World AIDS Day: Remembering The Invisible War That Wages On

By: Joon Kim

Every year on December 1st, individuals across the world embrace the significance of a single red ribbon, worn on clothes, shared on social media, and stuck to public buildings. To many, this red ribbon may appear as just another trend or decoration, yet to the 40.8 million individuals concurrently living with acquired immunodeficiency syndrome (AIDS) as of 2024, a red ribbon holds far more meaning than just that.¹ In fact, December 1st is World Aids Day, a day of awareness for those suffering from the unseen illness, and an even greater recognition for a sneaky viral infection that continues to trump advances in modern-day medicine.

Inherently, the question that comes to you and I at this time: what virus could possibly collect this many victims? The answer, the human immunodeficiency virus (HIV). While most viruses infect cells, replicate, and leave, HIV creates its own rules. It acts as a spy, sneaking into your cells, locating and distorting its very blueprints, and then discretely hiding from the foresight of your very own immune system. This is all completed in an efficient 3-phase mechanism that makes HIV so difficult for scientists to combat. 

Phase 1, is entry. Initially, HIV scans for CD4+ T-cells, the main cell within your immune system that combats foreign disease.² HIV then binds to the surface of these T-cells using interactions between its very own glycoproteins gp120 and gp41, as well as the CD4 receptors on the T-cells.² As they latch on, with the additional help of co-receptor proteins CCR5 or CXCR4, HIV is able to fully secure itself to the T-cell via a connection fusion tube.²

This fusion tube marks the beginning of phase 2, editing the blueprints. After HIV has fused with the T-cell, it releases its viral RNA, the very genetic blueprint that can code for another HIV cell.² In doing so, HIV reveals another trick up its sleeve, the reverse transcriptase enzyme. In normal cells, DNA is typically converted into RNA, yet with the help of reverse transcriptase, HIV is able to turn the released viral RNA back into DNA (3). After doing so, another one of its secret weapons, the integrase enzyme, works its sleight of hand to discretely place the now viral DNA into the existing genome of the host T-cell.⁴ With the work of the two enzymes, the T-cell has now unknowingly been infected, with no way to trace back to where it started. ⁴

As a result, phase 3 commences. With a now infected T-cell, it can become active at any moment, producing additional viral RNA, structural proteins, and enzymes which work to assemble a viral capsid protein.⁹ The combination of such components sets the stage for more infections, allowing HIV to spread through the work of the immune system’s very own T-cells.⁹ 

Subsequently, over months and years, the relentless cycle of infection slowly degrades the body’s immune system.⁵ Eventually, the body becomes a shell of what it used to be, with much of the T-cells now infected by HIV.⁵ Thus, it has become a common misconception that AIDS is a separate disease or illnesses with its own unique symptoms, yet in reality, it is simply the progression of HIV infection at its most advanced stage.⁵ With the spread of HIV, the overall count of CD4+ T-cells drops continuously, reaching a level that leaves the body incredibly vulnerable to various forms of infection, diseases, and cancers.⁵ Illnesses that were once mild and easily treatable such as the common cold or fever may have far more drastic and long-lasting effects within those suffering from HIV, typically referred to as opportunistic infections.⁶ 

Inevitably, another question becomes seemingly apparent: why is there no cure? Unfortunately, due to HIV’s latent reservoirs within the body that carry the integrated DNA, current treatments are unable to pinpoint every minute DNA sequence and terminate HIV sequences entirely.⁷ However, modern-day medicine has advanced to develop antiretroviral therapies (ARTs), which aim to target various aspects of the HIV infection cycle.⁸ For instance, certain ART drugs act as entry inhibitors to block HIV from binding to the T-cell’s surface, while other drugs such as Integrase inhibitors may prevent HIV’s viral DNA from combining into the host-cell’s genome.⁸ Although ARTs appear as the most effective combatant against HIV, they are still limited to its overall impact, only suppressing HIV replication within an infected individual, as well as inhibiting transmission to others.⁸

World AIDS Day serves as a critical day of awareness and acknowledgement, for the millions of individuals who live their day-to-day lives to the fullest despite the degrading effects of AIDS. Simultaneously, this day acts as an appreciation for the decades of scientific innovation and medical advances in treating the deadly virus of HIV. Ultimately, while HIV may remain hidden to today’s medical technologies, the red ribbon of December 1st acts as a symbol of hope and resilience, as medical research inches us closer each day towards a potential end to such a health detriment. 

References

1. UNAIDS. Global HIV & AIDS Statistics — 2024 Fact Sheet [Internet]. UNAIDS. 2025 [cited 2025 Dec 9]. Available from: https://www.unaids.org/en/resources/fact-sheet

2. Wilen CB, Tilton JC, Doms RW. HIV: Cell Binding and Entry. Cold Spring Harbor Perspectives in Medicine. 2012 Apr 10;2(8):a006866–6.

3. Hu WS ., Hughes SH. HIV-1 Reverse Transcription. Cold Spring Harbor Perspectives in Medicine [Internet]. 2012 Jun 14;2(10):a006882–2. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475395/

4. Marchand C, Johnson AA, Semenova E, Pommier Y. Mechanisms and inhibition of HIV integration. Drug Discovery Today: Disease Mechanisms. 2006 Jun;3(2):253–60.

5. National Institute of Health. HIV and AIDS: The Basics [Internet]. hivinfo.nih.gov. 2024. Available from: https://hivinfo.nih.gov/understanding-hiv/fact-sheets/hiv-and-aids-basics

6. Cleveland Clinic. Opportunistic Infections (OIs): Causes, Transmission & Examples [Internet]. Cleveland Clinic. 2025 [cited 2025 Dec 9]. Available from: https://my.clevelandclinic.org/health/diseases/opportunistic-infections

7. Chen J, Zhou T, Zhang Y, Luo S, Chen H, Chen D, et al. The reservoir of latent HIV. Frontiers in Cellular and Infection Microbiology. 2022 Jul 28;12.

8. Spach DH, Wood BR. Core Concepts - Antiretroviral Medications and Initial Therapy - Antiretroviral Therapy - National HIV Curriculum [Internet]. Uw.edu. 2015 [cited 2025 Dec 9]. Available from: https://www.hiv.uw.edu/go/antiretroviral-therapy/general-information/core-concept/all

9. Rossi E, Meuser ME, Cunanan CJ, Cocklin S. Structure, Function, and Interactions of the HIV-1 Capsid Protein. Life. 2021 Jan 29;11(2):100.