September 2, 2025

Snika Gupta

Brooklyn Technical High School

12th Grade

HIV is a disease that has vastly impacted the globe, from epidemic to now affecting many disadvantaged communities. HIV is a retrovirus, and because of that, it has been incredibly difficult to find a cure for it. Retroviruses are viruses that do the opposite of what most viruses usually do, which is why they are called "retro." Instead of using DNA as their genomic material, they use RNA. Retroviruses rely on the enzyme reverse transcriptase to infect a host. Once they enter a cell, the retroviral RNA is converted into DNA and inserted into the host cell’s genome. The cell then produces more copies of the retrovirus, which spread to other cells.

There are many retroviruses, though their impact differs between animals and humans. Only six retroviruses affect humans: HIV-1, HIV-2, HTLV-1, HTLV-2, HTLV-3, and HTLV-4. These fall into two main subgroups that affect humans: oncoretroviruses and lentiviruses. Oncoretroviruses are cancer-causing viruses. In humans, these are the HTLVs, which can activate oncogenes or inactivate tumor suppressor genes, sometimes leading to cancer. Lentiviruses include HIV-1 and HIV-2. They are “slow viruses” that cause chronic diseases, most notably AIDS. 

Retroviral particles are called virions. They are about 80 to 100 nanometers in diameter, while a strand of human hair is about 80,000 to 100,000 nanometers thick. Structurally, virions have an outer lipid envelope with glycoproteins that protrude from the surface. Inside, the core protein contains the RNA genome along with enzymes necessary for replication. Despite their small size, retroviruses spread only through direct contact with bodily fluids.

The HTLV family includes HTLV-1, HTLV-2, HTLV-3, and HTLV-4, but most human cases involve HTLV-1. Even in this group, about 95% of carriers remain asymptomatic. HTLV-1 infects lymphocytes and, through its replication process, can cause cancer. Unlike HIV, HTLV-1 maintains genetic stability by replicating when the infected cell undergoes mitosis or by budding from the host cell’s surface. However, free HTLV-1 viral particles are weak, so the virus relies heavily on direct cell-to-cell contact or cell division for transmission. This feature feature explains the low viral load compared to HIV. Importantly, infected T-cells do not die after producing HTLV-1; instead, they continue to divide. HTLV-1 disrupts the host’s transcription factors, which regulate cell division, and this disruption can cause oncogenesis, or uncontrolled cell growth. As a result, tumors may form, and in the case of lymphocytes, leukemia can develop.

HIV-1 and HIV-2, on the other hand, primarily target the immune system, especially CD4 T-cells. HIV enters CD4 cells, replicates inside, and destroys the cell before spreading to others. The cycle repeats, causing a steady decline in CD4 cells. This is why CD4 cell counts are used to measure both the progression of infection and the extent of immune system damage. The body attempts to replace lost CD4 cells, but HIV replication overwhelms these efforts. With a weakened immune system, the person becomes vulnerable to opportunistic infections and other illnesses.

A major challenge with HIV is that its rapid reproduction leads to frequent mutations, which help it evade detection and treatment. A cure is especially difficult because the very cells needed to fight the infection—T-cells—are the ones being infected and destroyed. HTLV infections, by contrast, are much rarer and less studied, particularly in developed countries. Even among people with HTLV, only about 4% develop cancer.