Winning the Fight Against COVID-19

0

“If you know the enemy and know yourself, you need not fear the result of a hundred battles. If you know yourself but not the enemy, for every victory gained you will also suffer a defeat. If you know neither the enemy nor yourself, you will succumb in every battle.”

— Sun Tzu, The Art of War

For nearly a year, the world has been under attack. Not by missiles or bullets, despots or dictators, but by one of the earth’s smallest organisms – a virus. The coronavirus COVID-19 spread quickly, traveling the world in a matter of months once the first “recorded” case was found. It struck everywhere, laying siege to the vulnerable, elderly and susceptible. Through the summer months, we fought back with quarantines and face masks, while scientists and health professionals worked overtime to both learn about the disease and create a viable plan of action. In the last few months, the virus launched a massive offensive that hit us just when we thought we were headed toward victory. Aiding the virus in its fight against us is a sea of misinformation and ill-intended bravado meant to separate and weaken us. A divided population is a vulnerable population. The only way we can defeat this enemy is to do it together.

Regardless of its origin, it’s here and will have to be dealt with before worldwide progress continues, and apathy is no longer a viable solution. So, what can we do? What is the next step? Well, while getting ready to battle any enemy standing across the field, information is key. It is crucial to know what we are up against, our susceptibilities and risks, and how we can fight back in the most effective manner.

Know Your Enemy

Much is known about viruses today and how they operate, but mystery still surrounds the organism. For example, scientists know the biology of a virus, how it infects and reproduces; but the question of whether they are truly alive or not is still up for debate.

The existence of the virus was first hinted at in 1886 by Adolf Mayer as he studied the mosaic disease of the tobacco plant. He made the observation that healthy plants, when exposed to the leafy juice of a diseased plant, will itself become diseased. Mayer attributed the sickness to a bacterial agent present in the juice, but could find no evidence of a bacterium.

Six years later, Russian student Dmitri Ivanovsky repeated the Mayer experiment with a small change. He passed the juice of infected leaves through a Chamberland Filter, which was fine enough to filter out known bacteria. The plants still became  infected by the juice indicating that the infectious agent was something new. In 1898, scientist Martinus Beijerinck posited that the cause of the disease was a “living liquid virus,” coining the term that we use to describe the organism today. (The word “virus” is a Latin term meaning “poisonous substance.”) The actual existence of the virus was confirmed in 1931 with the invention of the electron microscope. The first images of a virus were produced in 1939.

Since that time, scientists have studied the organism(s) in depth in order to combat disease of all types. After all, viruses are the most abundant entities on Earth by an enormous margin and (it’s believed) one of the first. Whether or not a virus is an actual “living” organism is in question. They possess the key elements of a living organism: nucleic acids, DNA or RNA; but, cannot read or act upon the information they possess. A virus needs a host cell to continue.

The purpose of a virus is only reproduction. Once a host cell is “hijacked” the virus uses the cell’s inner machinery to create more of itself. Replication is quick, because a virus constitutes the bare minimum needed to infect and reproduce – nothing more. The structure of a virus is relatively simple (although there are exceptions). Most viruses include a genome (RNA or DNA) and a surrounding protein shell called a capsid. The capsid holds unique protein subunits that help to determine virus function. Some viruses are surrounded by a “greasy envelope” made from stolen pieces of the last cell they infected. Influenza, coronavirus, hepatitis C and HIV are examples of those with a greasy envelope. Soap can disrupt the greasy membrane of these viruses which makes washing hands a great weapon to use against them. Examples of non-enveloped viruses are those that cause the common cold and polio.

Once a virus is completely assembled and ready for infection, it is called a virion. The new virion then leaves the cell in which it was created with the mission of finding another host cell for replication. Once a virus is in a host’s system it reproduces as much as possible until stopped by the host’s inner defenses and/or anti-viral medications. While the virus is spreading throughout the host, it also looks to spread to another host body. For humans, the respiratory passages and open wounds are the easiest route to viral infection. Another mode of viral transportation is through the saliva of insects. Examples of insect-transmitted viruses are yellow fever and dengue fever. One viral host can infect multiple others. For example, one sneeze from a person suffering from the common cold emits 20,000 droplets containing viral particles. Touching or breathing in the droplets are all a cold needs to spread.

When inside a host, a virion must find a new cell to plunder. After one is located, it attaches itself to the cell’s surface and begins looking for a way inside. A virus can penetrate a cell in a number of ways. An enveloped virus can fuse with the host membrane and be pushed through. Some create a porous channel of entry and burrow through (polio) and some can “trick” the cell into letting them in by binding its outside proteins to a receptor on the cell membrane. Once inside, two things begin: the host cell alerts the body’s immune system that an invader is present (although some viral invaders can suppress the distress signal), and the virus hijacks the cell machinery and begins replicating. Like an invading army taking over a munitions plant, the virus utilizes the cells inner machinery to produce new versions of itself. After the cell fills up with virions ready for infection, they can punch holes in the cell membrane causing the infected cell to burst and die. Taking a different route to dispersal, enveloped viruses can wrap themselves in a piece of cell membrane and diffuse through, significantly weakening the cell but not immediately killing it. Other viruses acting as “sleeper cells” of invaders, such as HIV, can sew their genes into the genome of the cell they invaded and can reactivate when immune systems are weakened. This has happened throughout human evolution to the effect that viral DNA sequences make up 8% of our genome.

Making everything so much harder, viruses can mutate (evolve) at an alarming pace. The Influenza virus is notorious for its changing nature – it mutates so quickly that our scientists can barely keep up with it, having to create new vaccines every year. It is believed that COVID-19 mutated from a strain infecting bats to be able to infect humans. There is some evidence to suggest that COVID-19 jumped from bats to pangolins then to humans as the “spike protein” needed for human cell invasion is not found in bats but is found in pangolins. There are other differences in the human version that are not found in other animals, suggesting a third mutation.


Nader-T / stock.adobe.com

Our Current Enemy: COVID-19

We now know how viruses traditionally operate, so it is time to get a little more specific. We need to learn how our current enemy operates. What are its tactics and how is it different from other viruses in history? What makes it so dangerous?

COVID-19 stands for “Coronavirus Disease 2019” and is one of seven known strains of coronavirus. Four strains are quite common and produce mild symptoms in humans. There are now three strains that are more serious. The first was recorded after an outbreak in 2003, named SARS-CoV. It led to 8,000 infections and 774 deaths world-wide. The second was recorded after an outbreak in 2012, named MERS-CoV. It was relegated and stopped in the Middle East where it caused hundreds of deaths. The third and (hopefully) final dangerous strain is termed SARS-CoV2 or, by the common name of COVID-19. The main difference between our current enemy and the coronaviruses of the past lies in onset and severity of symptoms. The first two dangerous coronaviruses we have faced (SARS/MERS) produced acute and intense, serious symptoms in the infected allowing for immediate identification of the disease and quarantine. The older diseases worked quickly and “burned” themselves out before the spread grew. COVID-19 is more insidious. In most people, onset of symptoms is slow and often extremely mild allowing for a period of slightly symptomatic or even asymptomatic transmission which, if left unchecked, can (and has) spread quickly without resistance.

The survival of COVID-19 revolves around the spike protein that covers its outer envelope. These proteins hold multiple functions. They form a sort of suit of armor for the virus which shields the organism from direct contact, enabling it to survive on surfaces for a longer period of time than standard, and they act as keys to enter a host cell. (Soap and hand sanitizers can still disable the virus.) The spike proteins can bond to ACE 2 receptors on certain cells in the body, and trick the cell into allowing entry. Once inside, the replication begins.

The biggest threat posed by COVID-19 is its novelty. The human body has never seen it before and therefore has no immunity to it. As the virus infects our cells, our bodies have no idea how to fight it and, in some tragic instances, figures it out too late. Understanding this makes it easy to see how a weakened immune system can heighten the severity of the disease. The novelty of the virus also makes it more contagious than the influenza virus – it has nothing to stop it right now. Just as the human body is encountering it for the first time, so is science. No coronavirus vaccines existed before the outbreak and COVID-19 is a unique strain causing even more confusion.

Another unfortunate property of the new virus is the kind of cell that it infects. As the virus is inhaled through the nasal passages and mouth, it can travel to the deepest part of our lungs where it infects type II alveolar cells. These cells are responsible for the exchange of oxygen and carbon dioxide in the blood and are the cells in which the virus does the most damage. As the cells become infected, the body defends itself in all sorts of ways, including fluid buildup in the lungs resulting in shortness of breath and pneumonia. As the virus attacks more cells, fluid continues to fill the lungs and inflammation increases, potentially causing acute respiratory distress, abnormal blood clotting, organ failure and death. The more the virus is allowed to attack and destroy alveolar cells, the higher the chance a person will need to be put on a respirator to avoid organ failure. Again, this is a unique attack that we have rarely dealt with. In comparison, the rhinovirus (common cold) attacks upper respiratory cells causing mild distress, but generally leaving breathing untouched, whereas COVID-19 attacks breathing directly. At the time of this writing, COVID-19 presents a mortality rate 30 times higher than the influenza virus. It still presents as a mystery to science and everything from symptoms to transmission is still being studied.


Rawpixel.com / stock.adobe.com

All About Us: Susceptibility and Symptoms

Just as we must know our enemy, we must also know ourselves. Where are we vulnerable? Who is most at risk? How do we know when we are being attacked? These questions must be answered before we engage in battle in order to protect the vulnerable from falling.

Those with the biggest risk are the elderly, pregnant, and immune compromised. These are the people we must protect in this fight. The older a person is, the bigger the chance of a severe infection and in scientific terms, it makes sense. As we age, our immune system also ages and becomes weaker. We have already established that the more alveolar cells the virus manages to hijack, the bigger the chance of hospitalization or death, so it should come as no surprise that 8 out of 10 deaths due to COVID-19 happen to those 65 or older. In addition, older adults are often dealing with other ailments that could further hinder their immune response.

Persons of any age (this includes children) with underlying medical conditions are also at risk. Basically, any condition that can tax the immune system can elevate the chance of hospitalization or death due to COVID-19. As the virus continues its path of destruction, scientists have been on the front lines studying all aspects and have found that those with the following conditions are most at risk:

  • Cancer
  • Kidney Disease
  • COPD (Chronic Obstructive Pulmonary Disease)
  • Heart Conditions
  • Severe Obesity
  • Smoking
  • Sickle Cell Anemia
  • Type 2 Diabetes
  • HIV or Aids
  • Recent organ transplant

This list is not exhaustive, however, and other medical conditions could be added. If you have any medical condition at all, it is best to sit this one out until more information can be obtained.

Another group at risk are pregnant women, who are more apt to develop severe infection due to sharing of resources between the child and the mother. A pregnant woman with COVID-19 has a higher chance of adverse pregnancy outcomes such as pre-term birth. There is no scientific evidence that a baby can contract the virus when in the womb; however, once born, the child could become infected through contact with a COVID-19- positive adult. The effects in newborns have been mild with a few severe exceptions (most often when the child is born with a medical condition).

Those with lower risk are healthy children and adults. One of the biggest frustrations with the virus is that it can produce mild symptoms (or none) in younger people, causing the group to believe themselves immune. This is a fallacy. Science does not know the long-term complications of infection, and will not for a period of years. Also, if a person is experiencing mild symptoms or asymptomatic, they are still contagious and could spread the disease to those who are most vulnerable. (It is important to acknowledge that what we do to thwart the virus is not to protect solely ourselves, but also everyone else. Americans have always cared for and protected one another, especially on the battlefield. We leave no person behind. Again, it will take all of us to win this fight.)

There is some evidence to suggest that men are at higher risk than women to contract a severe case; however, scientists believe that this is due to gender behavior with men having higher levels of drinking and smoking, and displaying a more irresponsible attitude towards undertaking preventative measures. Early in the pandemic, some believed that people with certain blood types showed a higher risk of death by COVID-19 but since then, new research has shown no significant connection between blood type and mortality. One intriguing finding in this instance is that there appeared to be a greater chance of peoples with blood types B+ and AB+ testing positive for the disease, while an even greater chance exists that symptomatic people with blood type O less likely to test positive. One possibility for these findings may lie in the testing procedure itself.

Knowing who is most at risk is step one, recognizing an infection is the second. COVID-19 is a subtle and
confusing enemy. It attacks slowly, often pretending to be something else with its symptoms mirroring other diseases, particularly the flu. While the virus is busy infecting and replicating, host immune cells are attacking the invader, looking for a weakness. If the immune system has encountered the invading army before, the host system already has a blueprint for victory. If not, the immune system must find a new way of attack. The host experiences these attempts as symptoms and in severe cases, the immune system over-reacts (panics), contributing to multi-organ failure and shock. Just like the aforementioned flu, some symptoms of COVID-19 are: fever, cough, muscle aches, headache, sore throat, congestion, and in some cases, vomiting and diarrhea. These symptoms are standard to most viral infections, but some symptoms of COVID-19 are different than the common flu or cold and these are: loss of taste and smell, and shortness of breath or difficulty breathing. During the midst of our fight, it becomes important to get tested as soon as a person experiences any of the symptoms before mingling at work or in public. If someone is experiencing intense symptoms such as trouble breathing, persistent pain or pressure in the chest, confusion, the inability to wake or stay awake or blue-colored lips or face, they should seek medical attention immediately. All exposed should be tested. Science is still learning about the effect of the disease on our bodies and new symptoms are still being catalogued as they occur.


Gorodenkoff / stock.adobe.com

Fighting Back

1. The Scientific Method

Information is paramount when facing the unknown and in the beginning, science new very little about COVID-19. Scientists have only the prior coronavirus outbreaks to study, but as previously mentioned, the current virus is very different, presenting with new biology, symptoms and outcomes. In the beginning, scientists seemed to contradict itself on occasion, first not advocating for mask-wearing and then advocating for it. This frustrated the populace and people lost faith in the process; however, the change of ideas is simply science doing its job. As more information is gathered and more is learned, old suppositions are re-imagined and often changed. Science is a self-corrective process. This is not scientists being wrong, it is scientists making right. When looking for an answer, a decision to follow a particular train of thought can be wrong. This doesn’t mean the person looking for an answer is always wrong or that nothing is advanced. Instead, we have eliminated that train of thought and are moving closer to an answer. In other words, if Indiana Jones is searching for a lost treasure on a jungle island and makes a wrong turn, he has not necessarily wasted time. He has eliminated a route and section of the map, and can now narrow his search even further. He is closing in on his bounty.

Scientists all over the world have been working together and at a record pace to unlock the secrets of COVID-19. Within weeks of the first known case of the disease, scientists had sequenced its full genome and vaccine production had begun in earnest. We are watching scientists try to build a plane while they’re flying it. It is science, albeit quick and dirty, and it is our best defense against any pandemic.

2. The Counter-attack

While science continues to move forward, the lay-person has a job to do. The way to defeat an epidemic is to limit spread – hold our ground, letting the virus get no further. The U.S. has let the virus travel freely across our country for far too long. It’s time to get serious.

Our counter-attack is easy, comprised of three simple things. You already know what they are. Currently, the best ways to fight back are to:

  • Wear a mask in public.
  • Social-distance at six feet or beyond.
  • Quarantine when required.

The goal is to hold the virus at bay until science can find the answer. In fact, if all of us do what we need to, we can end it ourselves over time. Science has figured out that the easiest route of transmission for the virus is through respiratory droplets which can be halted by adequate face coverings and distance. We also have a responsibility to each other to quarantine when feeling symptoms and to get tested before attending a social function or meeting.

3. The Offensive

The best way to eliminate the COVID-19 virus is with a vaccine. Vaccines eliminated smallpox and polio
and nearly eliminated the measles, mumps and rubella. It is our best weapon to date against a microorganism attack. Vaccines take time to develop and, at the time of this writing, two vaccines have been produced with both claiming 95% effectiveness.

The goal of a vaccine is to produce an immune response in the inoculated person. Our immune systems have to learn how to fight each and every disease and the only way for our bodies to learn is to encounter the disease. A virus with 95% effectiveness means that the vaccine will produce an adequate immune response in 95% of people administered the vaccine. The U.S. Food and Drug Administration (FDA) will only approve a vaccine for use if it shows at least 50% effectiveness.

The two COVID-19 vaccines are both mRNA vaccines. This type of vaccine contains material from the COVID-19 virus that gives our body instructions to make a harmless protein that is unique to the virus. It essentially provides an instruction booklet on how to build an intruder. Once the protein (intruder) is built, the immune system recognizes it as a foreign invader and destroys it, making note of how it has done so. The hope is that if COVID-19 invades the body, the vaccinated person’s immune response will recognize the protein and destroy it, therefore killing the virus. Side effects of the vaccine may occur in some people and it is unknown how long the immunity will last. It is possible that in the future, we will expect to get yearly coronavirus vaccines as we do for influenza.

It is understandable if you are skeptical of the COVID-19 vaccine (or vaccines in general). There are some groups that advise against them and a lot of the information out there. Here is some more info to perhaps, ease your mind.

There is little chance that the vaccine will give you the disease. The two vaccines showing efficacy do not use a live virus. It is possible that some slight symptoms are recorded, such as fever, as the body learns to fight off the unique protein it created. Also, the body may take a few weeks to build immunity, so don’t run out into public immediately. Things take time. The vaccine will not alter your DNA, either. The mRNA provided
does not enter our cells or interact with our cellular DNA in any way.

The overall hope for a vaccine is to achieve what is known as “herd immunity.” For example, if 80% of a population is immune to a virus, four out of every five people exposed to the disease won’t get sick and the virus will spread slowly. Currently, nearly 0% of our population has immunity to COVID-19; therefore, five out of five people exposed will get sick. Depending upon the disease, usually 50-90% of the population will need to have immunity to achieve herd immunity. For COVID-19, over 70% immunity may be needed. It is expected that a workable vaccine will be available for everyone by late spring or early summer.


The Battle Ahead

We are in the midst of one of the biggest pandemics we have ever faced. It was a battle we thought we had won or at least were winning. The recent wave has proven us wrong. Science has learned as we all have, and it is up to us to use the information we have gained effectively. We know what it is, what it does and who it targets. We know how to fight it and how to win. Politics aside, as U.S. citizens, we have to work together to end this and get back to doing what we love to do – be it sports, movies, parties, concerts, or being with friends and family. We have the tools … we simply need to execute.

COVID-19 is insidious. In most people, onset of symptoms is slow and often extremely mild allowing for a period of slightly symptomatic or even asymptomatic transmission which, if left unchecked, can spread quickly without resistance.

One of the biggest frustrations with the virus is that it can produce mild symptoms (or none) in younger people causing the group to believe themselves immune. This is a fallacy.

Scientists all over the world have been working together and at a record pace to unlock the secrets of COVID-19.

 


References
Associated Press. (2020). What does COVID-19 vaccine effectiveness mean? Medical Press. Retrieved from https://medicalxpress.com/news/2020-11-covid-vaccine-effectiveness.html

Bwire, G. (2020). Coronavirus: Why men are more vulnerable. SN Comprehensive Clinical Medicine. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/

Canales, M., & Stegmaier, A. (2020). How it attacks. National Geographic. Special Issue 11.2020.

CDC. (2020). Understanding how COVID-19 vaccines work. Cdc.gov. Retrieved from https://www.cdc.gov/coronavirus/2019-ncov/vaccines/different-vaccines/how-they-work.html

D’Souza, G. & Dowdy, D. (2020). What is herd immunity…Johns Hopkins. Retrieved from https://www.jhsph.edu/covid-19/articles/achieving-herd-immunity-with-covid19.html

Gohealth. (2020). What’s the difference between coronavirus, COVID-19 and the flu? Gohealth urgent care. Retrieved from https://www.gohealthuc.com/library/what%E2%80%99s-difference-between-coronavirus-covid-19-and-flu

Goldman, B. (2020). What is a virus anyway? Scope 10k Stanford Medicine. Retrieved from https://scopeblog.stanford.edu/2020/04/02/whats-a-virus-anyway-part-1-the-bare-bones-basics/

Henig, R. M. (2020). In science we must trust. National Geographic. Special Issue 11.2020.

Mayo Clinic Staff. (2020). Pregnancy and COVID-19…Mayo Clinic. Retrieved from https://www.mayoclinic.org/diseases-conditions/coronavirus/in-depth/pregnancy-and-covid-19/

MGH News and Public Affairs. (2020). COVID-19 and blood type. Harvard Medical School. Retrieved from https://hms.harvard.edu/news/covid-19-blood-type

Vidyasagar, A. (2016). What are viruses? Livescience.com. Retrieved from https://www.livescience.com/53272-what-is-a-virus.html

Williams, V. (2020). How the virus that causes COVID-19 differs…Mayo Clinic. Retrieved from https://newsnetwork.mayoclinic.org/discussion/how-the-virus-that-causes-covid-19-differs-from-other-coronaviruses/

Share.

Leave A Reply