Maybe so - But surely using other countries as models for best Practice and using their data to perfect your own measures makes sense ? - See Italy & China for example. I dont i agi e 5e data is anywhere bear accurate in these areas, but 5he measures they put in place certainly stopped the spread.
Im no expert just going off what im reading.
I just cant see more testing ever producing anywhere bear an accurate number. Can you not still go off percentages of positives from smaller sample numbers ?
I'm not going to harp too much more on this, but we have different demographics from these countries and have a different culture--and yes, this does make a difference as to what we think is appropriate distance from someone on a cultural basis, as well as how we greet people and how close we are within families (multigenerational housing). Also, stats from far away don't help individual states or other local governments to make informed decisions.
I read an article that type A blood could be more susceptible to COVID-19 whereas type O is most resilient. Where I live, type A is very prevalent.
I work at a hospital in Washington State. We've had 3 deaths and positive cases over 20. They are NOT taking temps here. They are NOT testing healthcare workers. We cancelled our sugeries/procedures deemed "elective". We've limited who comes in/out to people with a reason to be there plus 1.
We also had anti-viral wipes and face masks w/eye shields go on backorder for us today.
Just stay home if you can people. It's gonna get ugly out there.
I had a medical appointment that had been scheduled and they told me to come on in. They took my temperature at the door and only let me in because I had no temp and I had an appointment. They weren't letting anyone who didn't have an appointment in. The waiting room was reconfigured and a lot of the chairs were gone. The chairs were set up in twos with about five feet of distance between each group of two chairs.
Why are the very young so unaffected? In a usual outbreak, the very young form another usually smaller peak of severe outcome because their immune system is not experienced enough. Not here. One possibility I read about (sorry, don't remember the reference) is that the immune system in some older people has seen something like this and uses the old ineffective antibodies to fight this instead of making new ones, causing the fatal lung flooding.
This is actually why the Spanish Flu of 1918 was so bad. Young people were making the wrong antibodies.
They found that a human H1 virus that had been circulating among humans since around 1900 picked up genetic material from a bird flu virus just before 1918 and this became the deadly pandemic strain.
Exposure to previous strains of flu virus does offer some protection to new strains. This is because the immune system reacts to proteins on the surface of the virus and makes antibodies that are summoned the next time a similar virus tries to infect the body.
But the further away the new strain is genetically from the ones the body has previously been exposed to, the more different the surface proteins, the less effective the antibodies and the more likely that infection will take hold.
This is what the authors suggest happened to the young adults in the 1918 pandemic. In their childhood around 1880 to 1900, they were exposed to a supposed H3N8 virus that was circulating in the population. This virus had surface proteins that were very different from those of the H1N1 pandemic strain. Their immune system would have made antibodies, but they would have been ineffective against the H1N1 virus.
“We believe that the mismatch between antibodies trained to H3 virus protein and the H1 protein of the 1918 virus may have resulted in the heightened mortality in the age group that happened to be in their late 20s during the pandemic.”
In 1918, a flu virus took only a few months to kill three times more people than World War I. Now, a new study suggests exposure during childhood may explain why it was so deadly.
www.medicalnewstoday.com