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Coronavirus infections in Iran are increasing again and the country’s epidemic looks to be heading for a second wave.

The first wave peaked at the end of March when the daily count of new cases briefly rose above 3,000. Throughout the following month new cases dropped steadily, reaching a low point on May 2 when only 802 were reported. Since then, though, they have been rising again.

Further evidence that Covid-19 is making a resurgence in Iran can be seen by comparing numbers of new cases with numbers of recoveries over the last three weeks.

Before May 2 the virus was clearly receding: there were more recoveries than new infections. Since May 2 the position has been reversed. There are now more new infections than recoveries, and the gap is widening.
 
Just heard from a friend who has flown from NSW back to Tasmania where they live. Was met at the airport and taken to a hotel and has been put there for 14 days quarantine. It's all paid for, and gets room service with a nice looking menu, and an expenses account to spend on food and drink.


In Canada, you have to show the border officiers your two week quarantine plan.
If it is not good enough (or no plan), you are put into quarantine at a local hotel.
Once your plan is ok, you may leave and go to another place for the balance of your 14 day quarantine.

I do wonder how much the Americans coming across the border will complain about this loss of freedom.
We will find out once the border between the two countries is opened for non-essential travel.
 
Some doubts about the effectiveness of the ChAdOx1 vaccine candidate (the Oxford vaccine) arising from response in animal models (all subjects shed viral RNA after SARS-CoV-2 exposure and produced a low titre of neutralising antibody).
Paper DOI: 10.1101/2020.05.13.093195

Meanwhile in China, another vaccine candidate, PiCoVacc (a traditional form using inactivated virus), appears to be fairly effective in animal models.
Paper DOI: 10.1126/science.abc1932
 
Some doubts about the effectiveness of the ChAdOx1 vaccine candidate (the Oxford vaccine) arising from response in animal models (all subjects shed viral RNA after SARS-CoV-2 exposure and produced a low titre of neutralising antibody).
Paper DOI: 10.1101/2020.05.13.093195

The Forbes article seems to be being heavily criticized by virologists, in particular because of the very high viral load given in the Oxford study.
 
The Forbes article seems to be being heavily criticized by virologists, in particular because of the very high viral load given in the Oxford study.
It is far from all doom and gloom though despite them still being infectious. The Oxford virus does seem to reduce the viral load and prevent pneumonia.
Here, we showed that a single vaccination with ChAdOx1 nCoV-19 is effective in preventing damage to the lungs upon high dose challenge with SARS-CoV-2. Similarly a recent study showed that a triple vaccination regime of a high dose of whole inactivated SARS-CoV-2 protected rhesus macaques from SARS-CoV-2 pneumonia7.

Viral loads in BAL fluid and lung tissue of vaccinated animals were significantly reduced, suggesting that vaccination prevents virus replication in the lower respiratory tract. Despite this marked difference in virus replication in the lungs, reduction in viral shedding from the nose was not observed. However, animals were challenged with a high dose of virus via multiple routes, which likely does not reflect a realistic human exposure. Whether a lower challenge dose would result in more efficient protection of the upper respiratory tract remains to be determined.

Several preclinical studies of vaccines against SARS-CoV-1 resulted in immunopathology after vaccination and challenge, with more severe disease in vaccinated animals than in controls810. Importantly, we did not see any evidence of immune-enhanced disease in vaccinated animals. The immune response was not skewed towards a Th2 response in mice nor in NHPs, there was no increase in clinical signs or virus replication throughout the study in vaccinated NHPs compared to controls and no markers of disease enhancement in lung tissue of NHPs, such as an influx of neutrophils were observed. These data informed the start of the phase I clinical trial with ChAdOx1 nCoV-19 on April 23, 2020. As of May 13, 2020, more than 1000 volunteers have participated in the clinical trials. This study is thus an important step towards the development of a safe and efficacious SARS-CoV-2 vaccine.
 
Cafes and bars open in Portugal this morning

11th and 12th year pupils go back to school
 
Seeing reports of French researchers suggesting that they've found evidence of Covid infection as early as mid November 2019 reminds me that, back in September a family friend (NHS A&E doctor) strongly advised us all to take up offers of flu jabs (which we did) as he had heard of reports of very virulent 'flus' being associated with the Southern Hemisphere winter 'flu season.

Almost certainly coincidental & all that, but I when I recalled this advice I thought that it would be unsurprising if researchers eventually push back Covid origins even further.
 
Some doubts about the effectiveness of the ChAdOx1 vaccine candidate (the Oxford vaccine) arising from response in animal models (all subjects shed viral RNA after SARS-CoV-2 exposure and produced a low titre of neutralising antibody).
Paper DOI: 10.1101/2020.05.13.093195
Yes I read that, disappointing.

Meanwhile in China, another vaccine candidate, PiCoVacc (a traditional form using inactivated virus), appears to be fairly effective in animal models.
Paper DOI: 10.1126/science.abc1932
Whereas this seems much more positive.
 
Seeing reports of French researchers suggesting that they've found evidence of Covid infection as early as mid November 2019 reminds me that, back in September a family friend (NHS A&E doctor) strongly advised us all to take up offers of flu jabs (which we did) as he had heard of reports of very virulent 'flus' being associated with the Southern Hemisphere winter 'flu season.

Almost certainly coincidental & all that, but I when I recalled this advice I thought that it would be unsurprising if researchers eventually push back Covid origins even further.

I'm always ready for the historical timetable of a novel virus to be revised, and just the other day I commented on this and linked to some BBC story about a choir in the UK who got sick in January after a contact came back from Wuhan in December.

In theory there are limits as to how far the timing can be pushed back though. Because we have seen how transmissible this virus is, how quickly it spreads in countries and between countries, and how much hospitalisation and death results. So if you push the timing back too far then you have to be able to explain why the disease did not explode around the world at that time, why it didnt cause levels of casualties that would be noticed, why it took so long for large and notable outbreaks to arrive elsewhere.

I am not complacent that the currently understood timeline of events is accurate, but if I want to think along the lines of the virus having been out there earlier than first thought, I suppose I'd have to assume that the number involved were relatively low, otherwise we would have seen healthcare swamped and certain quirks of symptoms sooner. And then it would be easy to speculate that maybe the virus changed at some point to be much more transmissible more quickly, and thats the stae where it would then start to get noticed by humanity.

Countries like Australia have often been in the news, very much including UK news, in recent years for having bad flu seasons, so there has been quite a lot of attention in that direction in recent times. These bad flu seasons were in part breaking records there because they had started to do a lot more testing, which also means we know a lot of their cases were influenza, and which type of influenza. I havent studied their last flu season recently but I think it started early and went on a long time, with more than one strain of influenza involved, and a very large number of positive influenza tests.

Anyway it is fair to say there are holes and assumptions in the global respiratory disease surveillance systems so I like to maintain some wiggle room on these topics, I try to keep my assumptions tentative and ready to change. It is completely expected that some early Covid-19 cases will have been missed and put down to being something else like influenza or some other cause of pneumonia. It would take sufficient numbers of them to raise any alarms at the time, so sporadic incidents of severe disease would have been easily overlooked.
 
Another implication of what I just said is that for coronaviruses that only rarely cause severe disease in humans (ie dont cause notable levels of severe illness at a particular time & place), its quite easy for us never to even notice they exist at all. Although several of the human coronaviruses that cause seasonal colds etc were discovered in the 1960's, I believe several others were only discovered this century, despite likely having been present in human populations for a long time before that. There could be others for all I know. A fair chunk of this modern coronavirus knowledge came from research that was motivated by the SARS outbreak, motivation that somewhat faded as the years went by. Obviously to say there is fresh incentive to study coronaviruses more closely now would be a rather large understatement.
 
Yeah thats a big reason you wont see me engaging with those topics too much at this stage. I will sound more pessimistic than I really am if I have to resort to moaning about journalism by press release too often, I'd rather just wait and celebrate any eventual proven successes once they are solid and the extent of their achievements more certain. Its a potential rollercoaster of hope and disappointment that I have no intention of getting on.
 
Seeing reports of French researchers suggesting that they've found evidence of Covid infection as early as mid November 2019 reminds me that, back in September a family friend (NHS A&E doctor) strongly advised us all to take up offers of flu jabs (which we did) as he had heard of reports of very virulent 'flus' being associated with the Southern Hemisphere winter 'flu season.

Almost certainly coincidental & all that, but I when I recalled this advice I thought that it would be unsurprising if researchers eventually push back Covid origins even further.

I dont really see how we could push it back much further when we see the exponential increase in cases after our first few known cases and the virus could be passed on fairly unfettered.
 
I wont have time to go looking for a writeup until this evening or maybe even another day, but its the awkwardly timed World Health Assembly meeting today, where all sorts of blame and politics and calls for investigations and new investigative powers and stuff like that will be on display. I've seen some live reports coming through but I dont have time to follow the detail now. I think I read a preview last night that suggested the WHO would get plenty of stick too. Anyone interested in covering this event?
 
I dont really see how we could push it back much further when we see the exponential increase in cases after our first few known cases and the virus could be passed on fairly unfettered.
Yeah, I get that and elbows response above is, as ever, helpful and measured.
That said, hearing that patients may have been x-rayed with characteristic lung symptoms as early as Nov 16 2019 suggests that infection/transmission may have been possible in early Nov/end October? I believe the average incubation being 5 days & symptomatic period 18 days, or there abouts.

Given that official first deaths were recorded months later it does make you question the 'intelligence'.
 
It turns out there was a bloody stupid story about that sort of thing in the Express a few days ago. Normally I wouldnt link to such a publication but I dont think I have any choice if I want to make this point.


The article never seems to end and eventually manages to accumulate some more reasonable points by the end.

Its often useful to look at what articles like that are failing to mention much or emphasise. In this case flu only just gets mentioned at all, with no important detail about the context of that winter. The flu season was early in this country last winter, and timing of flu epidemics are often used by the press to make dramatic claims. Because if you typically have flu peaks in December, January or February, that obviously affects the historical comparisons when you have a season that is earlier or later than that. The UK press have used this before in recent years with Australian flu epidemics in order to hype them up beyond the actual severity of epidemic (though thats not to say they didnt have some bad flu seasons in recent years) - its easy to make claims about the death rate being at a very high rate compared to the same stage of winter in other years, if the flu happens to be early that year. This is misleading, better to compare the peak death rate with the peak death rate of other seasons and not to be wedded to calendar weeks that the peaks happened on.

So yeah, context. Which I do have to say is quite interesting in this case and there is much that a decent article could make of things. Because unless my memory has gone completely wrong, this last winter was described as the most challenging one the NHS has faced. Its not necessarily that easy to find all the press articles about that now, because the pandemic has obviously generated 8 gazillion articles which share some common search terms. But here is just one example:


I'm certainly not sure I have a full picture. It looks complicated and like a number of factors came together to make the winter very challenging for the NHS. Deeper analysis of the cases that drove the situation would need to be undertaken, but the early flu season certainly satisfies some of my questions about it. All the same, as I've mentioned before, its all down to numbers in many ways - countries would generally be expected to miss sporadic cases unless they had some advanced warning of what to be on the lookout for, and even then would not find it hard to overlook cases until the numbers requiring hospital treatment caused unusual levels of demand that were harder to miss.
 
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