatric patients never know they’re ill. 

An April study of pediatric patients in China found that 90% of children studied were either asymptomatic or developed mild or moderate symptoms compared to 6% who developed severe or critical infections.

A study from the CDC – the largest research sample of children with the corona virus to date – found that 18% of pediatric COVID-19 patients in the US reported no symptoms. Nearly three-quarters of the children in the study developed fever, cough, or shortness of breath, compared to 93% of adults.

The Chinese study of pediatric patients similarly found that more than 10% of infants had severe infections compared to 7% of kids from age 1 to age 5, 4% of kids ages 6 to 10, 4% of teenagers between 11 and 15, and 3% of older teenagers.

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1 hour ago, MR.CLEAN said:

Please share this science.  Should I hold my breath?

 

 

A nine-year-old boy who contracted Covid-19 in Eastern France did not pass the virus on despite coming into contact with more than 170 people, according to research that suggests children may not be major spreaders of the virus.

The boy was among a cluster of cases linked to Steve Walsh, the Hove-based businessman who became the first Briton to test positive for coronavirus after attending a sales conference in Singapore in January.

Walsh unwittingly passed the infection on when he joined 10 British adults and a family of five at a chalet in the ski resort of Contamines-Montjoie in the Haute-Savoie region after flying in from London.

Most of the chalet guests contracted the virus, but an investigation by Public Health France found that the nine-year-old did not pass it on to either of his siblings nor anyone else, despite coming into contact with 172 people, all of whom were quarantined as a precaution, and having lessons at three separate ski schools.

 

A report on the investigation published in Clinical Infectious Diseases describes how tests revealed the boy to be infected with Sars-Cov-2, the virus that causes Covid-19, and also influenza and a common cold virus. While both of his siblings caught the latter infections, neither picked up the corona virus.

“One child, co-infected with other respiratory viruses, attended three schools while symptomatic, but did not transmit the virus, suggesting potential different transmission dynamics in children,” Kostas Danis, an epidemiologist at Public Health France told the French news agency AFP.The boy had only mild symptoms and when tested was found to have levels of virus that were barely detectable. The low level of infection is thought to explain why he did not infect other people.

The researchers believe that since children typically have only mild symptoms, they may transmit the virus far less than infected adults. “Children might not be an important source of transmissions of this novel virus,” they write.

Why children generally escape the worst of the virus is not well understood, but many scientists suspect that their immune response is somehow able to clear the infections more rapidly than older adults, who tend to be hit much harder by the illness.

 

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1 hour ago, MR.CLEAN said:

Please share this science.  Should I hold my breath?

School closures are likely to have a relatively small impact on the spread of Covid-19 and should be weighed against their profound economic and social consequences, particularly for the most vulnerable children, according to a UK review.

The research, led by University College London (UCL), is the first to look at evidence behind many governments’ decision to shut schools and keep pupils at home.

According to the UN’s education body, Unesco, more than 90% of the world’s pupils have been affected by closures.

The UCL-led survey concludes that the evidence to support the closure of schools to combat Covid-19 is “very weak”, and statistics from influenza outbreaks suggest school closures “could have relatively small effects on a virus with Covid-19’s high transmissibility and apparent low clinical effect on schoolchildren”.

The research team reviewed 16 studies of recent outbreaks of other coronaviruses, including the 2003 Sars epidemic in mainland China, Hong Kong and Singapore, and found that school closures did not help control the epidemic.

“We know from previous studies that school closures are likely to have the greatest effect if the virus has low transmissibility and attack rates are higher in children. This is the opposite of Covid-19,” said thereview’s lead author, Prof Russell Viner, of UCL Great Ormond Street Institute of Child Health.

“Data on the benefit of school closures in the Covid-19 outbreak is limited but what we know shows that their impact is likely to be only small compared with other infection-control measures such as case isolation and is only effective when other social isolating measures are adhered to.”

Viner, who is president of the Royal College of Paediatrics and Child Health, said the benefit gained from closing schools had to be weighed against the costs. “Children’s education is damaged and their mental health may suffer, family finances are affected, key workers may need to stay home to look after children and vulnerable children may suffer most.”

He also highlighted the need to start working out how to return students to education and keep them in school safely.

“Countries that have closed schools, such as the UK, have to now ask hard questions about when and how to open schools. Interventions in schools, such as closing playgrounds, keeping students in constant class groups/classrooms, increasing spacing between students in classes, reducing the school week and staggering school start and break times across years or classes should be considered if restrictive social distancing policies are to be implemented for long periods of time.”

 

Prof Neil Ferguson, of Imperial College London, who is one of the key epidemiologists advising the government, said: “While school closure as a measure on its own is predicted to have a limited effectiveness in controlling Covid-19 transmission, when combined with intense social distancing it plays an important role in severing remaining contacts between households and thus ensuring transmission declines.”

Robert Dingwall, a professor of sociology at Nottingham Trent University, said the UCL survey suggested the public health benefits of school closures were not proportionate to the social and economic costs imposed on children and their families.

“It also underlines how the assumptions used in modelling the Covid-19 pandemic may rest on very flimsy foundations in terms of scientific evidence. This work suggests that UK schools could and should begin to reopen as soon as practicable after the initial wave of cases has passed through.”

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4 hours ago, Sailbydate said:

The science is, "Because Ashley says so".

Yeah I don't think thats accurate, and by extension very fair ;-) When asked yesterday in the presser he immediately cited one paper from Wuhan (which is linked to above)... and noted there were others too... (also linked to above)... so there is actual empirical science behind the position...

TBH as a center-righter I feel pretty lucky to have Ashley running his part of the show, given the plethora of idiots stumbling around the civil sector...

Having said that, I'm keeping the kids at home for the foreseeable future.. but if giving some people the opportunity to go back to work whilst their kids are at school is seen to be a low risk way of helping the economy recover, then I feel like the govt are stuck between a rock and a hard place - more and more pressure by opposition and some industry to modify restrictions to help with economy, and yet whatever ever mods they attempt to make are accused of being sub-optimal ones...

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1 hour ago, rh3000 said:

Having said that, I'm keeping the kids at home for the foreseeable future.

Wise choice, IMO.

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5 hours ago, rh3000 said:

Having said that, I'm keeping the kids at home for the foreseeable future.. 

In spite of my comments regarding the 'science as we understand it' regarding the infection of children and their potential to shed the virus to others I agree this is an entirely prudent response. 

The longer we maintain distance between as much of the populace as we can while getting on as able with restoring economic activity and 'more normal lives' (whatever those will be for the next while), the lower the risk that we'll face the sort of issue countries/territories like Hong Kong/Singapore/Japan are now facing. They each posted an apparently successful initial response to CoViD-19 only to encounter a larger second wave that their first response did little to mitigate - even while that first response was being lauded by many public health experts worldwide.  This disease needs no help; a little complacency is all that's required for it to quickly overwhelm.

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the more we find out  about this virus the more logical ( and financially manageable) eradication becomes

 

if it mutates fast enough to defeat vaccination in short periods of time ( which seems possible to likely given its over its 30th variation in 4-5 months )

then the hammer and dance become more of a perpetual way of life than a one or two off

 

if antibodies are temp to extremely temporary .. same

 

if vaccinations give the same results for produced anti bodies as the natural ones ... same

 

we are holding on the lucky streak .. it could still reverse at a great rate of knots .. but there is a case for some optimism allowed

 

 

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2 hours ago, phill_nz said:

if it mutates fast enough to defeat vaccination in short periods of time ( which seems possible to likely given its over its 30th variation in 4-5 months )

From what I've heard and read It actually mutates quite slowly compared to other viruses. So at least there is that...

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https://www.startpage.com/row/search?q=corona+virus+mutations&l=english

 

i was going to quote a couple

but just looking at them .. they differ  from every point of possibility

this virus really has a lot of heads spinning and throwing a lot of conventional wisdom out the door in so many ways

 

while a few of those articles come from not so reliable sources .. you cant throw them all out on that basis and just keep the reliable ones that agree .. there really isn't any

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5 hours ago, rh3000 said:

From what I've heard and read It actually mutates quite slowly compared to other viruses. So at least there is that...

Over 30 distinct RNA mutations (strains) now in ~5 months, some more virulent, others less (the most virulent can shed 270 times more viral load than the least), although all using one of at least 6 known variations of spike proteins to attach to ACE2 as the human transmission vector.....  draw your own conclusions about its rate of mutation, and the significance of the mutations.

Many of the articles indicating a slower rate of mutation were based upon research performed in late January and early February where variously 4-6 strains were known and 3 were predominant.  For those interested in further information regarding strain distinctions, nextstrain.org has become the defacto leader in reporting information relating to strains. 

For example, New York seems to have experienced the most deadly European derivative of the disease also experienced by Italy and Spain (via SIngapore) whereas the West coast states of the US such as Washington State seem to have experienced the (so far) less virulent Wuhan version of the virus - although degree of virulence and degree of mortality are not related. 

SCIENTISTS: THE CORONAVIRUS HAS ALREADY MUTATED INTO 30+ STRAINS

ONE STRAIN, FOR EXAMPLE, APPEARED TO GENERATE 270 TIMES THE VIRAL LOAD.

BY DAN ROBITZSKI / APRIL 21 2020

New research suggests that SARS-CoV-2, the virus that causes COVID-19, could have already mutated into more than 30 separate strains.

The study found that different strains can generate vastly different levels of viral load as others, the South China Morning Post reports, making them far more dangerous.

One strain, for example, appeared to generate 270 times the viral load — meaning the infected person produces 270 times as much of the virus— than the least potent strain.

That makes it far harder to fight off infections and facilitates spread, hypothetically explaining why some cases of COVID-19 are significantly worse than others.

“Sars-CoV-2 has acquired mutations capable of substantially changing its pathogenicity,” Li Lanjuan, one of China’s most prolific epidemiologists and a researcher at Zhejiang University, wrote in the study, which was shared online in the preprint server MedRxiv on Sunday but hasn’t yet been vetted by the peer-review process or published in an academic journal.

In the research, Li isolated different strains and, under laboratory conditions, measured how quickly and effectively they could infect and kill off host cells.

This table shows the epidemiological information about the  11 strains analyzed from the Chinese coronavirus patients

The paper also traced different strains to outbreaks in different parts of the world, finding that the version of SARS-CoV-2 that spread across Europe and New York were far more efficient killers than the one that hit other parts of the U.S. such as Washington State.

This graphic shows the deadly strain that hit Europe (in blue) and the mild strain that mostly hit the US such as Seattle (in orange)

“Drug and vaccine development, while urgent, need to take the impact of these accumulating mutations… into account to avoid potential pitfalls,” Li and her colleagues wrote.

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2 hours ago, Skipstone said:

Over 30 distinct RNA mutations (strains) now in ~5 months, some more virulent, others less (the most virulent can shed 270 times more viral load than the least), although all using one of at least 6 known variations of spike proteins to attach to ACE2 as the human transmission vector.....  draw your own conclusions about its rate of mutation, and the significance of the mutations.

Many of the articles indicating a slower rate of mutation were based upon research performed in late January and early February where variously 4-6 strains were known and 3 were predominant.  For those interested in further information regarding strain distinctions, nextstrain.org has become the defacto leader in reporting information relating to strains. 

For example, New York seems to have experienced the most deadly European derivative of the disease also experienced by Italy and Spain (via SIngapore) whereas the West coast states of the US such as Washington State seem to have experienced the (so far) less virulent Wuhan version of the virus - although degree of virulence and degree of mortality are not related. 

SCIENTISTS: THE CORONAVIRUS HAS ALREADY MUTATED INTO 30+ STRAINS

ONE STRAIN, FOR EXAMPLE, APPEARED TO GENERATE 270 TIMES THE VIRAL LOAD.

BY DAN ROBITZSKI / APRIL 21 2020

New research suggests that SARS-CoV-2, the virus that causes COVID-19, could have already mutated into more than 30 separate strains.

The study found that different strains can generate vastly different levels of viral load as others, the South China Morning Post reports, making them far more dangerous.

One strain, for example, appeared to generate 270 times the viral load — meaning the infected person produces 270 times as much of the virus— than the least potent strain.

That makes it far harder to fight off infections and facilitates spread, hypothetically explaining why some cases of COVID-19 are significantly worse than others.

“Sars-CoV-2 has acquired mutations capable of substantially changing its pathogenicity,” Li Lanjuan, one of China’s most prolific epidemiologists and a researcher at Zhejiang University, wrote in the study, which was shared online in the preprint server MedRxiv on Sunday but hasn’t yet been vetted by the peer-review process or published in an academic journal.

In the research, Li isolated different strains and, under laboratory conditions, measured how quickly and effectively they could infect and kill off host cells.

This table shows the epidemiological information about the  11 strains analyzed from the Chinese coronavirus patients

The paper also traced different strains to outbreaks in different parts of the world, finding that the version of SARS-CoV-2 that spread across Europe and New York were far more efficient killers than the one that hit other parts of the U.S. such as Washington State.

This graphic shows the deadly strain that hit Europe (in blue) and the mild strain that mostly hit the US such as Seattle (in orange)

“Drug and vaccine development, while urgent, need to take the impact of these accumulating mutations… into account to avoid potential pitfalls,” Li and her colleagues wrote.

Yes - like all viruses it mutates, again you seem to miss my point. So a single unvetted paper has some stats in it concerning mutations... The 270x statement is a classic. Read it again, and consider it could be written in the opposite way and still be 100% true and accurate "one of the strains was found to have 270 times a smaller viral load than the most virulent"...

And as I specifically stated, how does this compare to the rate of mutations in other viruses?... The article does not mention this... Without this comparison we continue to play games ourselves... This is just another demonstration of journalism's shameful game of finding and inch and taking a mile.

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@SkipstoneI appreciate (if not always understand) the info you’re providing

32 minutes ago, rh3000 said:

And as I specifically stated, how does this compare to the rate of mutations in other viruses?... 

 Yes, this I’d like to know too. And, presumably, would a single vaccine work?

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35 minutes ago, rh3000 said:

This is just another demonstration of journalism's shameful game of finding and inch and taking a mile.

are you complaining that you're too dumb to understand an article or that others are too dumb to understand it?

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2 hours ago, MR.CLEAN said:

are you complaining that you're too dumb to understand an article or that others are too dumb to understand it?

It depends who you ask I guess :-)

And I'd like to retract my original statement and re-clarify as 

"This is just another demonstration of some in journalism who play this shameful game of finding an inch of data and making a mile of a story."

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3 hours ago, rh3000 said:

Yes - like all viruses it mutates, again you seem to miss my point. So a single unvetted paper has some stats in it concerning mutations... The 270x statement is a classic. Read it again, and consider it could be written in the opposite way and still be 100% true and accurate "one of the strains was found to have 270 times a smaller viral load than the most virulent"...

And as I specifically stated, how does this compare to the rate of mutations in other viruses?... The article does not mention this... Without this comparison we continue to play games ourselves... This is just another demonstration of journalism's shameful game of finding and inch and taking a mile.

Very few papers are peer reviewed at release through this period for the very reason that they're published on completion to help facilitate further research or point to vectors for research not yet being performed.  The issue isn't whether a virus is 270 times more (or less) virulent, rather the extent to which mutations have and are occurring, and the difficulties with treating CoViD-19 as though it's one illness when the reality is that its impacts on one community may be significantly greater or more difficult to combat than on another so framing an effective AND appropriate public health response has been more difficult.  The greater virulence in NY for example c.f Washington State's less virulent strain.  Note that virulence may point to differing infection rates or the proportion of 'serious' cases, but is not inherently linked to mortality rate...

Mutation rate comparisons between viruses aren't particularly useful in themselves...

The highest per base pair per generation mutation rates are found in viruses, which can have either RNA or DNA genomes. DNA viruses have mutation rates between 10−6 to 10−8 mutations per base per generation, and RNA viruses have mutation rates between 10−3 to 10−5 per base per generation.  (source: Wikipedia link below)

FWIW I can provide you this... taken from this Johns Hopkins Bloomberg School of Public Health paper  

SARS-CoV-2 Evolution

Phylogenetic analysis of 30 publicly available SARS-CoV-2 samples concluded that emergence of SARS-CoV-2 in the human population likely occurred in mid-November 2019.

The sequences have limited variability in consensus sequences, suggesting the outbreak was initiated from either a single introduction into humans or from a very few animal-to-human transmission events.

The mutation rate has been estimated in various groups, ranging from about 1.05x10–3 to1.26x10–3 substitutions per site per year, which is similar to some estimates of MERS-CoV mutation rates. As more viral genomes are made publicly available, scientists will better be able to track viral evolution and mutation rates, so the exact estimates will vary

 

For a basic understanding of mutation rate principles; https://en.wikipedia.org/wiki/Mutation_rate

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Not sure if you listened to this - mutations well covered in great detail, despite being older than that published date of research paper, still incredibly informative

https://www.rnz.co.nz/national/programmes/saturday/audio/2018739526/james-hadfield-nz-phylogeneticist-tracking-covid-19-s-spread

... phylogeneticist Dr James Hadfield. Based in Wanaka but employed by Seattle's Bedford Lab, he works on the open source Nextstrain platform: this allows scientists all over the world to share and compare genetic information about SARS CoV-2 and other viruses in one central location, and then track their rate of mutation and their spread in real time. 

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4 hours ago, Xlot said:

@SkipstoneI appreciate (if not always understand) the info you’re providing

 Yes, this I’d like to know too. And, presumably, would a single vaccine work?

I've addressed the question of the estimated rate of mutation above. 

As for whether a single vaccine (or other preventative) would work, that's entirely down to the science.  In the case of a vaccine, successfully targeting a universal attribute such as the spike protein on the outside of the virus cell that it uses to attach to the ACE2 receptor enzyme would likely address all known strains - until the virus mutated further to attach in a different way or bypass this protein spike altogether.  

A few mainstream articles below that point to the difficulty of developing vaccines for corona viruses and explain how a vaccine might work;

https://nymag.com/intelligencer/2020/04/will-there-be-a-coronavirus-vaccine-maybe-not.html

https://www.newstalkzb.co.nz/news/science/covid-19-coronavirus-how-a-vaccine-will-work-explained/

https://www.nzherald.co.nz/world/news/article.cfm?c_id=2&objectid=12324650

 

And for those that might like to dig a little deeper...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151553/

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6 minutes ago, rh3000 said:

Not sure if you listened to this - mutations well covered in great detail, despite being older than that published date of research paper, still incredibly informative

https://www.rnz.co.nz/national/programmes/saturday/audio/2018739526/james-hadfield-nz-phylogeneticist-tracking-covid-19-s-spread

... phylogeneticist Dr James Hadfield. Based in Wanaka but employed by Seattle's Bedford Lab, he works on the open source Nextstrain platform: this allows scientists all over the world to share and compare genetic information about SARS CoV-2 and other viruses in one central location, and then track their rate of mutation and their spread in real time. 

No.  Hadn't heard this - listening now, thanks.  Nextstrain is a game-changer compared to prior epidemics and pandemics in the speed with which strains can be identified and tracked, responses identified and deployed, research initiated and shared, and the efficacy of actions or counter measures tested and refined for wider use or discarded with minimum ill effect.

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Of course the other absolute last resort option may be to pull Aotearoa off the wall, put her back together, split Te Aihe’s crew into two and use her to line up against Te Kahu and refine match racing skills while Boat 2 is being constructed and Te Aihe is off globetrotting.

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18 minutes ago, Forourselves said:

Of course the other absolute last resort option may be to pull Aotearoa off the wall, put her back together, split Te Aihe’s crew into two and use her to line up against Te Kahu and refine match racing skills while Boat 2 is being constructed and Te Aihe is off globetrotting.

Surely you realize that an AC50 is too large to qualify as a Protocol-compliant non-surrogate training boat, don't you?

By all means, they should give that a try...

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6 hours ago, accnick said:

Surely you realize that an AC50 is too large to qualify as a Protocol-compliant non-surrogate training boat, don't you?

By all means, they should give that a try...

The F50’s obviously did which was why INEOS were able to compete in SailGP. The wording is up for interpretation as a surrogate is defined in the protocol but excludes class yachts such as the TP52 or “any existing class” of which the AC50 is an existing class. 

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34 minutes ago, Forourselves said:

The wording [of surrogate] is up for interpretation as a surrogate is defined in the protocol but excludes class yachts such as the TP52 or “any existing class” of which the AC50 is an existing class. 

Yes, but the protocol says explicitly "Surrogate Yacht means any monohull yacht exceeding 12 m LOA…", so multis can't be surrogates.

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On 4/21/2020 at 9:24 AM, Priscilla said:

Leopard and spots comes to mind although dog would be more apt in that loudmouths case.

Whats with the absolutely puerile standard of the fourth estate in Aotearoa.

MediaWorks is broke so they would have thankfully paid Paul peanuts for his latest lame effort.

 

 

 

Hey brought in his own sponsor. Milford investments, they would have paid for everything and Paul gets a time slot to do whatever he likes after 9:30pm I love it. He's the only one holding the government to account..... 

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50 minutes ago, NZL4EVER said:

Hey brought in his own sponsor. Milford investments, they would have paid for everything and Paul gets a time slot to do whatever he likes after 9:30pm I love it. He's the only one holding the government to account..... 

I'm no Paul Henry fan so don't know what else I might have missed... But I caught a single segment the other night where he made himself an utter prick completely down the "wrong" side of an argument supporting one of his guests over another arguably more reasoned and rational guest.  And then did the Paul Holmes flip at the end where he glibly and speedily wound up the segment agreeing with the guest (he'd by then dismissed) that he'd spent the whole segment being a prick towards and beating down...  I'm not sure why anyone would want to put themselves anywhere near any show he was involved in.

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2 hours ago, RobG said:

Yes, but the protocol says explicitly "Surrogate Yacht means any monohull yacht exceeding 12 m LOA…", so multis can't be surrogates.

Nope. It was amended to “yacht”

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1 hour ago, NZL4EVER said:

He's the only one holding the government to account..... 

Other than the fucking virus!

jesus wept

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1 hour ago, NZL4EVER said:

He's the only one holding the government to account..... 

What along with Mike Hosking and Leighton Smith.

Guys a waste of space plain and simple but please humour me with one example where Paul Henry is doing the great political accountability mahi you admire so greatly.

https://nzherald.co.nz/entertainment/news/article.cfm?c_id=1501119&objectid=11737753

https://thestandard.org.nz/paul-henry-we-all-pay-for-his-unending-bigotry/

 

 

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25 minutes ago, Forourselves said:

Nope. It was amended to “yacht”

Oh yeah, I used the one marked "final" instead of "v6" or whatever. Apparently that was amendment 1, so any other version would have done. :-)

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