Yeah that… 
Makes sense and I will try to get study source from my friend next time we speak. Still curious to see those numbers.
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However, “that” (post-inoculation) immune-system “busy” period (of developing immunity against target Influenza strains) seems to be (thought) to only last ~2 weeks ? Imagine how much “busier” one’s immune-system might (comparatively) be if it were instead a live Infuenza infection that one’s system were to grapple with (within a similar 2-week time period - or later, following an Influenza inoculation). As well, each years (3 or 4 variant selected) Influenza strains will differ - making upcoming Influenza inoculation brews not necessarily representative of previously studied Influenza inoculation brews. 
Indeed, it is (in my personal experience) quite true that (particularly marginal due to age/disease-states, and already “busied”) immune-systems can be “compromised”. Few objective “transferrables”, though.
Hmmm… kind of a damned if you do and damned if you don’t scenario perhaps.
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Yes - something perhaps like “varying degrees of challenges”, without easily demarcated “certainties”. (Perhaps) the primary “constants” remain: death; taxes; dentists; ER bills; demagogues; and parasites.
And as well, widespread pervasiveness of ClickBait Acres in our Crave New World readily engenders:
Source: https://en.wikipedia.org/wiki/List_of_fallacies
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With a high prevalence of “glycemic” related conditions in many populaces, this info may be of interest:
(The Lancet, April 23, 2020):
“Practical recommendations for the management of diabetes in patients with COVID-19”
(Science Alert, April 23, 2020):
“Scientists May Have Found The Human Cell Types Most Vulnerable to The New Coronavirus”
In a huge, multi-institutional effort involving dozens of scientists, researchers combed through multiple RNA-sequencing datasets, compiling information for thousands of different kinds of cells in humans, non-human primates, and mice. In particular, the team were looking for gene expression patterns for hundreds of cell types in the lungs, nasal passages, and intestine - areas of the body that we know can harbour SARS-CoV-2.
“Because we have this incredible repository of information, we were able to begin to look at what would be likely target cells for infection,” says chemical physicist Alex Shalek from MIT. “Even though these datasets weren’t designed specifically to study [SARS-CoV-2], it’s hopefully given us a jump start on identifying some of the things that might be relevant there.”
Ultimately, the analysis revealed that only a small minority of human respiratory and intestinal cells have genes that express both ACE2 and TMPRSS2. Amongst the ones that do, three main cell types were identified: lung cells called type II pneumocytes (which help maintain air sacs, known as alveoli); intestinal cells called enterocytes, which help the body absorb nutrients; and goblet cells in the nasal passage, which secrete mucus. …
… Among the new results, the team also made a puzzling discovery. A family of immune proteins called interferons, which usually help the body to fight off infections, turns out to stimulate the ACE2 gene that produces the ACE2 protein.
Just why that is remains unknown, but it means that one of our body’s natural defence mechanisms against pathogens, in this instance, could actually end up promoting SARS-CoV-2, by up-regulating production of the receptor the virus uses to cling on to cells. If so, it could be an example of a sneaky evolutionary adaptation, although the researchers say there’s a lot more work to be done to figure out what’s going on here.
“This isn’t the only example of that,” Ordovas-Montanes explains. “There are other examples of coronaviruses and other viruses that actually target interferon-stimulated genes as ways of getting into cells. In a way, it’s the most reliable response of the host.”
.
Original Research Paper:
“SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells
and is detected in specific cell subsets across tissues”
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(STAT, April 23, 2020):
[British Medical Journal (BMJ), April 22, 2020]:
Editorial: “Remdesivir in covid-19”
.
(STAT, April 23, 2020):
(AJEM, April 14, 2020):
“Cardiovascular complications in COVID-19”
Myocardial injury and myocarditis.
Prior viral illnesses, including Middle East respiratory syndrome coronavirus (MERS-CoV), have been associated with myocardial injury and myocarditis with troponin elevation, thought to be due to increased cardiac physiologic stress, hypoxia, or direct myocardial injury. One of the first reports of myocardial injury associated with SARSCoV-2 was a study of 41 patients diagnosed with COVID-19 in Wuhan, China, wherein 5 patients (12%) had a high-sensitivity troponin I above the threshold of 28 pg/mL. Subsequent studies have found that myocardial injury with an elevated troponin level may occur in 7-17% of patients hospitalized with COVID-19 and 22-31% of those admitted to the intensive care unit (ICU). Myocarditis has also been identified with high viral loads and mononuclear infiltrates identified on autopsy of some patients with COVID-19. In fact, one study suggested that up to 7% of COVID-19 related deaths were due to myocarditis. Acute myocarditis presents across a variable range of clinical severity and is a significant diagnostic challenge in the COVID-19 era. Patients with COVID-19 can present with chest pain, dyspnea, dysrhythmia, and acute left ventricular dysfunction. In patients with myocarditis and myocardial injury, serum troponin values will be abnormal. The electrocardiogram (ECG) can demonstrate a range of findings, in some cases mimicking acute coronary syndrome (ACS).
The ECG abnormalities result from myocardial inflammation and include non-specific ST segment-T wave abnormalities, T wave inversion, and PR segment and ST segment deviations (depression and elevation). Echocardiography and consultation with cardiology, if either are available, is encouraged, as differentiating myocarditis and ACS is difficult. Echocardiographic evaluation is more likely to demonstrate a focal wall motion abnormality with active, significant ACS while severe forms of COVID-19-related myocarditis will show either no wall motion defects or global wall motion dysfunction. ECG and echocardiographic abnormalities in the setting of COVID-19 are markers of illness severity and are correlated with worse outcomes. Moreover, troponin elevations in patients with COVID-19 infection have been directly associated with an increased risk of adverse outcome in those patients with severe infection, including mortality.
Acute myocardial infarction.
Severe systemic inflammation increases the risk of atherosclerotic plaque disruption and AMI.
Acute heart failure and cardiomyopathy.
Acute heart failure can be the primary presenting manifestation of COVID-19 infection. One study found that acute heart failure may be present in 23% of patients in their initial presentation for COVID-19, with cardiomyopathy occurring in 33% of patients. Another study found that heart failure was present in 24% of patients and was associated with an increased risk of mortality.
Dysrhythmias.
Palpitations may be a presenting symptom in over 7% of patients with COVID-19. A range of dysrhythmias have been encountered in patients with COVID-19 infection.
Venous thromboembolic event.
Patients with COVID-19 are also at an increased risk of VTEs. Systemic inflammation, abnormal coagulation status, multiorgan dysfunction, and critical illness are all potential contributing factors to the increased risk of VTE.
Medication interactions.
Many of the newly studied medications interact extensively with other cardiovascular drugs, including antihypertensives, antiarrhythmics, anticoagulants, antiplatelets, and statins. Current medications under study include antivirals (e.g., remdesivir, ribavirin, lopinavir/ritonavir, favipiravir), antimalarials (e.g., chloroquine, hydroxychloroquine), azithromycin, corticosteroids, and biologics (tocilizumab).
Somehow, the idea of “viruses in space” is more interesting than “viruses that have cohabited with life-forms all along” (perhaps preceding bacterial forms, in some viewpoints). Yet, by not conforming to our standard definitions of what constitutes a life-form, such remarkable little buggers (having seeming evolutionary “intentions”, and ingenious and robust adaptive-ity to their biochemical circumstances), might be termed “closest” to what one might call “terrestrial aliens” (through our own prisms, anyway). Despite our tendencies to “anthropomorphize”, we are (to all such microbes) “just another substrate”.
Looks like we’ll have to keep a close eye on Georgia.
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Yes- living cells.
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Life After Ventilators Can Be Hell for Coronavirus Survivors
Some never fully recover, and those who do often must relearn basic skills such as walking and swallowing.
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I am slap dab in between Ga and NC… eh who knows??
Seems like Ga is double of NC… and still rising… while SC is even lower than NC…
With ATL CHAR CHAS and Myrtle Beach, one would think SC would be ate slap up…
Even MB is lower than my town…
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GA has something NC does not… “ATL”, one of the busiest airports in the world, with untold infected parties arriving on international flights for how-knows-long before things started getting shut down…
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Explain Charlotte… 
both are mega towns… and both are exactly 2 hours from me… Columbia is 3… but it is smaller than either ATL or CHAR… even here, we have international flights, Phil… do not forget, we have people coming from Germany and Sweden all the time, with BMW, Michegan and Lockheed… SC is a manufacturing state, mostly textiles and car/carp parts now days… but we were the place for cotton, tea and tobacco…
My state is surrounded by infected…
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So defensive.
Hartsfield–Jackson Atlanta International Airport has been the world’s busiest airport every year since 2000
But CLT is 34th so don’t feel too bad. And if it helps, I’ve been there plenty. I usually stop at the Five Guys by the gate I typically get. It’s a nice airport.
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I prefer to fly out of GSP as it is a lot smaller… and because it’s cheeaper to connect to larger flights later. 
Yeah I know… I just hope there is no big flair ups… by June 1… everything should be reopening… then we need to keep an eye out in the fall and spring… it’s not over by a long shot.
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