The human immunodeficiency virus (HIV) is a retrovirus that primarily targets and weakens the immune system, specifically CD4+ T-cells and macrophages. Its distinctive shape and internal organization are fundamental to its ability to infect human cells and replicate.
The Overall Architecture of HIV
The HIV virion is largely spherical, with a diameter typically ranging from 100 to 120 nanometers. This outer appearance conceals a sophisticated internal arrangement of distinct layers, each playing a role in the virus’s infectious cycle. The outermost layer is a lipid envelope, which HIV acquires from the host cell’s plasma membrane during the budding process. This envelope incorporates host cell proteins, such as major histocompatibility (MHC) molecules.
Beneath the lipid envelope lies a layer of matrix proteins, specifically p17. This matrix layer associates with the inner surface of the viral membrane, providing structural support and maintaining the virion’s integrity. Further inward, a conical capsid, composed of 1,500 to 3,000 copies of the p24 protein, encloses the viral core. This cone-shaped capsid forms a protective shell around the genetic material and associated enzymes, safeguarding them until the virus enters a host cell.
Key Components and Their Roles
Within the HIV virion reside several molecular components, each with a specific role in the viral life cycle. The core of the virus, encased by the p24 capsid, contains two identical copies of the single-stranded RNA genome. These RNA strands are bound to nucleocapsid proteins (p7), which protect them from degradation.
Within the core are enzymes essential for replication once the virus infects a cell. These include reverse transcriptase, which converts viral RNA into DNA; integrase, which inserts viral DNA into the host cell’s genome; and protease, which cleaves viral polyproteins into their functional forms during maturation. Protruding from the lipid envelope are trimeric complexes of envelope glycoproteins, consisting of gp120 and gp41 subunits. The gp120 subunit is exposed on the outer surface and binds to host cells, while gp41 is a transmembrane protein that mediates fusion with the host cell membrane.
How HIV’s Structure Enables Infection
The precise arrangement of HIV’s components is fundamental to its ability to infect human cells. Infection begins with the attachment of the virion to a target host cell, primarily CD4+ T-cells and macrophages. This attachment is mediated by the gp120 glycoprotein on the viral surface, which binds to the CD4 receptor on the host cell.
Upon binding to CD4, gp120 undergoes conformational changes that expose binding sites for co-receptors, typically CCR5 or CXCR4. Engagement of these co-receptors triggers further structural changes in both gp120 and gp41. These changes in gp41 lead to its insertion into the host cell membrane, initiating fusion of the viral and cellular membranes. This allows the viral core, containing the RNA genome and enzymes, to enter the host cell’s cytoplasm.
Once inside the cytoplasm, the conical p24 capsid protects the viral genome as it is transported towards the nucleus. The capsid then uncoats, releasing the viral RNA and enzymes into the cytoplasm. Reverse transcriptase converts the viral RNA into double-stranded DNA, and integrase inserts this newly synthesized viral DNA into the host cell’s chromosome, establishing a permanent infection.