Primary Causes & Pathophysiology
HIV binds CD4 receptors (helper-cell docks) with CCR5 or CXCR4 coreceptors (entry helpers). It infects CD4 T cells (helper cells), macrophages (eater cells) and dendritic cells (alert cells). Reverse transcription (RNA to DNA copying) with integration (viral DNA insertion) creates latency (hidden inactive virus). Ongoing replication (virus copying) depletes helpers and drives activation (chronic immune firing). Weak defence then allows opportunistic growth (weak-immunity germs) and cancers.
Lentivirus (slow retrovirus) depletes CD4 helpers through direct killing and chronic activation
Related retrovirus spreads by same routes with slower CD4 decline but similar AIDS risk
Mucosal inoculation (genital lining entry) without condoms allows virus to reach immune cells
Direct bloodstream entry bypasses mucosa and seeds rapid systemic spread
Maternal viraemia (virus in blood) passes to child without preventive maternal therapy and infant prophylaxis (preventive drugs)
Undiagnosed viraemia sustains transmission while low CD4 allows opportunistic disease before care