In this blog post, we’ll explore why pandemics spread repeatedly by examining the relationship between a virus’s genetic material, mutations, and the immune system, and look at the potential of science and technology to prevent them.
In 2015, another “epidemic storm” struck South Korea. The Middle East Respiratory Syndrome (MERS) resulted in 186 confirmed cases in South Korea, 38 of whom lost their lives. At the time, the MERS outbreak sent shockwaves through South Korean society and served as a catalyst for raising public awareness about infectious diseases.
It is often said that as science advances, human life becomes more prosperous. Many diseases—including cancer—that were once considered incurable or intractable are now being treated. However, from the SARS outbreak in 2003 to MERS in 2015, human society has suffered severe blows every time an infectious disease has ravaged the population. So why do humans always suffer damage whenever these “micro-storms” strike? Are infectious diseases simply an unavoidable natural disaster?
It is not easy to completely prevent the outbreak of infectious diseases through human effort alone. The reason for this lies in the fact that viruses were the primary cause of the epidemics that struck South Korea. Of course, the occurrence and spread of infectious diseases vary greatly depending on the type of disease, its mode of transmission, and the level of disease control measures, and it is indeed possible to prevent infections and minimize damage. However, due to the nature of viruses, it is difficult to completely eliminate the possibility of mutations and the emergence of new infectious diseases.
To understand how viruses can be the cause of this “microscopic natural disaster,” we first need to examine how proteins are produced in the human body. The human body relies on proteins both functionally and structurally. For example, the motor protein myosin plays a crucial role in muscle movement, while the protein keratin—found in hair, skin, and nails—helps protect the body.
When producing these proteins, cells use DNA as a blueprint. RNA is synthesized based on the genetic information in DNA, and proteins are synthesized using the information from the RNA. So why do we go through the two-step process of DNA and RNA to produce proteins? One reason is to maintain DNA as a stable repository of genetic information, while copying only the necessary information onto RNA for use in protein synthesis. While DNA preserves genetic information relatively stably, RNA—depending on its type—does not persist for long within cells and is easily degraded. In particular, messenger RNA (mRNA), which is directly used in protein synthesis, serves to transmit information from DNA to the ribosomes. Cells transfer the necessary genetic information to mRNA, use it to produce proteins, and then degrade the mRNA when it is no longer needed, thereby regulating protein production levels. Furthermore, RNA is chemically less stable than DNA, and in the case of RNA viruses, errors are prone to occur during genome replication, leading to the accumulation of mutations. In short, humans transfer genetic information stored in DNA to RNA and use it to produce proteins; it is important to note that RNA is relatively less stable than DNA and can be easily degraded.
Let’s return to the topic of viruses. Viruses possess genetic material, which they transfer into the cells of their host—the human body. Depending on the type of virus, either DNA or RNA serves as the genetic material, and the virus’s genetic information utilizes the host cell’s protein synthesis system to produce the proteins necessary for the virus. The viral proteins and genetic material synthesized in this way are then reassembled to form new viruses. In other words, once viral genetic material enters our cells, our cells are utilized for viral replication; as time passes and large numbers of viruses are produced, the host cells become damaged or destroyed, allowing new viruses to spread to surrounding cells.
The human body detects these viruses and triggers various immune responses, such as producing antibodies or eliminating infected cells. One of the key ways immune cells detect viruses is by recognizing proteins present on the virus’s surface. The immune system recognizes antigens, such as viral surface proteins, and produces corresponding antibodies to neutralize the virus or enable immune cells to eliminate the virus and the infected cells.
Now, let’s consider viruses that use RNA as their genetic material. A significant number of RNA viruses can produce a wide variety of variants because mutations occur at a relatively high frequency during the process of replicating their genome. If, among these mutations, a variant emerges that alters the structure or antigenicity of the viral surface protein, it may partially evade recognition by the existing immune system. In such cases, the body’s immune response may fail to completely eliminate the virus, allowing it to continue replicating and producing new variants. This is one of the reasons why it is difficult to prevent the spread of infectious diseases caused by viruses, and it is also related to why the flu recurs season after season. However, not all RNA viruses mutate to the same extent; the occurrence of mutations and the ability to evade the immune system vary depending on the type of virus, its replication mechanism, and selective pressures.
For example, influenza viruses undergo antigenic subvariation, in which changes accumulate in surface proteins such as hemagglutinin (HA) and neuraminidase (NA), as well as antigenic major variation, in which new subtypes emerge as the genomes of different influenza A viruses undergo reassortment. Antigenic drift is a process involving the accumulation of relatively minor genetic changes; it plays a key role in the recurrence of seasonal epidemics by partially evading existing immunity. In contrast, antigenic shift can occur through genetic reassortment—the rearrangement of genetic fragments when different influenza A viruses simultaneously infect a single cell—and may lead to the emergence of a new viral subtype, potentially resulting in a large-scale epidemic or a pandemic. The 1918 Spanish flu, the 1957 Asian flu, and the 1968 Hong Kong flu are representative examples of influenza pandemics, and a pandemic caused by a new influenza A (H1N1) virus also occurred in 2009. Therefore, rather than assuming that antigenic shifts occur at regular intervals, we must also consider that it is difficult to accurately predict when a new pandemic influenza will emerge.
Just as humans study ways to mitigate damage in preparation for unavoidable natural disasters, research to overcome these “microstorms” is also ongoing. In the past, the Korea Institute of Science and Technology Information (KISTI) conducted research using supercomputers to analyze the mutation patterns of influenza viruses and predict the likelihood of mutations, and since then, research on viruses and infectious diseases utilizing supercomputers, artificial intelligence, and big data has continued. Furthermore, research is underway in various fields, including antiviral drugs that target viral RNA or proteins, therapeutic technologies that target infected cells and genetic material, and virus diagnosis and treatment technologies utilizing nanotechnology. While completely eradicating infectious diseases is no easy task, we can significantly reduce the damage caused by epidemics by understanding the characteristics of viruses, detecting them early, treating them effectively, and developing technologies to prevent their spread.
Quelling this storm to prevent tragedies like MERS from recurring remains a critical challenge that the fields of life sciences, medicine, and public health must address together even today.
