Coronavirus - worldwide spread and control

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This has already been shown to be incorrect. I wrote this post about it earlier. On average more than 10 years of life are lost for each COVID death, and much more than 10 years for some.
Thank you for the reminder.

The paper wants to specify:
Instead to say: If somebody has died from covid-19, he has lost his life.
They now say: If somebody has died from covid-19, he has lost 11.8 years (on average).

11.8 years, if I am allowed mix the numbers of women and men. They make even some more particulars. E.g.
If a 80 years old woman has died from covid-19 and had one morbidity, she has lost 8.92 years (on average).
If a 80 years old woman has died from covid-19 and had six morbidies, she has lost 2.6 years (on average).
They used ten year time frames, so for a 89 year old woman it´s the same, but one gets the idea.

So, in this manner they say that the statements, that people have lost only one or two years, are wrong.
They drew their numbers from a given WHO table and the new Italian deaths.
But is this really an accurate telling? I this capturing the empirical reality?

E.g. it could be that the deaths have occured not over the whole distribution of possible deaths, but at the side where they die quite soon. And because there is to date no data - if I am not wrong (they don´t elaborate) - which can tell if this is the case or not, their conclusion cannot reflect such an input either. If this were the case, they should have elaborate, though the paper is not very clear anyway.

But in accordance, they simply can compare their results with a table from the UK, which says for instance:
If one has died from asthma, he has lost 21.6 years (on average).
If one has died from pneumonia, he has lost 13.1 years (on average).
If one has died from chronic obstructive pulmonary disease, he has lost 8.2 years (on average).

Asf. If one has died from a car accident - probably even far worse!

https://en.wikipedia.org/wiki/Years_of_potential_life_lost
 
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I wonder.... if severity is all to do with the amount of viral inoculation received, then could many of us have had tiny inoculations of viral particles that subsequently help our resistance to the virus without us ever developing COVID-19?

I’m not talking about the type of immunity gained from actually developing a full blown infection, but rather a sub-threshold readiness? Can the immune system even work like this?

If it can, could this be one of the reasons that endemic viruses become less virulent over time?

Perhaps it’s not that the virus is any different, only that the general population, even if never fully infected, have mostly encountered particles of that virus and have had some immune response to it? Not perhaps an immune response sufficient to be ready to totally squash any subsequent infection, but perhaps sufficient to make the body more prepared?

Might this mean that over time individuals at large would need a greater initial inoculation to actually develop COVID-19, and if they do develop the infection, it is less severe?

I had been thinking that if virulence were an evolution of the virus itself (rather than a change in the human population) that the tendency would be in the other direction. Ie that the virus would tend towards increasing virulence because of the way we move people who become severely affected.

My thinking goes like this: It’s the most severely ill that end up in hospital where they potentially spread their severe version of the virus to medical staff, carers, cleaners, etc, each of whom can potentially take it out to the wider population. Yet the less severe are asked to isolate at home, and perhaps therefore don’t spread the virus so far. If this were the case then the more virulent forms would become more widespread.

Yet it seems that severity is dependent on how great the initial inoculation is. (I don’t really have evidence for this... it’s just what I have picked up from reading.... so bear with me). So perhaps over time we will all become partially exposed, and so develop some resistance (if not full immunity) to the worst effects of the virus??

Or am I indulging in wishful thinking and unsubstantiated optimism? :p
 
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Or am I indulging in wishful thinking and unsubstantiated optimism?

I don't know if it's wishful thinking but it sounds implausible. In order to mount an immune response to a virus the immune system has to muster all sorts of co-operative forces in response to a danger signal (or three). A bit of virus hitting the throat and wandering in to the bloodstream without replicating will not raise a danger signal. T cells will not have pieces of virus presented to them. B cells will not get any encouragement to make antibody. Low level exposure to foreign proteins if anything may tolerise (i.e. block an immune response making it easier for the virus to invade).

I am a bit sceptical about the mantra that when infections become endemic they are milder. The reasons why historically infections taken to new continents caused catastrophic elimination of indigenous people are complex. And I suspect any loss of virulence is very much dependent on which virus. In fact with flu endemic virus repeatedly throws up more virulent forms (as well as less virulent ones), not just antigenically new forms.
 
SVT Nyheter -
Infektionsläkaren: Vi måste granska de höga dödstalen i Sverige


https://www.svt.se/nyheter/inrikes/infektionslakaren-vi-maste-granska-de-hoga-dodstalen-i-sverige

The infectious disease clinician:
We have to examine the high death rates in Sweden


The infectious disease clinician Erik Salaneck, at Uppsala Academic Hospital, says that the authorities must examine the high death rates in Sweden compared to other Nordic countries.
- It is very important that we bring this up for a meaningful discussion and review - are we on the right track? he says in SVT's Weekend Studio.

It was a viewer who asked the question of Sweden's high death rate to the infectious disease clinician Erik Salaneck in the weekend studio.

- That is a very important issue. Different ways of reporting have been discussed, but it can't differ that much between Denmark, Norway, Sweden and Finland, he said and continued:

- We must realize that we have a higher mortality rate than our neighboring countries. It is significantly higher and we must look at this in light of us having had a different strategy than our neighboring countries. Is it solely because of this or not?

- It is very important that we bring this up for a meaningful discussion and review - are we on the right track, have we done the right thing? says Erik Salaneck, an infectious disease clinician at Uppsala Academic Hospital, in the Weekend studio.

Can we sum everything up now?

- I definitely don't think so. But one has to raise the issue.

"Will be followed up"

The Public Health Authority states that “the development of the epidemic and the death toll is something that is being closely monitored now, and will be followed up further in evaluations later on when we know more about how different countries were affected. No one has the facts yet, and just as the infectious disease clinician says, it is too early to sum things up in this situation, ”writes press secretary Sara Rörbecker in an e-mail to SVT News.

She continues:

“Unfortunately, covid-19 has spread in the elderly care sector in Sweden. The death toll reflects this because it is primarily elderly - people over 70 - who are most at risk of death in covid-19. "

Deputy state epidemiologist Anders Wallensten tells SVT that it is deeply unfortunate that the infection has entered the care facilities of the elderly in Sweden and that it should be evaluated how this happened and what measures can be taken.

Is there a way to think about the strategy?

- Of course, we have to think about how we can prevent many deaths, but it should also be remembered that other countries that have adopted very strict measures have this ahead of them, they have very few infected.
 
Yes and we also know that there are very high rates of asymptomatic transmission in adults so people can certainly be very infectious without any coughing.

How do we know this? It is frequently hypothesised, but never demonstrated.

(note, it is important not to misinterpret raw test results without considering sensitivity and specificity...)
 
And I suspect any loss of virulence is very much dependent on which virus. In fact with flu endemic virus repeatedly throws up more virulent forms (as well as less virulent ones), not just antigenically new forms.

I think the shift in virulence is a microevolutionary dance between the viruses and their hosts - as the hosts change their behaviour (and use treatments etc.) and develop immunity from exposure to prior versions of the virus, the virus adapts. This can lead to oscillatory patterns.
I think there is strong evidence to suggest shift in virulence of Influenza seems to be proportional to the level of genetic shift over time.
 
Very interesting:



The article is paywalled but the first bit is interesting. Livestreaming! Transparency!

Sunday Times said:
The government’s former chief scientific adviser is convening a rival panel of experts to offer advice on easing the lockdown.

Tomorrow Sir David King will chair the first meeting of the group, which is designed to act as an independent alternative to the government’s Scientific Advisory Group for Emergencies (Sage).

The move comes after weeks of unease about the transparency of Sage decision-making. It has emerged that 16 of the 23 known members of the committee, which meets in secret, are employed by the government.

The independent group will broadcast live on YouTube and take evidence from global experts. It aims to present the government with “robust, unbiased advice” and some evidence-based policies to tackle the Covid-19 pandemic.

The committee will formally submit its recommendations...
 
How do we know this? It is frequently hypothesised, but never demonstrated.

(note, it is important not to misinterpret raw test results without considering sensitivity and specificity...)

Perhaps I am mistaken but I thought it had been demonstrated by this study?:

Temporal dynamics in viral shedding and transmissibility of COVID-19

Abstract
We report temporal patterns of viral shedding in 94 patients with laboratory-confirmed COVID-19 and modeled COVID-19 infectiousness profiles from a separate sample of 77 infector–infectee transmission pairs. We observed the highest viral load in throat swabs at the time of symptom onset, and inferred that infectiousness peaked on or before symptom onset. We estimated that 44% (95% confidence interval, 25–69%) of secondary cases were infected during the index cases’ presymptomatic stage, in settings with substantial household clustering, active case finding and quarantine outside the home. Disease control measures should be adjusted to account for probable substantial presymptomatic transmission.

https://www.nature.com/articles/s41591-020-0869-5
 
https://www.theguardian.com/world/2...-19-transmission-is-understood-say-scientists

UK lockdown must not be lifted until Covid-19 transmission is understood, say scientists

Studies into spread of the disease will centre on those working in the health and social care sectors as cases continue to rise

Researchers say relaxing social distancing should occur only once it is understood why new infections of the disease are still being diagnosed in their thousands every day.

....

And last week, several groups launched studies aimed at providing answers. These include projects to analyse how virus-laden aerosols behave in the air in a bid to understand how the disease is passed between humans. In addition, other schemes will target healthcare workers to investigate how the virus is being spread to them from patients and then on to others.

The importance of this latter approach was revealed in recent figures for cases of Covid-19 which have shown a drop in numbers of new cases in hospitals but reveal significant rises among health and social care workers.

This point was stressed by epidemiologist Anne Johnson at University College London. She said cutting transmissions of Covid-19 to health and social care workers had now emerged as a major priority. “Half of all new infections reported last week were among healthcare workers,” she told the
Observer. “This has now become the leading edge of the spread of the disease.”

This view was backed by infectious diseases expert Tom Wingfield of the Liverpool School of Tropical Medicine. “The numbers show that the rate of decline of new cases is slower in the UK than other European countries and that is likely to be down to transmission occurring within health and social care settings, transmission in the community despite social distancing and, to a lesser extent, chains of transmission that are still occurring within households, especially in larger households or shared accommodation.”

I think constant lack of PPE in care homes, community, downgrading of what PPE is needed, not knowing who’s infected and who’s not, lack of proper planning and not having as strong a lockdown as other European countries, has something to do with it..
 
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Wallensten: Därför har Sverige betydligt högre dödstal än grannländerna
https://www.di.se/nyheter/wallensten-darfor-har-sverige-betydligt-hogre-dodstal-an-grannlanderna/

English Google translation :
https://translate.googleusercontent...derna/&usg=ALkJrhh-BG93IoTXuH_zNPM1MwbaF8yQQw

Wallensten: That is why Sweden has a significantly higher death rate than neighboring countries
Sweden's high death toll in covid-19 stands out in comparison with our Nordic neighboring countries. An important explanation is that the infection entered the country's elderly homes early, explains Anders Wallensten at the Public Health Authority.
[...]
 
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Danmarks plan: 300 000 coronatester i veckan

https://www.svt.se/nyheter/inrikes/danmarks-plan-300-000-tester-i-veckan

"Denmark's plan: 300,000 coronate tests per week
UPDATED YESTERDAY 20:44
PUBLISHED YESTERDAY 18:48

Until last week, Denmark had tested more than twice as many for covid-19 as Sweden in relation to population size. And testing will be expanded even more to be able to control the spread of infection as the country now opens up more and more.

In Denmark, restrictions are now gradually being introduced to stop the coronavirus. Schools, hairdressers and preschools have reopened, while at the same time increasing the test capacity for each week.

Part of the infection tracking is also about people who have tested positive themselves to contact those with whom they have been in contact, so that they in turn should also go and test themselves.

- We need to keep the infection down now and we will do that with the help of more tests and more infection tracking, says Allan Randrup Thomsen, professor of virology to SVT's Agenda.

Tested far more than Sweden
In Sweden, people who are cared for in hospitals and elderly homes are primarily tested, but also more and more employees in care and care. Nevertheless, Denmark is one step ahead.

Last week, April 20-26, Denmark tested around 68,000 people, while 24,000 people were tested in Sweden.

This is despite the fact that the Public Health Authority hoped to test up to 100,000 a week in just a few weeks as early as April.

That was not the case and now the hope is that 100,000 Swedes will be able to be tested in mid-May instead.

In Denmark, the goal is to be able to perform 300,000 tests a week and that everyone who wants to be able to test themselves."
 
This study found that children are at a similar risk of infection to the general population:

Epidemiology and transmission of COVID-19 in 391 cases and 1286 of their close contacts in Shenzhen, China: a retrospective cohort study

Qifang Bi*, Yongsheng Wu*, Shujiang Mei*, Chenfei Ye*, Xuan Zou, Zhen Zhang, Xiaojian Liu, Lan Wei, Shaun A Truelove, Tong Zhang, Wei Gao, Cong Cheng, Xiujuan Tang, Xiaoliang Wu, Yu Wu, Binbin Sun, Suli Huang, Yu Sun, Juncen Zhang, Ting Ma*, Justin Lessler*, Tiejian Feng*

Summary
Background
Rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Wuhan, China, prompted heightened surveillance in Shenzhen, China. The resulting data provide a rare opportunity to measure key metrics of disease course, transmission, and the impact of control measures.

Methods From Jan 14 to Feb 12, 2020, the Shenzhen Center for Disease Control and Prevention identified 391 SARS-CoV-2 cases and 1286 close contacts. We compared cases identified through symptomatic surveillance and contact tracing, and estimated the time from symptom onset to confirmation, isolation, and admission to hospital. We estimated metrics of disease transmission and analysed factors influencing transmission risk.

Findings Cases were older than the general population (mean age 45 years) and balanced between males (n=187) and females (n=204). 356 (91%) of 391 cases had mild or moderate clinical severity at initial assessment. As of Feb 22, 2020, three cases had died and 225 had recovered (median time to recovery 21 days; 95% CI 20–22). Cases were isolated on average 4·6 days (95% CI 4·1–5·0) after developing symptoms; contact tracing reduced this by 1·9 days (95% CI 1·1–2·7). Household contacts and those travelling with a case were at higher risk of infection (odds ratio 6·27 [95% CI 1·49–26·33] for household contacts and 7·06 [1·43–34·91] for those travelling with a case) than other close contacts. The household secondary attack rate was 11·2% (95% CI 9·1–13·8), and children were as likely to be infected as adults (infection rate 7·4% in children <10 years vs population average of 6·6%). The observed reproductive number (R) was 0·4 (95% CI 0·3–0·5), with a mean serial interval of 6·3 days (95% CI 5·2–7·6).

Interpretation Our data on cases as well as their infected and uninfected close contacts provide key insights into the epidemiology of SARS-CoV-2. This analysis shows that isolation and contact tracing reduce the time during which cases are infectious in the community, thereby reducing the R. The overall impact of isolation and contact tracing, however, is uncertain and highly dependent on the number of asymptomatic cases. Moreover, children are at a similar risk of infection to the general population, although less likely to have severe symptoms; hence they should be considered in analyses of transmission and control.

[My bolding]

Research in context

Evidence before this study

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been accompanied by a substantial increase in research and publications ranging from transmissibility of SARS-CoV-2 to clinical characteristics of the infection. As of March 23, 2020, our search of PubMed using keywords (“COVID-19” OR “SARS-nCoV-2” OR “novel coronavirus”) AND (“serial interval” OR “incubation period” OR “attack rate”) yielded 14 articles that have estimated either the serial interval or incubation period of coronavirus disease 2019 (COVID-19) and one that investigated the secondary attack rate. However, most of these estimates have come from either Wuhan or publicly available case data; in both instances, incomplete capture of infections and cases might have produced biased estimates.

Added value of this study
This study is, to our knowledge, the first analysis of SARS-CoV-2 transmission and COVID-19 natural history based on a large primary dataset of cases and close contacts, for which the mode of surveillance (ie, symptom-based versus contact-based) was sufficiently documented and RT-PCR testing was nearly universal. We present one of the first estimates of the serial interval, secondary household attack rate, and dispersion (ie, tendency towards super spreading) for SARS-CoV-2 based on active surveillance data. We found that the attack rate does not differ significantly by age, with on average 7% of close contacts becoming infected, around 80% of these contacts showing any symptoms, and 3% of infections manifesting severe disease at initial assessment. We also found that contact- based surveillance in Shenzhen reduced the duration an infected individual transmits in the community by 2 days. These findings are important for understanding the burden of COVID-19 and for strategic planning across the world.

Implications of all the available evidence
These results shed further light on how SARS-CoV-2 is transmitting, how severe it is, and how effective control measures can be in specific contexts. We provide a key piece of evidence supporting intensive contact tracing and highlighting that children might be an important target for interventions aimed at reducing transmission, even if they do not get sick.

They also found that 20% of cases were asymptomatic at the time of the first clinical assessment. @Snow Leopard I don’t think the relatively high rates of asymptotic cases being reported by this and other studies could possibly all be the result of false positive test results (which I understand should only be about 0.5% for the RT-PCR test)? This is from the discussion:

Focusing on cases detected through contact-based surveillance adds nuance to previous characterisations of COVID-19. Since RT-PCR testing of contacts is near universal, we can assume these cases are more reflective of the average SARS-CoV-2 infection than cases detected through symptomatic surveillance. In the contact-based surveillance group, any tendency for cases to be male or older (beyond the underlying population distribution) disappears. Furthermore, in this group, 20% of cases were asymptomatic at the time of first clinical assessment and nearly 30% did not have a fever. This observation is consistent with a reasonably high rate of asymptomatic carriage, but lower than that suggested by some modelling studies,19 although RT-PCR has imperfect sensitivity.20

https://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(20)30287-5.pdf
 
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They also found that 20% of cases were asymptomatic at the time of the first clinical assessment. @Snow Leopard I don’t think the relatively high rates of asymptotic cases being reported by this and other studies could possibly all be the result of false positive test results (which I understand should only be about 0.5% for the RT-PCR test)? This is from the discussion:

Yes, with 99.5% specificity, we would only expect 6-7 of the 98 positives to be false positives. (from Bayes' Theorem). The ratio of false to true positives of a study like this is likely to be lower because it is a selected population with a known risk factor.
But not reporting symptoms at the first clinical assessment neither demonstrates that these cases were infectious at this point in time, nor does it demonstrate that they did not subsequently develop noticeable symptoms. In that sense, I'd suggest they were tested in the narrow "presymptomatic" incubation period and suggestions of infectiousness during this time is still speculative.

I am glad the study provides good evidence to dispel the nonsense about children somehow having greater resistance to the virus.
 
I think by now the EU should have gathered statistics from different countries and impacts from different strategies, for trying to understand what´s up with this virus.

But this doesn´t seems to be the case, instead the EU website looks as unclear as other ones. There is no concept.


In Germany everything looks fine, corona-wise. But it seems that there is no strategy anymore.

Hospitals are quite empty, economy is going down, side effects on health are likely to take place.
 
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