Human Immunodeficiency Virus (HIV) is a retrovirus that primarily targets critical cells of the immune system, specifically T cells. This infection leads to a progressive weakening of the body’s defenses, ultimately making it vulnerable to various illnesses.
Understanding CD4+ T Cells
HIV largely targets a specific type of white blood cell known as CD4+ T cells, often referred to as helper T cells. These cells are key components of the adaptive immune system, coordinating immune responses. They do not directly attack pathogens but instead secrete signaling molecules called cytokines that activate other immune cells, such as B cells, cytotoxic T cells, and macrophages.
A healthy adult typically maintains a CD4+ T cell count between 500 and 1500 cells per cubic millimeter of blood, reflecting a robust immune capacity.
How HIV Invades and Replicates in T Cells
HIV invades and replicates within a CD4+ T cell through specific binding and entry. The viral envelope glycoprotein, gp120, on the surface of HIV first attaches to the CD4 receptor on the T cell. This binding induces a conformational change in gp120, allowing it to then interact with a co-receptor, typically CCR5 or CXCR4, also present on the T cell surface. This dual-receptor engagement facilitates the fusion of the viral envelope with the T cell membrane, allowing the viral contents to enter the cell.
Once inside the T cell, the viral RNA genome is converted into a double-stranded DNA copy through a process called reverse transcription. This step is catalyzed by the viral enzyme reverse transcriptase. The newly synthesized viral DNA then travels to the cell’s nucleus, where another viral enzyme, integrase, facilitates its integration into the host cell’s DNA. The viral DNA, known as a provirus, becomes a permanent part of the T cell’s genetic material.
The integrated provirus can remain dormant or become active, using the host cell’s machinery to produce new viral RNA and proteins. This involves the host cell’s transcription and translation processes, which generate long chains of viral proteins. These proteins are then cleaved into functional units by another viral enzyme called protease. New viral RNA and proteins assemble near the cell’s surface, forming new, immature HIV particles. These newly formed virions then bud off from the infected T cell, maturing into infectious particles capable of infecting other healthy cells.
The Devastating Effects on T Cell Count and Function
The replication of HIV within CD4+ T cells leads to significant damage and depletion of these crucial immune cells. Lysis, or bursting, of infected T cells occurs as new viral particles bud from their membranes, reducing the overall CD4+ T cell count.
HIV infection also triggers programmed cell death, known as apoptosis, in both infected and uninfected bystander T cells. Even uninfected bystander T cells can undergo this self-destruction, contributing to the progressive loss of CD4+ T cells.
Surviving infected T cells often become dysfunctional, losing their ability to perform their roles in immune coordination. They may exhibit a reduced capacity to activate other immune cells or produce cytokines, compromising the overall immune response. This functional impairment, combined with the direct and indirect cell death, results in depletion of the CD4+ T cell population over time.
Immune System Collapse and AIDS Progression
The progressive depletion and dysfunction of CD4+ T cells due to HIV infection lead to severe immunodeficiency. With fewer functional helper T cells, the immune system becomes increasingly unable to mount effective responses against various pathogens. This leaves the body highly susceptible to infections that a healthy immune system would typically manage without difficulty.
This weakened state allows for the emergence of opportunistic infections, which are illnesses caused by microorganisms that are usually harmless in individuals with intact immune systems. These can include bacteria, viruses, fungi, and parasites, leading to life-threatening conditions. The occurrence of specific opportunistic infections, or a significant drop in CD4+ T cell count, signals the progression to Acquired Immunodeficiency Syndrome (AIDS).
A diagnosis of AIDS is typically made when an individual’s CD4+ T cell count falls below 200 cells per cubic millimeter of blood, or when certain AIDS-defining opportunistic infections manifest. While HIV infection without treatment often progresses to AIDS within 9 to 11 years, modern antiretroviral therapy (ART) has revolutionized HIV management. ART helps to reduce the viral load and preserve CD4+ T cell counts, significantly improving immune function and preventing progression to AIDS.