Tuesday, February 16, 2021

On The Origin Of The Home Of COVID-19 - 21

I. Where

This series asks what others have also asked (e.g. Where Did SARS-CoV-2 Come From?).

But, Dredd Blog asks the question "where" in terms of not the planet, not the nation, not the state, county, city, nor mammal, but in terms of what single-celled microbe host did the SARS-CoV-2 virus come from.

Microbes are the most abundant single-celled life in and/or on the human body (see video below).

Further, what food source (animal host) does that particular microbe have a mutualistic/symbiotic relationship with?

The candidates which have microbes that SARS-CoV-2 comes from are: avian food (e.g. poultry/birds chickens, turkeys, and ducks); bovine food (e.g. cattle, buffalo, beefalo); porcine food (pork); and, offal from any or all of those (see On The Origin Of The Home Of COVID-19 - 15). 

The predecessor of SARS-CoV-2 is SARS-CoV-1, which had a food related fingerprint:

"On 16 November 2002, an outbreak of severe acute respiratory syndrome (SARS) began in China's Guangdong province, bordering Hong Kong. The first case of infection was traced to Foshan. This first outbreak affected people in the food industry, such as farmers, market vendors, and chefs."

(SARS-CoV-1 outbreak, emphasis added). This series also hypothesized that SARS-CoV-2 comes from damaged or killed (by antibiotics and other toxins) microbes in those food animals during mass production by the food industry (see "III. Big Slaughter Economy" here).

The general scenario is that poor living conditions, in terms of too many animals in a small space, unsanitary conditions, overuse of antibiotics and other drugs/chemicals, along with the food that such animals are fed, cause the demise and/or death of a vast number of microbes within those for-food animals.

As animal-inhabiting-microbes sicken or die within those for-food animals, their replication system composed of machines (ribosomes, ribozymes, etc.) degenerate or malfunction, and cease to properly replicate the viruses within them.

The viruses and microbes within a microbiome (e.g. intestinal microflora) of those for-food animals become damaged or malformed, which we then describe with words such as "mutant", "replicant", "variant", "pathogen", and the like.

When we humans or other animals (e.g. offal-eating mink) ingest any such for-food animal, we ingest any damaged microbes and viruses within them.

II. How

How can SARS-CoV-2 navigate from the enteric realm's microbiome (i.e. microbes in the intestines) into other body locations?

Are viruses alive?

Long story short, that would be, among others, "vascular endothelial cells" where there are ACE-2 entry receptors:

"ACE-2 is an Entry Receptor for SARS-CoV-2" (ACE-2: The Receptor for SARS-CoV-2) ...

"The vascular endothelium is the inner-most structure that coats the interior walls of arteries, capillaries and veins. Endothelial cells (EC) were described to anchor to an 80-nm-thick basal lamina (BL). Both EC and BL constitute the vascular intima, establishing a hemocompatible surface, estimated a total combined surface area of 3000–6000 m2 in the human body, comprising 1 to 6 × 1013 EC ... From their first description in 1865 until the early 1970s, this monolayer was regarded as a mere inert barrier separating blood cells from the surrounding tissue."...

"ACE-2 is a type I transmembrane metallocarboxypeptidase with homology to ACE, an enzyme long-known to be a key player in the Renin-Angiotensin system (RAS) and a target for the treatment of hypertension. It is mainly expressed in vascular endothelial cells ..."

(Vascular Endothelial Cell Biology: An Update, emphasis added). Note that ACE-2 is a good fit for SARS-COV-2 in the abundant realm of vascular endothelial cells.

In the normal, healthy enteric environment there are protections from improper crossing-over from microbiome to bloodstream:

"The intestinal barrier prevents the passage of gut microbiota into the circulation yet allows nutrients to be absorbed. Bacteria that do manage to cross the intestinal epithelium are prevented from entering the bloodstream, despite the close proximity of blood vessels to epithelial cells. “We wondered why bacteria would not easily enter the blood vessels and reach the liver ... thus, we hypothesized that the endothelial cells of the blood vessels might generate a barrier [to bacteria],” explains corresponding author Maria Rescigno."

(Gut endothelial cells — another line of defense). This begs the question how is the determination made as to which microbe is friend and which is foe?

The same question applies to those in the mass animals-for-food industry: what specific microbe contains the SARS-CoV-2 virus?

The vast crowd of microbes, good and bad, must be distinguished for a safe application of microbial justice to take place.

Do the police fire shotguns into a crowd ... or must their arrests be specific and based upon a search warrant identifying with particularity the subject to be arrested?

Every defense has an offense it would seem:

"Antibiotics can selectively decrease tissue invasion and eliminate aggressive bacterial species or globally decrease luminal and mucosal bacterial concentrations, depending on their spectrum of activity. Alternatively, administration of beneficial bacterial species (probiotics), poorly absorbed dietary oligosaccharides (prebiotics), or combined probiotics and prebiotics (synbiotics) can restore a predominance of beneficial Lactobacillus and Bifidobacterium species."

(Therapeutic Manipulation of the Enteric Microflorain Inflammatory Bowel Diseases:Antibiotics, Probiotics, and Prebiotics). In the responses to unhealthy events in the microbiome, a lot is known and a lot is unknown (Enteric microflora contribute to constitutive ICAM-1expression on vascular endothelial cells).

It is known that a lot of the problems are engendered by what goes into our mouths:

"Enteric bacteria typically enter the body through the mouth. They are acquired through contaminated food and water, by contact with animals or their environments, by contact with the feces of an infected person. Every year, millions of cases of foodborne illness and thousands of associated deaths occur in the United States, and the illness burden is even higher in developing countries. Much of this burden could be prevented with better science and prevention tools. We are working to meet national goals to decrease the burden of bacterial diarrheal illness by the year 2020." 

(Enteric Diseases Epidemiology Branch, emphasis added). And so it goes.

III. Closing Comments

The transfer of  "'mutant', 'replicant', 'variant', 'pathogen', and the like" entities mostly takes place undetected:

"In this decision analytical model of multiple scenarios of proportions of asymptomatic individuals with COVID-19 and infectious periods, transmission from asymptomatic individuals was estimated to account for more than half of all transmissions."

(SARS-CoV-2 Transmission From People Without COVID-19 Symptoms, emphasis added). Clearly, the knowledge base must be improved before we can competently proceed to avoid the next pandemic.

The next post in this series is here, the previous post in this series is here.

Video Index (time - subject)

00:21 - microbes are oldest life forms on Earth
01:03 - 10 times more microbes than human cells in us
01:31 - 100 times more microbial genes than human genes in us
02:00 - microbes are 99% of our make-up; they keep us alive
02:20 - microbes are vital for keeping us alive and healthy
04:20 - microbes talk with a molecular language
07:50 - quorum sensing (like a census) to know population count
08:20 - Intra species communication (shape of words) dialects
10:50 - microbes communicate with other microbes (multi-lingual)
11:20 - they take a census of all other microbes around them
12:30 - synthetic molecules-words interrupt communication
13:50 - synthetic molecules-words confuse the microbes
15:00 - they have collective, community behaviors
15:20 - microbes made the rules for multi-cellular development
16:00 - microbes invented multi-cellular behavior inside us
17:15 - the team

Dr. Bonnie L. Bassler, Princeton University: