An infectious diseases doctor muses on COVID-19

I recently retired from my 45-year career as an Infectious Diseases consultant and can claim some authority and interest in the  COVID-19 pandemic. No one has, so far as I can tell talked about some curious aspects of this outbreak. 

Why don't all people in closed settings like in Wuhan or on the Diamond Princess cruise ship acquire the virus? Three explanations occur to me. 

A) Viruses require compatible binding sites on cells so that they can enter and infect them. Most cells, do not have the appropriate binding sites on their cells. It is known that  COVID-19 binds primarily to respiratory cells and to a lesser extent to gastrointestinal cells. It does not bind to or infect muscle cells or brain cells for example. It may also be that individuals may lack binding sites for  COVID-19. We know that some people cannot be infected with the HIV virus because of cell surface characteristics. It is possible that this is also the case for  COVID-19. It might be that there are racial or other genetic differences that make some less likely to be infected and so unable to pass the infection on. Related to this, three cities in the USA are hotspots. Two, New Orleans and Detroit, are predominantly African-American. Preliminary data from Detroit shows a disproportionately high  rate among African-Americans. The article from a port side think-tank attempts to link this to poverty and crowding. (Detroit has lost 60% of its population so calling it “crowded” might be a bit rosy.) I will admit that cultural factors might play a role in the outbreak in Michigan’s largest city, but genetic factors could confound this analysis. I’d be interested in the racial and ethnic data on infected cases in  a mixed population like in New York City. Unfortunately, political correctness in a leftist enclave like NYC make it unlikely that material that could be construed as racist would be released in a timely and unbiased form. 

B) The well-known interferon phenomenon has been known for at least 50 years. It seems that a cell infected with many kinds of viruses produces proteins that cause itself and nearby cells to become resistant to being infected with other unrelated viruses. The interferon effect lasts for weeks. 

I’m envisioning widespread influenza infection in a population followed shortly by the introduction of  COVID-19. The new virus would not be able to infect most of the people exposed, truncating the infection as has apparently happened in Wuhan itself as well as in Korea, Japan, and Singapore during their winter influenza seasons. There are serologic tests that can determine recent viral infection. These can be done in parallel to doing serologic testing for  COVID-19. It may be possible to determine in hindsight why some were spared the infection. Unfortunately, trying to foster active influenza outbreaks in an attempt to protect populations from  COVID-19 is too theoretical to be tried.

C) It is very probable that the virus itself changes as it passes down through a contagion chain. I read articles in which researchers are able to tell whether one infected individual’s virus is related to that of another individual. The evolved viruses introduced in any one area might be less contagious or have altered binding sites than those elsewhere. 

D) It may be that many individuals in various populations may have been exposed to an infectious agent with antigenic elements shared with  COVID-19 and are immune as a result. If this were the case, we might find a natural and probably benign vaccine.

Another observation is that  COVID-19 Is a serious illness for those over 70 and for those with underlying chronic diseases, and generally is just the flu for younger folks-exactly like ordinary influenza. There are numerous statistical analyses of influenza outbreaks showing excess mortality among elderly and sickly in midwinter, but the death rates fall three or four months later to well below baseline; that is to say, it seems that flu causes folks who are already dying to die a few months earlier.

I have no idea why we would think that medical treatment will have any huge impact. Only about 50% survive. Folks who are on ventilators are seldom healthy after getting off. Every survivor of a stay in the ICU on a ventilator that I've seen is diminished, dazed. Many do not enjoy their remaining life. I offer this iconoclastic observation for what it’s worth.

Erwin Haas was an Army flight surgeon in Vietnam and a Kentwood city commissioner. His forefathers were drunks, smugglers, bootleggers, gamblers and he continues their Libertarian traditions. He Blogs here.

I recently retired from my 45-year career as an Infectious Diseases consultant and can claim some authority and interest in the  COVID-19 pandemic. No one has, so far as I can tell talked about some curious aspects of this outbreak. 

Why don't all people in closed settings like in Wuhan or on the Diamond Princess cruise ship acquire the virus? Three explanations occur to me. 

A) Viruses require compatible binding sites on cells so that they can enter and infect them. Most cells, do not have the appropriate binding sites on their cells. It is known that  COVID-19 binds primarily to respiratory cells and to a lesser extent to gastrointestinal cells. It does not bind to or infect muscle cells or brain cells for example. It may also be that individuals may lack binding sites for  COVID-19. We know that some people cannot be infected with the HIV virus because of cell surface characteristics. It is possible that this is also the case for  COVID-19. It might be that there are racial or other genetic differences that make some less likely to be infected and so unable to pass the infection on. Related to this, three cities in the USA are hotspots. Two, New Orleans and Detroit, are predominantly African-American. Preliminary data from Detroit shows a disproportionately high  rate among African-Americans. The article from a port side think-tank attempts to link this to poverty and crowding. (Detroit has lost 60% of its population so calling it “crowded” might be a bit rosy.) I will admit that cultural factors might play a role in the outbreak in Michigan’s largest city, but genetic factors could confound this analysis. I’d be interested in the racial and ethnic data on infected cases in  a mixed population like in New York City. Unfortunately, political correctness in a leftist enclave like NYC make it unlikely that material that could be construed as racist would be released in a timely and unbiased form. 

B) The well-known interferon phenomenon has been known for at least 50 years. It seems that a cell infected with many kinds of viruses produces proteins that cause itself and nearby cells to become resistant to being infected with other unrelated viruses. The interferon effect lasts for weeks. 

I’m envisioning widespread influenza infection in a population followed shortly by the introduction of  COVID-19. The new virus would not be able to infect most of the people exposed, truncating the infection as has apparently happened in Wuhan itself as well as in Korea, Japan, and Singapore during their winter influenza seasons. There are serologic tests that can determine recent viral infection. These can be done in parallel to doing serologic testing for  COVID-19. It may be possible to determine in hindsight why some were spared the infection. Unfortunately, trying to foster active influenza outbreaks in an attempt to protect populations from  COVID-19 is too theoretical to be tried.

C) It is very probable that the virus itself changes as it passes down through a contagion chain. I read articles in which researchers are able to tell whether one infected individual’s virus is related to that of another individual. The evolved viruses introduced in any one area might be less contagious or have altered binding sites than those elsewhere. 

D) It may be that many individuals in various populations may have been exposed to an infectious agent with antigenic elements shared with  COVID-19 and are immune as a result. If this were the case, we might find a natural and probably benign vaccine.

Another observation is that  COVID-19 Is a serious illness for those over 70 and for those with underlying chronic diseases, and generally is just the flu for younger folks-exactly like ordinary influenza. There are numerous statistical analyses of influenza outbreaks showing excess mortality among elderly and sickly in midwinter, but the death rates fall three or four months later to well below baseline; that is to say, it seems that flu causes folks who are already dying to die a few months earlier.

I have no idea why we would think that medical treatment will have any huge impact. Only about 50% survive. Folks who are on ventilators are seldom healthy after getting off. Every survivor of a stay in the ICU on a ventilator that I've seen is diminished, dazed. Many do not enjoy their remaining life. I offer this iconoclastic observation for what it’s worth.

Erwin Haas was an Army flight surgeon in Vietnam and a Kentwood city commissioner. His forefathers were drunks, smugglers, bootleggers, gamblers and he continues their Libertarian traditions. He Blogs here.