I am asking seriously, because severity of symptoms is every bit as important--arguably more important from a public health perspective--as the incidence of symptoms.
A crucial distinction is frequently glossed over in the Pandemic Panic Narrative: the pathogenicity of the SARS-CoV-2 virus vs its virulence.
Pathogenicity is a measure of the virus' ability to cause disease. Virulence is a measure of how severe that disease is.
For example, the viruses which lead to the common cold during cold and flu season have relatively high pathogenicity (because "everyone" literally gets a cold now and then) yet relatively low virulence (mild fever, body aches, congestion and cough for a few days).
Influenza virus, on the other hand, tends to be much more virulent--higher fever, greater aches, longer duration.
SARS-CoV-2 virus, based on the totality of described symptoms and severity that I have seen, appears to be either as virulent or somewhat more virulent than influenza.
This is where one has to be cautious with anecdotal evidence and testimony: a person might plausibly describe symptoms using severe language (the most colorful expression of the experience of COVID I have seen is "felt like hammered dog sh*t!"), yet not feel the need for medical attention or hospitalization, with symptoms resolving naturally within a few days or perhaps a couple of weeks.
If a person has symptoms but does not need medical attention is that a public health crisis or concern? If "everyone" comes down with a mild cold or the equivalent, does that warrant public health interventions such as quarantine of exposed individuals?
If "everyone" is spending several days in the hospital after developing symptoms, does that warrant public health interventions?
That you have not had a history of influenza like illness personally is reflective of the novel nature of the SARS-CoV-2 virus. Even people with robust immune systems are likely, all things being equal, to experience at least some symptoms, because their bodies have no information on how to fight it off--at least some exposure is necessary for the body to develop antibodies and otherwise "program" the immune system to fight this new pathogen.
How serious an individual case of COVID-19 is will always be a matter of individual assessment. That is as it should be. Yet the impact of COVID-19 on the community, just like the impact of any infectious pathogen, will always be driven not by individual appraisals of individual cases, but by the broad changes in the utilizations of public health resources brought on by the illness.
Understanding those changes requires data, not anecdotes.
Peter, I don't know if you saw my conversation with a patient about blood pressure, but the hospital which sent them back home with no warnings about BP falling under severe covid infection why they waited to see if they should come back to the hospital when "they could no longer breathe" despite the fact that the hospital knows they have to use pressers for certain patients, more than others, depending on the BP meds they were taking.
For instance, calcium channel blockers (CCBs), not much need for Bp increasing drugs.
But Angiotensin-converting enzyme inhibitors (ACE) and particularly ACE II inhibitors are known to be affected by the SARS-CoV-19 virus and require frequent presser use.
From a recent article (7-13-2020):
Conclusions
"The RAS and ACE2/angiotensin-(1тАУ7)/MAS axis play important roles in various physiological and pathophysiological contexts. Both SARS-CoV-2 and SARS-CoV use ACE2 as the receptor for entry into host cells. Because ACE2 is highly expressed in various organs and tissues, SARS-CoV-2 not only invades the lungs but also attacks other organs with high ACE2 expression. The pathogenesis of COVID-19 is highly complex, with multiple factors involved. In addition to the direct viral effects and inflammatory and immune factors, the downregulation of ACE2 and imbalance between the RAS and ACE2/angiotensin-(1тАУ7)/MAS axis may also contribute to the multiple organ injuries in COVID-19. The spike glycoprotein of SARS-CoV-2 is a potential target for the development of specific drugs, antibodies, and vaccines. Restoring the balance between the RAS and ACE2/angiotensin-(1тАУ7)/MAS may help attenuate organ injuries in COVID-19."
At the risk of sounding snarky, define "sick".
Sick enough to go to the doctor?
Sick enough to require hospitalization?
Or sick enough to crawl into bed for 7-10 days?
I am asking seriously, because severity of symptoms is every bit as important--arguably more important from a public health perspective--as the incidence of symptoms.
A crucial distinction is frequently glossed over in the Pandemic Panic Narrative: the pathogenicity of the SARS-CoV-2 virus vs its virulence.
Pathogenicity is a measure of the virus' ability to cause disease. Virulence is a measure of how severe that disease is.
https://www2.tulane.edu/~wiser/protozoology/notes/Path.html
For example, the viruses which lead to the common cold during cold and flu season have relatively high pathogenicity (because "everyone" literally gets a cold now and then) yet relatively low virulence (mild fever, body aches, congestion and cough for a few days).
Influenza virus, on the other hand, tends to be much more virulent--higher fever, greater aches, longer duration.
SARS-CoV-2 virus, based on the totality of described symptoms and severity that I have seen, appears to be either as virulent or somewhat more virulent than influenza.
This is where one has to be cautious with anecdotal evidence and testimony: a person might plausibly describe symptoms using severe language (the most colorful expression of the experience of COVID I have seen is "felt like hammered dog sh*t!"), yet not feel the need for medical attention or hospitalization, with symptoms resolving naturally within a few days or perhaps a couple of weeks.
If a person has symptoms but does not need medical attention is that a public health crisis or concern? If "everyone" comes down with a mild cold or the equivalent, does that warrant public health interventions such as quarantine of exposed individuals?
If "everyone" is spending several days in the hospital after developing symptoms, does that warrant public health interventions?
That you have not had a history of influenza like illness personally is reflective of the novel nature of the SARS-CoV-2 virus. Even people with robust immune systems are likely, all things being equal, to experience at least some symptoms, because their bodies have no information on how to fight it off--at least some exposure is necessary for the body to develop antibodies and otherwise "program" the immune system to fight this new pathogen.
How serious an individual case of COVID-19 is will always be a matter of individual assessment. That is as it should be. Yet the impact of COVID-19 on the community, just like the impact of any infectious pathogen, will always be driven not by individual appraisals of individual cases, but by the broad changes in the utilizations of public health resources brought on by the illness.
Understanding those changes requires data, not anecdotes.
Peter, I don't know if you saw my conversation with a patient about blood pressure, but the hospital which sent them back home with no warnings about BP falling under severe covid infection why they waited to see if they should come back to the hospital when "they could no longer breathe" despite the fact that the hospital knows they have to use pressers for certain patients, more than others, depending on the BP meds they were taking.
For instance, calcium channel blockers (CCBs), not much need for Bp increasing drugs.
But Angiotensin-converting enzyme inhibitors (ACE) and particularly ACE II inhibitors are known to be affected by the SARS-CoV-19 virus and require frequent presser use.
From a recent article (7-13-2020):
Conclusions
"The RAS and ACE2/angiotensin-(1тАУ7)/MAS axis play important roles in various physiological and pathophysiological contexts. Both SARS-CoV-2 and SARS-CoV use ACE2 as the receptor for entry into host cells. Because ACE2 is highly expressed in various organs and tissues, SARS-CoV-2 not only invades the lungs but also attacks other organs with high ACE2 expression. The pathogenesis of COVID-19 is highly complex, with multiple factors involved. In addition to the direct viral effects and inflammatory and immune factors, the downregulation of ACE2 and imbalance between the RAS and ACE2/angiotensin-(1тАУ7)/MAS axis may also contribute to the multiple organ injuries in COVID-19. The spike glycoprotein of SARS-CoV-2 is a potential target for the development of specific drugs, antibodies, and vaccines. Restoring the balance between the RAS and ACE2/angiotensin-(1тАУ7)/MAS may help attenuate organ injuries in COVID-19."
https://ccforum.biomedcentral.com/track/pdf/10.1186/s13054-020-03120-0.pdf