Organisms have been competing for biological domination since the beginning of life. Evolutionary adaptations arise from genetic mutations, which propel biodiversification and allow organisms with favourable traits to survive and reproduce. This is the foundation of Charles Darwin’s Theory of Evolution, explaining the rise of antimicrobial resistance and contagious viruses, while also offering solutions to these threats in public health and medicine. 

Mutations in the DNA of pathogens allow them to adapt to our immunological defences and invade our bodies. Conversely, the variation in our immune cells allows us to detect and defend against pathogens as a counter-adaptation. Medicine has advanced dramatically in the recent decades, with novel vaccines, antivirals and antibiotics being developed quicker than ever before. Unfortunately, persistent pathogens have found a way to survive attacks from our immune systems and drugs, making it difficult to devise an effective cure for these infections. Take HIV, for instance: the virus activates programmed cell-death in our CD4+ T immune cells and alters their metabolism as a survival mechanism (Gougeon, 2003; Palmer et al., 2016). In turn, this directly reduces the immune system’s ability to defend against the virus. This is further complicated by the high mutation rate of HIV, leading to rapid resistance to various treatment options (Gupta et al., 2018). 

Fortunately, scientific discoveries are helping us develop solutions for infectious diseases. It was found that HIV is susceptible to immune responses in its initial immature stages, which has become a target of the current pursuits in vaccine development for the virus (Picker et al., 2012). Vaccines are beneficial in these cases because they expose memory cells in order to inactive microbial antigens, which are a key cell involved in our active immune responses. This allows our bodies to tackle the pathogens more efficiently, reducing the symptoms and long-term effects of infection. 

Another emerging treatment option is through CRISPR-Cas9 technology. Originally discovered as a bacterial defence system against viruses, CRISPR allows scientists to precisely edit genes. This technology is being explored not only for its potential to correct genetic disorders, but also as a weapon against pathogens. Researchers are looking into using CRISPR to target viral DNA in infected human cells, cutting it out before the virus can replicate (Mengstie & Wondimu, 2021). If successful, CRISPR could be a game-changer in the fight against diseases like HIV, influenza, and even the next pandemic.

However, HIV is just one example of this ongoing evolutionary arms race between pathogens and humans. The phenomenon isn’t restricted to just viruses; bacteria and fungi have also become significant opponents. The rise of antibiotic resistance in bacteria is an alarming and rising public health issue today. Antibiotics are increasingly losing their efficacy due to misuse and overprescription. Pathogens like Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) have developed multiple resistance mechanisms, including the production of enzymes that break down the antibiotic molecules before they can exert their effect (Reygaert, 2018). Methicillin-resistant Staphylococcus aureus (MRSA) is a prime example of antibiotic resistance. Initially, methicillin was developed to treat penicillin-resistant strains of bacteria. However, as methicillin became widely used, new strains of S. aureus emerged that could resist the potent drug. MRSA infections are now incredibly difficult to treat and pose a serious public health threat, particularly in hospitals and healthcare settings where immunocompromised patients are most vulnerable (Collins et al., 2010).

Vaccines are not as effective against bacteria and fungi due to the more complex structures of these organisms. So how do we stay ahead in this race? One promising area of research is the development of next-generation antibiotics and antivirals. Researchers are now investigating bacteriophages—viruses that specifically infect bacteria—as a potential solution to antibiotic-resistant infections. These phages, which evolve alongside bacteria, could be used to target and destroy harmful bacterial strains without the collateral damage caused by traditional antibiotics (Plumet et al., 2022).

While scientific innovation is key to staying ahead in the evolutionary arms race, public health policies play an equally important role. Misuse of antibiotics, for instance, has significantly accelerated the rise of antibiotic-resistant bacteria outside healthcare settings (David & Daum, 2010). Governments and healthcare organisations are now pushing for stricter regulations on antibiotic prescriptions and promoting the responsible use of these drugs. Global collaboration is also essential. Pathogens don’t respect national borders, and the spread of infectious diseases is a global issue. Initiatives like the World Health Organisation’s Global Antimicrobial Resistance Surveillance System (GLASS) are crucial in monitoring and controlling the spread of resistant pathogens worldwide. By sharing data and resources, countries can better coordinate their responses to emerging threats, mitigating the risks posed to global health.

The dynamic shifts in power between humans and pathogens continues to unfold in this evolutionary arms race. While scientific innovation is allowing the development of new tools, from vaccines to gene-editing technologies, we must also adopt policies that promote responsible drug use and global cooperation. In this race, staying at the top of our game requires constant vigilance, innovation, and adaptation—because pathogens certainly aren’t slowing down. The stakes are high, but with continued research and collaboration, we have the potential to maintain the upper hand in this ever-evolving battle for survival.

References

Collins, J., Rudkin, J., Recker, M., Pozzi, C., O'Gara, J. P., & Massey, R. C. (2010). Offsetting virulence and antibiotic resistance costs by MRSA. Isme Journal, 4(4), 577-584. https://doi.org/10.1038/ismej.2009.151 

David, M. Z., & Daum, R. S. (2010). Community-Associated Methicillin-Resistant Staphylococcus aureus: Epidemiology and Clinical Consequences of an Emerging Epidemic. Clinical Microbiology Reviews, 23(3), 616-+. https://doi.org/10.1128/cmr.00081-09 

Gougeon, ML. Apoptosis as an HIV strategy to escape immune attack. Nat Rev Immunol 3, 392–404 (2003). https://doi.org/10.1038/nri1087

Gupta, R. K., Gregson, J., Parkin, N., Haile-Selassie, H., Tanuri, A., Forero, L. A., Kaleebu, P., Watera, C., Aghokeng, A., Mutenda, N., Dzangare, J., Hone, S., Hang, Z. Z., Garcia, J., Garcia, Z., Marchorro, P., Beteta, E., Giron, A., Hamers, R., . . . Bertagnolio, S. (2018). HIV-1 drug resistance before initiation or re-initiation of first-line antiretroviral therapy in low-income and middle-income countries: a systematic review and meta-regression analysis. Lancet Infectious Diseases, 18(3), 346-355. https://doi.org/10.1016/s1473-3099(17)30702-8 

Mengstie, M. A., & Wondimu, B. Z. (2021). Mechanism and Applications of CRISPR/Cas-9-Mediated Genome Editing. Biologics-Targets & Therapy, 15, 353-361. https://doi.org/10.2147/btt.S326422

Palmer, C. S., Cherry, C. L., Sada-Ovalle, I., Singh, A., & Crowe, S. M. (2016). Glucose Metabolism in T Cells and Monocytes: New Perspectives in HIV Pathogenesis. EBioMedicine, 6, 31–41. https://doi.org/10.1016/j.ebiom.2016.02.012

Picker, L. J., Hansen, S. G., & Lifson, J. D. (2012). New Paradigms for HIV/AIDS Vaccine Development. In C. T. Caskey, C. P. Austin, & J. A. Hoxie (Eds.), Annual Review of Medicine, Vol 63 (Vol. 63, pp. 95-111). https://doi.org/10.1146/annurev-med-042010-085643 

Plumet, L., Ahmad-Mansour, N., Dunyach-Remy, C., Kissa, K., Sotto, A., Lavigne, J. P., Costechareyre, D., & Molle, V. (2022). Bacteriophage Therapy for Staphylococcus Aureus Infections: A Review of Animal Models, Treatments, and Clinical Trials. Frontiers in cellular and infection microbiology, 12, 907314. https://doi.org/10.3389/fcimb.2022.907314

Reygaert, W. C. (2018). An overview of the antimicrobial resistance mechanisms of bacteria. Aims Microbiology, 4(3), 482-501. https://doi.org/10.3934/microbiol.2018.3.482