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New Updates from Dr Mansoor Mohammed Immunologist and functional Genomics Scientist on Corona Virus

How it's spread and details of the virus and precautions you need to take

Two days ago we posted another article from World Leading Functional Genomics Scientist and Immunologist Dr Mansoor Mohammed on the Corona Virus.

Information without the hype and just the facts.

Dr Mohammed has now added this article to the information he wants to share with people about Corona Viruses ability to survive outside the human host and much more 

Dr Mansoor states:

The data collected by Dr. Doremalen and colleagues demonstrate that:
1. SARS-CoV-2 can survive in the aerosolized droplets of our sputum (the saliva and mucus
we emit when we cough, sneeze or even when we simply speak or exhale vigorously).
These microdroplets of our sputum can remain airborne for several hours, and within
them, the SARS-CoV-2 virus can stay alive for up to 3 hours. One would imagine
(correctly) that this does not bode well for being in poorly ventilated, densely
populated environments for prolonged periods during this outbreak.

2. Dr. Doremalen’s study further concluded that the SARS-CoV-2 virus can survive for much
longer periods once they settle – up to 24 hours on cardboard surfaces and up to 2-3
days on plastic and stainless-steel surfaces. Interestingly, copper seems to possess an
inherent anti-viral property – killing the SARS-CoV-2 virus within 4 hours of contact.

3. The porous and fibrous nature of most clothing items makes studying the survivability of
SARS-CoV-2 on them very difficult. Some studies suggest that the virus has a shorter
survivability on clothing fabrics, but those data are far from conclusive. It would be
more conservative to assume that the virus can survive on clothing for at least several
hours (until otherwise clarified)
Now that we have a sense of the survivability of the SARS-CoV-2 virus outside of a host (human
cells), let’s consider some practical ramifications.

Wearing a mass may very well protect you from passing on the virus through your own emitted
sputum (should you be carrying the virus) or from contracting it yourself via airborne
transmission from others. However, aerosolised droplets can be as small as 1-5 micrometres in
size – about 1/30th the width of a human hair. Accordingly, if you choose to wear a mask, you
should ensure that it meets the appropriate filtration specifications. Importantly, masks do not
protect you from touching surfaces upon which viral particles have settled, nor do they
prevent you from transporting them to other surfaces (or other humans).
The take home point here is that wearing a mask does not replace proper hygiene habits, nor
does it replace an intelligent awareness of your environment. We cannot stress this enough.
Engender in yourself and your loved ones, a thorough handwashing habit when leaving
places of high human traffic – shops, public transportation etc – and when returning home, or
to your workplaces.
It is likely worth a gentle reminder of a few of the ghastliest surfaces we often overlook...none
of which are in bathrooms (which of course are germ zones):
1. Handrails. The handrails of escalators have been shown to be some of the filthiest
surfaces in communal areas
2. The containers that are used to place your belongings in as you pass through airport
security are quite literally filthier than the toilets of those same airports
3. Your cell phones are subject to relentless sputum bombs from your mouth day in day
4. Your laptops and other mobile devices

While on the topic of surfaces and cleanliness, the following have been shown to rapidly
inactivate coronaviruses:
1. ~70+ % alcohol solutions
2. 0.5% hydrogen peroxide

3. 0.1% sodium hypochlorite

4. 1⁄4 cup of bleach per 1 gallon of cold water. Please note that a diluted bleach solution
should be used within 24hours, as it loses its disinfecting properties over time
Please exercise extreme caution when interreacting with any of these agents. Under normal
circumstances we would not even recommend some of these disinfectants. However, these
are not normal circumstances.
- Another repeated question we have been asked is in regard to the infection cycle
of COVID-19 and the concept of viral shedding

In our first missive we highlighted that the SARS-CoV-2 virus seems to enter human cells by
binding to the ACE2 cell surface receptor. Think of the ACE2 receptor as the door through
which the coronavirus enters the human cell. Unsurprisingly, these receptors are expressed on
cells of the lower respiratory tract. Interestingly, these receptors are also expressed on cells of
the cardiovascular system (more on this later).
To recap, the SARS-CoV-2 virus binds and enters human cells via the X-linked ACE2 gene
product (which is an enzyme/receptor). Because the ACE2 gene is X-linked, it is likely
differentially expressed in women and men – women have 2 copies of the ACE2 gene, while
men have only 1.
The role of the ACE2 gene in the COVID-19 pandemic is definitely something that we will be
keeping a closer eye on in the coming weeks/months.
(A point of note: a number of clinicians have mistaken the ACE2 gene for the primary ACE
gene. However, the primary ACE gene is located on chromosome 17...and should not be
confused with the ACE2 gene...which is located on chromosome X).
While it must be stressed that these are extremely early observations:
Dr. Zunyou Wu, MD, PhD, chief epidemiologist at the Chinese Center for Disease Control and
Prevention, has presented data showing that more than 40% of people with severe COVID-19
infection had baseline hypertension and cardiovascular disease. Among those with severe
illness, the next most common comorbidity was diabetes, which was about half the rate of
those with underlying cardiovascular disease. Moreover, more men appear to present with
more severe symptoms than women.
Does the difference in expression of the ACE2 gene in men and women explain why there
appears to be a preponderant morbidity and mortality in males? The epidemiologic data
surrounding the COVID-19 outbreak is still extremely sparse and it would be irresponsible to
draw premature conclusions. However, it would be equally irresponsible to leave any strong
associations unexplored. The central role the ACE2 receptor plays in both the infectious cycle
of the SARS-CoV-2 virus as well as in the cardiovascular system; the male/female dimorphism
of the expression of the ACE2 gene; the apparent preponderance of male morbidities and
mortalities; and the confounding comorbidity of cardiovascular disease; all suggest that this is an angle or query that must be further explored.

Moreover, can other genes involved in the risk of chronic inflammation, cardiovascular and
pulmonary disease be used to stratify risk of severity in the COVID-19 infected population?
At The DNA Company we have studied the novel genomic underpinnings of chronic
inflammation, cardiovascular and pulmonary disease susceptibility in thousands of patients.

We intend to aggressively evaluate these insights to determine if they might allow for a better
stratification of COVID-19 infected patients. 

As we discussed in our original missive, it is not the general severity of the COVID-19 outbreak that is concerning. Rather, it is the strain on our healthcare system that is alarming (see below). Any – stress any – insights that better stratify the at-risk COVID-19 infected population will likely not only impact patient survivability, but radically influence the saturation capacity of our healthcare system and response.
Regardless of where the research on ACE2 and underlying cardiovascular comorbidity leads
us, what we do understand is that once the SARS-CoV-2 virus enters the human cell it shows its
true disturbing colours. 

Dr. Wolfel and colleagues from the Institute of Microbiology, Munich,
Germany, have shown that the SARS-CoV-2 virus co-opts the resources and inner machinery of
the human cell in an alarmingly fast manner. All viruses co-opt their host cells to reproduce.
Once they have drained the resources of their host cells, they then erupt from the host cell in
all the glory of their offspring (trust me when I say it’s not an image you want to ponder for too
long). This phenomenon is known as viral shedding. It is the viral shedding that populates your
sputum with millions of viral particles as per our discussion above. The SARS-CoV-2 virus seems
to be shedding faster than previous coronaviruses – and if very early studies are confirmed – at
a rate of 1000X more than the previous SARs coronavirus. 

Said simply, COVID-19 infected patients are apparently spewing 1000X more viral particles per volume of sputum than patients infected with previous coronaviruses...and they are doing so often before they are even symptomatic!
Now to be clear, and to re-emphasise, the degree of viral shedding does not equate to the
severity of the viral infection. We are still dealing with a virus, which for the vast majority of
infected individuals, will lead to only nominally more severe symptoms than the common flu (if
even that). However, for a percent of the infected population (estimated at about 3-4%),
COVID-19 will be a life or death struggle. When combined with the extremely high rate of
transmission (as addressed above) and the symptomologies experienced by those with severe
manifestations of the infection (pulmonary and cardiovascular co-morbidities), it is simply a
numbers game before our healthcare systems become saturated, and we lose the ability to
care for not only COVID-19 patients, but acute trauma patients, child-birthing women, cancer
patients etc., all of whom will demand care from the very system drained by this pandemic.
With these further insights, the conclusion of our initial missive is all the more relevant and
With a mature and purposeful approach to limiting the spread of the COVID-19 outbreak, we
can keep not only ourselves and our loved ones safe, but our communities, and the most at
risk within them, as well. This mature approach will, and must, require a sense of communal


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