Coronavirus Severity and Viral Load

I’ve been hearing mostly anecdotal stuff on the news that healthcare workers or people that have more continuous exposure to Coronavirus and patients are developing more severe symptoms of the disease.

I have found some articles about this with a little googling.

https://www.newscientist.com/article/2238819-does-a-high-viral-load-or-infectious-dose-make-covid-19-worse/

The article says higher infectious dose of influenza for example causes worse symptoms, people with higher viral load have more severe symptoms.

So is this some kind of circular logic like people with a weak immune system allow the virus to multiply in greater numbers?

Is it a fact that hospital workers who are around the patients are getting sicker than the average infected patient that picked it up at the grocery store from a small amount of virus on a grocery cart?

Is this a common thing with most diseases and does more severe symptoms also mean more likely to die from it in this context?

Viruses, unlike bacteria, cannot replicate without access to the host’s cells. This means that each individual virus can only infect a single cell, producing hundreds or thousands of copies of itself before the cell undergoes necrosis (non-programmed cellular death), rupturing and expelling the product virions, some of which will go on to affect other cells. The host’s immune system cannot ‘see’ inside the virus inside the cell but the cells produce class I major histocompatibility complex proteins (MHC class I) which will display fragments of protein from the virus upon the cell surface. The host’s immune system produces cytotoxic T-cells which recognize a particular antigenic peptide bound to an MHC molecule, ‘informing’ the immune system of the presence of a pathogenic invader. The T cell releases cytotoxic factors to kill the infected cell which prevents viral replication and release of new virions. The immune system will also develop antigen-specific antibodies, which essentially tackle the pathogens, deactivating and removing them from the body. (There are also intrinsic proteins in the cells called interferons, which deactivate the virus before it can replicate and prompt the host’s immune system, but these don’t work against novel viruses; these are the reason you can be exposed to millions of different types of viruses every day and not be infected.)

It takes time for the host immune system to respond to an new infection; several days to a couple of weeks in most cases, so the higher viral load means more infected cells, and therefore more replications in geometric scale prior to developing immune response, and such a mass of infected cells can overwhelm the host immune system’s ability to destroy virions faster than they are produced. So, having a few infected cells may be just enough to provoke an immune response without developing any evident signs or symptoms, but a massive viral load may overwhelm the immune response of even the most healthy adult. Child, whose immune systems are running at hyperspeed all the time because every pathogen is essentially novel to them, are able to control most infections, hence while the so-called ‘childhood diseases’ like chickenpox and measles are essentially just an irritation for them but can be lethal or have serious and long-lasting consequences for adults.

It is also the case that doctors and nurses, who are in essentially intimate contact (e.g. direct mass contact with droplets or aerosols containing large quantities of virions) are getting exposures deeper within the respiratory system (deep within the pleura of the lung) which causes a much faster and more severe onset of the disease than infection from incidental contact that may only reach the trachea. This results in a faster and more severe onset of the COVID-19 disease before the immune system can even begin to respond, and thus, a more severe progression and greater potential for pleurisy (inflammation of lung tissues), pleural effusion (fluid leaking into the space between the lung and chest wall), or interstitial lung disease (fibrosis) as well as the potential for bacterial co-infection leading to bacterial pneumonia (bacteria colonizing in the lung requiring antibiotic treatment) instead of the more mild bronchial infection resulting in only induced asthma and acute bronchitis in most patients.

There is increasing evidence of aerosol transmission of the SARS-CoV-2 virus, which would explain how rapidly it is able to spread with even casual (non-intimate) contact, but while causal contact will only result in intermittent exposures to aerosols or fine droplets, doctors and nurses working in an enclosed environment with multiple patients are essentially surrounded by the virus at all times. This overwhelms the normal protections and procedures used in hospitals (which are essentially the equivalent of Biosafety Level 2 in operating and exam rooms, and nothing in waiting areas and other areas of the hospital), and since medical personnel are now having to reuse one-use protective equipment such as respirator masks it means that exposure is almost certain as they repeatedly re-don contaminated gear. At this point, the masks are essentially hopeful pleading to prevent infected medical personnel from spreading the contagion to uninfected patients, although again given the infectiousness of this pathogen that may be futile.

So, yes, a higher initial ’viral load’ can lead to faster, more acute, and potentially more life-threatening progression of viral infection and disease, and people in hospitals are significantly more likely to be exposed to both large amounts of virions and in a form (aerosol or fine droplets) which is more likely to be inhaled deeply into the lungs where the infection can do more damage before the host’s immune response is prompted.

Stranger

“Viral Load Distribution in SARS Outbreak”, Emerging Infectious Diseases, 2005 Dec; 11(12): 1882–1886.

From the paper:

Severity of illness did not differ between block E patients and non-E block patients when they were first seen at the hospital, despite higher viral load in block E patients. However, the death rate was higher in block E. We have previously demonstrated that patients with high initial and peak viral loads in nasopharyngeal samples were more likely to show a less favorable disease course and lower survival rate (8,18). Patients living in E7 who had highest nasopharyngeal viral loads explains why their death rate was higher than for those living in other units. The dilution effect resulted in a decreased viral load as the disease spread to other units and in a lower death rate.

Stranger

Thanks, that’s interesting about having a larger amount of virions making their way deeper into the lungs causing much more severe symptoms as opposed to ones that only make it as far as the trachea, that seems common sense in a way but I never really gave it much thought.

Could all this play a role in herd immunity? Like say if younger people that don’t have regular contact with the elderly or immunocompromised could be exposed to a controlled small amount of the Coronavirus. I guess it wouldn’t be a vaccine per se but possibly works as well?

I also wonder if we will see death rates go up considerably among those frontline healthcare workers.

The problem is that while younger people certainly have less incidence of severity and overall less poor outcomes (death, fibrosis of lung tissue, cardiovascular complications) there are some who have severe responses even without any evident underlying health issues, so we just can’t tell who will be fine and who won’t. In the days before vaccination, controlled exposure was used, albeit more as a means to assure that people didn’t get sick at inconvenient time, and a certain amount of mortality was just accepted as part of playing the game of life. Now that we have means to test for, quarantine, and immunize people without direct exposure, those kinds of risks are just deemed as unnecessary and ethically unacceptable except in very restricted cases, e.g. vaccine trials with tight controls.

That is the fear; not only the deaths of the very people who are working tirelessly to care for the ill, but that we may lose a significant portion of the frontline medical workers (not just doctors and nurses but anyone else who is exposed as well) and therefore all medical support will be impacted. We have difficulty producing enough doctors and nurses as it is, and as far as general health care and elder care aides there are few enough people willing to do that kind of work for the paltry level of pay, hence why that vocational group is largely populated by people in poverty and immigrants.

Stranger