Misconceptions About Infections

Being sick is an integral and regrettable part of the human experience, and the average person will likely fall victim to a few symptomatic viral infections every year. Despite being nearly uniformly familiar with the feeling of being acutely sick, many people still maintain an inaccurate understanding of what exactly is going on in their bodies during the course of their “cold”.

What is a Cold?

The common cold, as it is generally understood, is a relatively mild upper respiratory tract infection by any of a small set of similar viral pathogens. The most common of these viruses is the Rhinovirus, and it is the focus of the majority of common cold research in the scientific research community at this point in time. The rhinovirus infects the epithelial (outer layer cells) in your upper respiratory tract, leading to irritation and swelling consistent with sore throats. The irritation also leads to mucus production and a systemic immune response that can result in a fever and other symptoms that fall under the purview of a common cold. But how does the virus cause your body to enter into such a state of misery?

In short, it doesn't; you do. The symptoms of a cold are not the virus damaging your body, so much as they are your body trying to contain destroy the virus. It is true that if you don't have an immune system (as is the case for certain unfortunate people with mutations in genes of the immune system; think of the bubble boy) then the cold virus will still kill you, and would likely cause many of the same symptoms, however in the case of a mild infection the majority of these symptoms originate from your own cells.

To anthropomorphize things, the goal of the rhinovirus (or any virus) is to produce more copies of itself. At the simplest level, a virus is nothing more than a bundle of genetic material that travels from cell to cell in a protective container of lipids and proteins. Viruses are unable to move themselves, cannot replicate on their own, and indeed cannot “do” anything per se, as they do not fit most classical definitions of what constitutes life. In order to reproduce, a virus needs to use some of the manufacturing machinery located within cells of its host organism - in the case of the common cold, it is best suited to reproducing in respiratory epithelial cells. Once a virus is set up in a cell, it would be “happiest” to just remain there and produce copies of itself ad infinitum. At some point, the cell would likely burst open or tear apart due to the sheer number of viral particles that it contained, or the lack of normal cellular processes that it was able to engage, but in the meantime millions of viral particles would likely be produced, which could then exit the cell and enter nearby cells where the process can be repeated. One of the body's best ways to combat this is, in many circumstances, to kill the cells that are infected with viruses.


Indeed, it is believed that many infected cells may undergo a programmed cell death that enables us to shut down these viral factories before they reach maximum capacity. Some cells will likely die, especially early in the infection, from viral damage, and this death coupled with signals from the virus itself will recruit white blood cells to the site of infection. These cells are specialized to engulf and destroy invading pathogens, or to produce toxic molecules and antibodies that destroy infected cells and viral particles respectively. As white blood cells stream into the site of infection, blood vessels increase in diameter in order to slow localized blood flow, thereby allowing cells to escape the blood stream and enter tissues. As cells enter tissues and blood vessels expand, patients will experience the classical symptoms of redness, swelling, and pain that are central aspects of an acute inflammatory reaction. If the response is severe enough, these cells will also release inflammatory mediator molecules that travel through the blood to the brain, where they alter certain chemical pathways to produce a set of behaviors commonly called “sickness behavior”.

Sickness behaviors include social withdrawal, decreased appetite, and most notably fever. Fevers occur when certain inflammatory molecules act on the hypothalamus portion of the brain in such a way that they effectively raise the normal temperature of the body by a few degrees (or higher, in severe cases). While it is difficult to determine the true purpose of sickness behavior from a disease resolution standpoint, it is easy to speculate as to the cause. For example, viruses are able to reproduce most readily at certain temperatures which mirror those found in the sites of the body where they reproduce; for example, rhinovirus reproduces best at the temperature of cells near the mouth and nose where it is slightly cooler, and it cannot grow at the warmer temperatures found deep within the lungs and the rest of the body. A fever raises the body temperature enough that it is able to make the environment somewhat less hospitable for the invading virus, thereby aiding the immune system in clearing the threat as soon as is possible. Social withdrawal and decreased appetite are more complex social behaviors, which likely have an evolutionary advantage rather than an immediate host advantage. These actions are likely able to help prevent the spread of disease through human contact and food contamination, thereby protecting the population as a whole.

By killing infected cells, the immune system reduces the ability of the virus to reproduce and enables its clearance from the body, but in the process it damages host tissues. This damage is typically the major driver of the sore throats that typically accompany respiratory infections, as swelling and death of cells in the throat epithelium contribute to localized pain that is familiar to us all. The mucus secretion that leads to congestion stems from inflammatory signals that cause a special mucus producing cell known as the Goblet cell to release increasing amounts of this complex compound, which fills the airways in order to prevent viral particles from reaching the epithelium and enable their clearance. Coughing aids in the removal of mucus and virus, and stems from stimulation of specialized nerve cells in the throat.

In essence, while the pathogen that causes the cold has the potential to cause damage on its own, the immune system has this same potential. These two forms of damage - pathogen induced and host induced - are effectively opposite ends of a single spectrum. Increased inflammatory damage will typically result in less pathogen induced damage and, however if the combined damage is above the threshold that the host can tolerate, the damage will be catastrophic. In these cases of runaway inflammation, without treatment the host can easily die from extremely high fevers or other issues that destroy normal bodily functionality. The immune response to any disease, be it viral, bacterial, or parasitic, is a balancing act that requires clearance of the offending agent without irreparably damaging the host, and people with a competent immune response are almost always able to achieve this response with ease. For this reason, common colds are not a major threat to the majority of the human population, and only when age or disease alters the immune response does this balance shift in a pathogenic direction.

Treating Infections

As most people are aware, there is no treatment for the common cold or for the majority of viruses that plague the human population, which means that those infected with these viruses are only able to receive symptomatic treatments. These treatments typically aim to combat the immune system's effects that have been causing the host to feel ill, which is why asprin and tylenol-containing drugs will typically reduce swelling and lower a fever, thereby eliminating certain aspects of sickness behavior and inflammatory responses. In essence, these drugs likely slightly shift the balance of power between viral and host damage. In practice, however, no scientific studies to date suggest that there is any significant danger in taking these drugs; if they do allow for viruses to grow slightly better, the difference is largely negligible, and the tradeoff for patient comfort likely makes up for the issue. Indeed, the biggest drug related issues for treating the cold are those raised by patients that want to be treated with antibiotics, even though these drugs are ineffective against viruses of any kind.

In summary, viruses want to use host cells to replicate themselves, and they will do so at a cost to the fitness of the host. The host, in turn, seeks to eliminate this virus, and in doing so it inevitably engages certain responses that cause significant collateral damage, with this damage causing the classical symptoms of the common cold and many other viral infections. This inflammatory response helps to resolve the infection, and so long as it does not permanently damage host functional processes it is likely for the best in the long run. In time, viruses are eliminated from the body, and the immune system produces antibodies to ensure that these diseases don't re-infect their original host. Inflammatory responses dissipate, causing sickness behaviors to wane and allowing swelling to subside. Over the course of the next few days, epithelial cells regrow and in 1-2 weeks most people will not even be able to tell that they recently suffered from a cold, provided that they are not so unfortunate as to have to deal with a secondary bacterial infection.


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