5 Things For Consideration In Addressing Viral Infections
Understanding the sequential process behind a virus infection is key. Not just for COVID-19, but for any other virus that can get into our bodies via the inhalation of airborne droplets or aerosols.
As the global economy starts to regain its footing and people start going out again, the concern about the COVID-19 pandemic shifts to when a second wave of infections may appear.
That’s a valid concern. We have seen how infectious this virus is, and how severe the consequences of an unmitigated infection can be.
And of course, Gilead isn’t going to let this money spinner get away from them. As CNBC reports, Gilead will be selling their remdesivir for a good chunk of moolah:
The majority of patients treated with remdesivir will receive a five-day treatment course using six vials of remdesivir, the company said. That would bring the government cost to $2,340 for patients on the five-day treatment and $3,120 for commercially insured patients.
The longer, 10-day treatment course will cost governments $4,290 per patient and $5,720 for a U.S. patient with private insurance.
But there are always things that we ought to be mindful about in this entire sequence of events leading to an infection, if we are even aware of the sequence, which is outlined in this article:
- The virus gains entry into the body.
- The virus infects a cell and reprogrammes it to only produce copies of the virus RNA/DNA strands. These virus copies can then proceed to infect other healthy cells and amplify the effects of virus multiplication exponentially.
- Infected cells continue producing virus copies, until antibodies tag the infected cells as infected and programme them to commit suicide via apoptosis.
- These dead cells send out signals to phagocyte cells so that the phagocytes can find them, engulf them and digest them up. This process is known as phagocytosis. The digested RNA/DNA strands are broken back down into their constituent nucleic acids so that new cells can be synthesised to replace the dead ones.
- Signals in the form of pro-inflammatory cytokines can also be sent out to kill these infected cells by force if the rate of phagocytosis is less than the rate of infection. Too many infected or apoptotic cells aren’t good for our health.
Hence, taking appropriate care of these 5 stages can greatly reduce the risk of contracting an infection. But what can we do about these stages?
The virus gains entry into the body
Viruses are able to penetrate our mucous membranes to gain access into our body. It’s not just about the SARS-CoV-2 virus, but any other Tom, Dick or Harry flu virus penetrates the mucous membranes in a similar way.
Hence, the whole idea of social distancing and wearing masks is there. Inhale less droplets that potentially infected people are exhaling, and the risk of contracting an infection is much lower.
In fact, don’t even go out. Be a hermit. Limit one’s exposure to the virus by limiting social contact. In doing so, the chances of infection can go down to zero. Unfortunately, most people are social beings and cannot stand being a hermit. Staying home on a lockdown can drive many people insane and irrational, in fact.
If one does have to go out, masks are important. So is keeping a safe distance from other people.
The virus infects a cell and reprogrammes it to only produce copies of the virus RNA/DNA strands. These virus copies can then proceed to infect other healthy cells and amplify the effects of virus multiplication exponentially.
When the virus infects a cell, the cell essentially becomes hypnotised. It cannot do what it is supposed to do anymore, and only exists to do the bidding of its new master, the virus particle.
The infected cell becomes a photocopier machine and starts churning out more copies of the virus particles, which can then leave the cell and proceed to infect other healthy cells.
As such, infection rates can be increased exponentially. One infected cell becomes two. Two become four. Four become eight. The thing that matters is the doubling time — how much time does it take for one infected cell to become 2?
The initial infection, if not cleared out quickly enough, can proceed into the development of all the full blown symptoms. Some people may be able to deal with the infection satisfactorily such that they do not experience any major symptoms, but they can still be carriers of the virus if their bodies are still working to eliminate the virus completely.
Infected cells continue producing virus copies, until antibodies tag the infected cells as infected and programme them to commit suicide via apoptosis.
Keeping one’s immune defenses up against infection is also important. For example, the body’s production of the immuoglobulin A (IgA) antibody also helps in preventing infection, as it is said here that:
In fact, IgA has long been known to be able to act as a mucosal barrier to infection by preventing attachment of viruses to epithelial cells, and experimental studies in vivo have demonstrated that virus-specific IgA antibodies can protect the host from infection and resolve chronic infection.
Certain strains of probiotic bacteria, such as Lactobacillus rhamnosus GG (LGG), may promote the production of IgA in the body.
When the infected cells and virus particles have been tagged by the virus-specific antibodies, they get inactivated by apoptosis and lie there, dead. They then have to be decomposed down by phagocytosis or lysis.
These dead cells send out signals to phagocyte cells so that the phagocytes can find them, engulf them and digest them up. This process is known as phagocytosis. The digested RNA/DNA strands are broken back down into their constituent nucleic acids so that new cells can be synthesised to replace the dead ones.
The apoptotic cells are then cleared up by the phagocytes, which include the macrophage cells in our immune system. The apoptotic cells send out signals to the phagocytes to find them, digest them and decompose them down back into their constituent nucleic acids.
What we can see here is a sequential process, which can be simplified into:
Infection → Multiplication → Antibody tagging/Apoptosis → Phagocytosis
- If we do take proper precautions to prevent infection, the whole problem can be eliminated right from the start.
- However, if we do get infected by just one virus particle, this virus particle can reprogramme cells in the body to produce multiple copies of itself.
- Antibody tagging deactivates the infected cells, which commit suicide via apoptosis.
- Phagocytosis then proceeds to clear out the dead infected cells so that their constituent nucleic acids can be reused for the synthesis of new cells.
Remdesivir focuses on Stage 2 by preventing virus particles from attaching themselves onto other healthy cells, which thus results in a reduction of the virus multiplication rate.
However, phagocytosis is an important procedure that cannot be ignored. Antibody support is key, but in the final analysis, dead apoptotic cells that aren’t cleared by phagocytosis quickly enough will be producing pro-inflammatory signals when they turn necrotic.
It’s essentially the same thing as food waste. Food waste that is left in a rubbish bin for a long while decomposes and gives off a bad smell. However, if waste removal services are clearing the bin regularly, the accumulation of the decomposition and the bad smell will be much less.
Phagocytosis functions as the waste removal process in this analogy. When phagocytosis isn’t working well…
Signals in the form of pro-inflammatory cytokines can also be sent out to kill these infected cells by force if the rate of phagocytosis is less than the rate of infection. Too many infected or apoptotic cells aren’t good for our health.
If phagocytosis cannot eliminate all the virus particles or infected cells efficiently enough, other immune cells such as the natural killer cells (NKCs) or the dendritic cells (DCs) are called on to aid the elimination process. The NKCs and DCs are signalled by the complex pro-inflammatory cytokine signalling cascades that the macrophages can present, and proceed to produce their own cytokine signallers.
Interferon alpha (IFN-α), for instance, is a cytokine that is produced mainly by the DCs. In large amounts, IFN-α is pro-inflammatory and pyrogenic — it can cause body temperatures to rise, as it is in the case of a fever.
Apoptotic cells that have turned necrotic will also produce pro-inflammatory signals.
The macrophage cytokine signals can also signal a violent cell death via pyroptosis, which releases even more pro-inflammatory cytokines into the mix of an already complicated pro-inflammatory signalling cascade.
As such, all these signalling cascades, if not properly regulated, can contribute to the development of a terrible cytokine storm, which can eventually lead into human death, or permanent organ damage even.
What are the key takeaways here?
There are a few key points here:
- We need to understand that infection and recovery are a sequential process. Recovery is rapid when the clearance rate of the infectious agents far exceeds their multiplication rates.
- Social distancing and providing sufficient barriers to reduce the possibility of infection is highly important if one does have to go out. Practising social responsibility in an environment where the infection potential is high can go a long way to not only protect myself, but also to protect the people around me whom I will be interacting with. These are external measures for protection.
- Internally, we can keep a good defense against infection by consuming the necessary nutrients that can aid in preventing infection and support clearance of the infected cells.
Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 2 ebooks (available on Amazon.com in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should.
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