For those interested in understanding the progression of SARS CoV2. Brief excerpts, emphasis added. See also: Notes from a Dr. David Brownstein Treating Patients.
Human ingenuity and people coming together to fight CV19 is heartening and wonderful.
Version 1, not peer reviewed*. See the full PDF: Face Masks Against COVID-19: An Evidence Review.
...The preponderance of evidence indicates that mask wearing reduces the transmissibility per contact by reducing transmission of infected droplets in both laboratory and clinical contexts. Public mask wearing is most effective at stopping spread of the virus when compliance is high. The decreased transmissibility could substantially reduce the death toll and economic impact while the cost of the intervention is low. Thus we recommend the adoption of public cloth mask wearing, as an effective form of source control, in conjunction with existing hygiene, distancing, and contact tracing strategies. We recommend that public officials and governments strongly encourage the use of widespread face masks in public, including the use of appropriate regulation.
DIGLLOYD: in my view, the CDC, WHO and US Surgeon general leaders should pay a heavy price for in effect likely killing thousands of people by their lying malfeasance. They should never again be allowed to lead or to practice medicine and be prosecuted with prison time if it can be shown they acted in bad faith.
I for one will never again trust these organizations, because at the leadership level they are political and politically-correct organizations, even as most researchers under them might all be fine people with the best intentions.
* Note that “peer review” has a certain value, but it is frequently a euphemism for cliques that reject views not conforming to their own, and by itself is frequently of questionable value in view of incestuous amplification of viewpoints.
Working around the clock for two weeks, a large team of Stanford Medicine scientists has developed a test to detect antibodies against the novel coronavirus, SARS-CoV-2, in blood samples.
In contrast to current diagnostic tests for COVID-19, which detect genetic material from the virus in respiratory secretions, this test looks for antibodies to the virus in plasma, the liquid in blood, to provide information about a person’s immune response to an infection.
The test was launched April 6 at Stanford Health Care. It differs from an externally developed test that Stanford researchers used for a prevalence study during recent community screening events.
The Stanford-developed test takes two to three days for results. Stanford Health Care is able to test 500 samples per day, and the organization hopes to scale up quickly. The effort has been led by Scott Boyd, MD, PhD, associate professor of pathology and a leading expert in antibody research.
...the Stanford test detects two different types of antibodies: IgM antibodies, which are made early in an immune response and whose levels usually quickly wane, and IgG antibodies, whose levels rise more slowly after infection but usually persist longer.
Stanford’s test for COVID-19, caused by the novel coronavirus, is rapidly expanding capacity to serve patients in the Bay Area and beyond. Researchers hope to soon be able to process more than 1,000 tests per day...
The Stanford Clinical Virology Laboratory now tests hundreds of patient samples each day from around the Bay Area and beyond for COVID-19, the respiratory illness caused by the novel coronavirus sweeping the globe. Within the next week, the lab hopes to be able to conduct more than 1,000 tests per day. Results are typically delivered within 36-48 hours.
Feb 3 2020, Nature: A pneumonia outbreak associated with a new coronavirus of probable bat origin by eng Zhou, Xing-Lou Yang, […]Zheng-Li Shi
Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats. Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans. Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China.... we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus.
...we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus.
.. Coronaviruses have caused two large-scale pandemics in the past two decades, SARS and Middle East respiratory syndrome (MERS)8,9. It has generally been thought that SARSr-CoV—which is mainly found in bats—could cause a future disease outbreak.... Here we report on a series of cases caused by an unidentified pneumonia disease outbreak in Wuhan, Hubei province, central China. This disease outbreak—which started from a local seafood market...
... ACE2 is known to be a cell receptor for SARS-CoV14... We show that 2019-nCoV is able to use all ACE2 proteins, except for mouse ACE2, as an entry receptor to enter ACE2-expressing cells, but not cells that did not express ACE2, indicating that ACE2 is probably the cell receptor through which 2019-nCoV enters cells (Fig. 3). We also show that 2019-nCoV does not use other coronavirus receptors...
.. Since this paper was accepted, the ICTV has designated the virus as SARS-CoV-2.
DIGLLOYD: this is not proof of origin. If no bats were sold in Wuhan (some claim this) then WTF? It remains a possibility that a virus escaped from the biolab in that city. With all key information suppressed by the CCP, we will probably never know.
Even so, the cruel and filthy wet markets for wildlife, especially wildlife like bats and monkeys and pangolins ought to be stopped. Why not ban all travel to/from China until these wet markets are closed? No negotiation on this point—if the virus originated in the wet markets, then it is the only intelligent thing to do given the enormous damage caused, which will happen again.
Robin D writes:
It is no coincidence that Bats are implicated because they are unique mammals. Like humans, bats are mammals that maintain a warm body temperature that protect them from disease. But while our body temperature rests around 98.6°F and spikes a few degrees when we’re sick, bats’ body temperatures can regularly jump to as high as 105°F. Flying also requires a tremendous amount of activity for bats, which has caused their immune systems to become very specialized. When they fly they have a peak body temperature that mimics a fever, - It happens at least twice a day with bats -- when they fly out to feed and then they return to roost. And so the pathogens that have evolved in bats have evolved to withstand these peaks of body temperature. This poses a potential problem when these diseases cross into another species. In humans, for example, a fever is a defense mechanism designed to raise the body temperature to kill a virus. A virus that has evolved in a bat will probably not be affected by a higher body temperature....something that is very evident in Covid 19 where its signature is a high fever that doesn't abate.
Why does the disease transfer in the first place? -- "zoonotic spillover" or transfer.
The underlying causes of zoonotic spillover from bats or from other wild species have almost always -- always -- been shown to be human behavior. When a bat is stressed -- by being hunted, or having its habitat damaged by deforestation -- its immune system is challenged and finds it harder to cope with pathogens it otherwise took in its stride. It is believed that the impact of stress on bats would be very much as it would be on people. It would allow infections to increase and to be excreted -- to be shed. You can think of it like if people are stressed and have the cold sore virus, they will get a cold sore. That is the virus being 'expressed.' This can happen in bats too. That means they can carry a whole slew of pathogens without suffering from them.
Various wide-ranging articles.
Various wide-ranging articles, many technical but including politically-correct blog posts, such as avoiding naming place of origin, evading the debate of best public health outcomes vs placing real and imagined and non-infections harms. The lack of reasoned debate is disturbing; it is not a self-evident primary.
Unsettled debate about viral load (how much virus is encountered initially) and how that effects dissease progression and outcome.
“We must be more concerned about situations where somebody receives a massive dose of the virus (we have no data on how large that might be but bodily fluids from those infected with other viruses can contain a million, and up to a hundred million viruses per ml), particularly through inhalation. “Unfortunately, we don’t yet know enough about the distribution of the COVID-19 virus throughout the body of the infected patients in normal, and unusual situations. “Under such circumstances the virus receives a massive jump start, leading to a massive innate immune response, which will struggle to control the virus to allow time for acquired immunity to kick-in while at the same time leading to considerable inflammation and a cytokine storm.
Computational fluid dynamics for sneezing. Someone coughing or sneezing in your face especially at close range is a really bad idea.
Respiratory infectious diseases can be spread by direct and indirect contacts or airborne transmission. Direct contact of droplet spray produced by coughing, sneezing or talking involves relatively large droplets containing organisms and requires close contact usually within 1 m. Indirect contact may take place after the droplets are removed from the air by surface deposition Airborne transmission is a major disease transmission mode of respiratory infectious diseases in indoor environments. This mode may take place by inhaling the droplets exhaled by respiratory activities or their residues after evaporation These droplets exhaled by infected patients may carry microorganisms and infect other people...
... So studies on droplet production process and atomization mechanisms of the respiratory activities are still strongly needed and also necessary for the study of the characterization of sneeze.
Effectiveness of Surgical and Cotton Masks in Blocking SARS–CoV-2: A Controlled Comparison in 4 Patients
This experiment did not include N95 masks and does not reflect the actual transmission of infection from patients with COVID-19 wearing different types of masks. We do not know whether masks shorten the travel distance of droplets during coughing.
DIGLLOYD: 4 subjects and tested at kissing distance (8 inches) and no N95 mask testing and no understanding of large droplet behavior = not very persuasive. The researchers also offer a highly misleading characterizations of “not effective” when the reduction in viral load in percentage terms for cotton masks would be hailed as a major breakthrough were it a prescription drug—see the tiny icon (minimized on purpose?) for the data and see for yourself which shows a 35% to 42% reduction for cotton masks (this is better than than the relative risk reduction claims for statins prescribed to millions). This is bias, not objective summarization.
I’d like to see the study repeated and confirmed at least 3 times by other researchers, and viral load assessed at 0.5m, 1m, 2m, 3m after repeated coughing as well as total room contamination in small rooms similar to elevator size as well as conference room size.
Temporal profiles of viral load in posterior oropharyngeal saliva samples and serum antibody responses during infection by SARS-CoV-2: an observational cohort study
Our study has several limitations. First, we could only include a few patients, and viral load and antibody titre data were not available everyday. This limitation is a common problem in studies of emerging infections such as SARS-CoV and MERS-CoV.16 The few patients enrolled does not allow for adjustment for potential confounding factors that could affect viral load or antibody response. Second, 48% of patients enrolled had chronic medical illness, which is a higher proportion than that reported in a large clinical series (24%).
DIGLLOYD: Observational studies are useful for suggesting hypotheses to investigate, but do not show causation nor can much be concluded from them—too many disparate factors.
The severe acute respiratory syndrome–associated coronavirus (SARS-CoV) is thought to be transmitted primarily through dispersal of droplets, but little is known about the load of SARS-CoV in oral droplets.
... We report large amounts of SARS-CoV RNA in the throat wash and saliva from probable SARS case-patients. This finding supports the possibility that SARS-CoV can be transmitted through oral droplets...
DIGLLOYD: so... block oral transmission, eg facial coverings are highly likely to have some meaningful benefit, even ones with marginal materials. And get everyone in the nation an N95 mask or two ASAP.
March 30 2020, CDC: Aerosol and Surface Distribution of Severe Acute Respiratory Syndrome Coronavirus 2 in Hospital Wards, Wuhan, China, 2020
This study led to 3 conclusions. First, SARS-CoV-2 was widely distributed in the air and on object surfaces in both the ICU and GW, implying a potentially high infection risk for medical staff and other close contacts. Second, the environmental contamination was greater in the ICU than in the GW; thus, stricter protective measures should be taken by medical staff working in the ICU. Third, the SARS-CoV-2 aerosol distribution characteristics in the GW indicate that the transmission distance of SARS-CoV-2 might be 4 m.
...Our study has 2 limitations. First, the results of the nucleic acid test do not indicate the amount of viable virus.
Second, for the unknown minimal infectious dose, the aerosol transmission distance cannot be strictly determined. Overall, we found that the air and object surfaces in COVID-19 wards were widely contaminated by SARS-CoV-2. These findings can be used to improve safety practices.
DIGLLOYD: sick people rapidly contaminate spaces they occupy.
Listing of links does not imply my agreement or disagreement or endorsement of any source.