Human Immunodeficiency Virus (HIV) is a retrovirus that specifically targets and undermines the body’s defense system. The virus invades certain immune cells, turning them into factories for producing more virus particles. Understanding which cells HIV attacks helps explain how the infection progresses and ultimately causes immune system failure.
The Primary Target: Helper T-Cells
The main target of HIV is the CD4+ T-cell, often called a Helper T-cell. These cells are central to the immune response because they coordinate the activity of other immune cells. They recognize foreign invaders and signal B-cells to produce antibodies and T-cells to destroy infected cells.
The mechanism of attack relies on molecular docking. The HIV envelope protein, gp120, first attaches to the CD4 receptor on the Helper T-cell surface. This binding changes the shape of gp120, allowing it to connect with a second receptor, called a co-receptor.
The co-receptors are typically either CCR5 or CXCR4, and the viral strain determines which one is used for entry. Once the virus binds to both the CD4 receptor and a co-receptor, the viral and cellular membranes fuse. This fusion allows HIV’s genetic material to enter the T-cell and begin replication.
The infected Helper T-cell produces new HIV particles, leading to two outcomes. The cell can rupture and die as new virus particles are released, or it can be destroyed by other immune cells. This continuous cycle results in a progressive decline in circulating Helper T-cells.
Other Immune Cells Attacked by HIV
While Helper T-cells are the primary victims, HIV also targets other immune cells that express the CD4 receptor and co-receptors. These secondary targets include monocytes, macrophages, and dendritic cells, which are part of the body’s first line of defense.
These cells play a distinct role compared to T-cells. Unlike Helper T-cells, which often die quickly, macrophages and dendritic cells are less susceptible to immediate death. This allows them to act as persistent “viral reservoirs” within the body.
In these reservoirs, the virus can maintain low production or remain latent, hiding from the immune system and antiretroviral medications. This persistence is a major challenge for achieving a complete cure. The virus can also infect microglia, the resident immune cells of the central nervous system.
Infection of microglia contributes to neurological symptoms associated with later stages of the disease. Macrophages and dendritic cells are also implicated in the initial spread of the virus. They capture the virus and efficiently pass it on to uninfected T-cells, facilitating systemic infection.
Immune Collapse: The Outcome of Cellular Destruction
The sustained destruction and dysfunction of Helper T-cells leads to progressive immune system failure. The loss of these coordinating cells means the body can no longer effectively defend against pathogens. The normal range for CD4+ T-cells is typically between 500 and 1,500 cells per cubic millimeter of blood.
When the CD4+ T-cell count drops below a specific threshold, the immune system becomes severely compromised. This stage is defined as Acquired Immunodeficiency Syndrome (AIDS). AIDS is confirmed when the CD4 count falls below 200 cells per cubic millimeter of blood.
The compromised immune state allows for the development of “opportunistic infections.” These are illnesses that a healthy immune system would typically fight off easily. They include certain types of pneumonia, fungal infections, and specific cancers that take advantage of the body’s weakened defenses.
The level of actively replicating virus in the blood, known as the viral load, is linked to the speed of cellular destruction. A high viral load indicates rapid viral production and a quick decline in CD4+ T-cells. Effective treatment suppresses the viral load, halting cell destruction and allowing the immune system to partially recover.