Molecular War: Why Some Diseases Can Be Cured While Some Can’t?
by Muhammad Danish Azarisman
Perhaps. The simple answer to “Can all diseases be cured?” would be “Perhaps”. In 2011, the Rinderpest virus, a virus with a 100% fatality rate, was declared successfully eradicated from the earth. If you told someone 20 years ago that such a disease could be eradicated, they may not have believed you. If we are told that cancer would be curable 20 years into the future, would we believe it? While the limitations of medical technology have yet to be determined, certain diseases appear to be more “treatable” than others.
Now, why is that? What differentiates treatable diseases from non-treatable diseases? Why can some diseases be cured while others cannot? Just as people differ in terms of their personalities and skills, our ability to tackle diseases can vary drastically depending on the underlying mechanisms of the disease. In this article, we will compare curable and incurable diseases to find out the factors that determine whether a disease is treatable or not, using examples of viral diseases and non-infectious diseases.
A viral disease or viral infection refers to a disease that is caused by a virus. Ranging from colds, the flu, and COVID-19, to norovirus and many more, some viruses can inflict severe adverse effects while others can be handled by our bodies on their own. First, we will take a look at treatable viral diseases.
Have you ever wondered what happens when you get a cold? You might feel hot and fatigued one day, but all of a sudden, you’re back on your feet the next day! This is what happens when your body does its job right. The pathogens inside your body are successfully flushed out by your body’s immune system. In other words, these simple infections are easily curable.
Common colds are usually caused by rhinovirus. Rhinoviruses enter your body through the mouth, ears, and eyes, breaching your body’s first line of defence. At first, these viruses fly under the radar, but when a certain virus population is reached, they change their behaviour and begin to damage the body. The immune system must stop them as fast as possible. First, your guard cells, known as macrophages, intervene. They are huge cells that guard every border region of the body. Most of the time, they alone can suffocate an attack because they can devour up to a hundred intruders each. They swallow the intruders whole and trap them inside a membrane. Then, the enemy is broken down by enzymes and killed. When the macrophages fight for too long, they call in heavy backup by releasing messenger proteins that communicate location and urgency, causing neutrophils to leave their patrol routes in the blood and move to the battlefield. The neutrophils fight so furiously that they kill healthy cells in the process. If this is not enough to stop the invasion, the brain of the immune system kicks in.
Now, this is the important part. Cells called dendritic cells are activated. Dendritic cells are specialised immune cells that present viral antigens on their surface to other cells of the immune system. In this case, dendritic cells will display viral antigens of the rhinovirus. In short, it reacts to the signals of the soldiers and starts collecting viral antigens from the rhinoviruses, ripping them into pieces and presenting the parts on their outer layer. They then travel to the closest lymph node where T cells and B cells are located. These cells will produce antibodies with specific characteristics obtained from the dendritic cell. With an army of antibodies, the rhinoviruses have no chance of winning, and you will be healthy and happy in no time. However, viral diseases are not always so easily dealt with. Case in point: the Ebola virus.
According to the World Health Organisation, the average case fatality rate of Ebola is around 50%, but this can rise to 98% when left untreated. What makes this virus so devastatingly deadly? During mild viral infections, dendritic cells will activate an army of anti-virus cells, support cells, and antibody factories that work together with the guard cells to wipe out the infection in a matter of days. But when Ebola strikes, it attacks the immune system directly. Some of the first cells it takes over are the dendritic cells, the brains of the immune system. The Ebola virus enters a dendritic cell by binding into receptors for cell transport. Once the virus makes its way inside, it dissolves its outer hull and releases its genetic material, nucleoproteins, and enzymes, taking over the cell, disabling the cell’s protective mechanisms, and reprogramming it. The cell now becomes a virus production machine and uses its resources to build Ebola viruses. Once the cell is saturated, it dissolves the cell membrane and millions of viruses are released into the tissue. The virus not only prevents the dendritic cells from activating the specialized and anti-virus forces, but it also manipulates them into sending signal proteins that trick cells into ending their own lives prematurely.
Compared to the common cold, the Ebola virus targets our main weapons first to turn the tide of battle in their favour. A manipulated dendritic cell commands T cells to instruct B cells to produce more Ebola viruses. So instead of having an army of antibodies to combat this virus, we have a literal Ebola virus factory inside our bodies. At the same time, Ebola infects the guard cells of the body macrophages and monocytes, not only circumventing their defences but also manipulating them to signal the release of fluid into the body. As the virus spreads, mayhem ensues throughout the immune system, not unlike setting off nukes around the body. From this point onwards, the virus infects more and more body cells while the body desperately struggles to stay alive.
Wow! Okay, Ebola is nasty. So, it’s time to panic, right? No, not even close. The severity of Ebola gets papers sold and YouTube videos shared, but it’s crucial to note that currently, the only way to get infected by Ebola is to come in contact with the body fluids of a person who shows symptoms or from an infected bat, such as through objects that have been contaminated with infectious Ebola secretions. Ebola has killed 5,000 people since June 2014, but the flu kills up to 500,000 people each year. For comparison’s sake, malaria causes up to one million deaths each year — that’s 3,000 people every single day! As we can see from the two viruses above, they both will manipulate our body systems, primarily our immune system as all viruses require hosts to live and multiply.
Viral diseases are scary. We are constantly exposed to risks of infection, and worst of all, we can’t see or sense them. But what is perhaps scarier is a disease that lurks inside you, waiting for a chance to strike and destroy you from the inside. The most notorious of these diseases is, of course, cancer. Cancer is a disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body. Cancer can start almost anywhere in the human body.
Normally, human cells grow and multiply to form new cells. When cells grow old or become damaged, they die, and new cells take their place. Sometimes this orderly process breaks down, and abnormal or damaged cells grow when they shouldn’t. These cells may form tumours, which are lumps of tissue. Tumours can be cancerous or not cancerous. Cancerous tumours spread into or invade nearby tissues and can travel to distant places in the body to form new tumours in a process called metastasis. On the other hand, non-cancerous tumours, or benign tumours, do not spread to other parts of the body. Once removed, benign tumours do not usually grow back, whereas malignant tumours often do.
Different cancers have different survival rates. To understand the difference in outlook between cancer types, researchers often use a statistic called the 5-year survival rate. This figure refers to the percentage of people who survive for 5 years after the diagnosis of cancer. The 5-year survival rate does not indicate whether a treatment has removed all signs of cancer, but it is useful for comparing the relative severity of different types of cancer. In this section, we will compare breast cancer, which has a relatively high 5-year survival rate, with pancreatic cancer, which has a low 5-year survival rate.
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The main factor which determines the survival rate of cancer is, in many cases, how early it can be detected. An early screening process enables countermeasures to be taken instantly and effectively. Breast cancers are usually detectable at early stages as most patients feel odd lumps externally on their breasts that would lead them to go for a check-up. Hence, early treatments such as surgery to remove the lump, chemotherapy, and radiotherapy can be done safely and accurately to eradicate the cancer cells, effectively “curing” the disease. This contrasts with pancreatic cancer, which is incredibly difficult to detect due to the position of the pancreas deep inside the body. Often, pancreatic cancer is only diagnosed once symptoms such as abdominal pain, dark-coloured urine, and blood clotting occur, by which time the cancer has already reached stage 3 or stage 4 and metastasised to other regions in the body. When this happens, survivability drops significantly.
Of course, they are more complexities that we need to consider when discussing cancer. For instance, some aggressive tumours can have multiple populations of slightly different cancerous cells. Over time, distinct genetic mutations accumulate in cells in various parts of the tumour, giving rise to unique subclones. For example, aggressive brain tumours called glioblastomas can have as many as six different subclones in a single patient. This is called clonal heterogeneity, and it makes treatment even more difficult because a drug that works on one subclone may have no effect on another.
Here is another challenge. A tumour is a dynamic interconnected ecosystem where cancer cells constantly communicate with each other and with healthy cells nearby. They can induce normal cells to form blood vessels that feed the tumour and remove waste products. They can also interact with the immune system to suppress its function, keeping it from recognizing or destroying cancer. If we could learn how to shut down these lines of communication, we would have a better shot at vanquishing a tumour permanently. Additionally, mounting evidence suggests we will need to figure out how to eradicate cancer stem cells. These are rare but seem to have special properties that make them resistant to chemotherapy and radiation. In theory, even if the rest of the tumour shrinks beyond detection during treatment, a single residual cancer stem cell could seed the growth of a new tumour. Figuring out how to target these stubborn cells might help prevent cancers from coming back.
Even if we solved those problems, we might face new ones. Cancer cells are masters of adaptation, adjusting their molecular and cellular characteristics to survive under stress. When they are bombarded by radiation or chemotherapy, some cancer cells can effectively switch on protective shields against whatever is attacking them by changing their gene expression. Malignant cancers are complex systems that constantly evolve and adapt. To defeat them, we need to find experimental systems that match their complexity and monitoring and treatment options that can adjust as the cancer changes.
Even though a lot has been covered, there is, in my opinion, still a lot more to what has been discussed in this article. In summary, it is safe to say that what differentiates an incurable disease from a curable one is how much we know about the disease itself. That being said, we may one day reach a point where we can devise treatments for every conceivable disease. Personally, I believe that with enough time and development, we can out-evolve pathogens. After all, we are learning more every day, and each new piece of information gives us one more tool to add to our arsenal.
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