HIV progressively destroys CD4+ T-helper lymphocytes, the master coordinators of adaptive immunity, creating immunodeficiency that permits opportunistic infections (OIs) by organisms normally controlled by intact cell-mediated immunity. HIV binds to the CD4 receptor and CCR5/CXCR4 coreceptors on T-helper cells, undergoes reverse transcription, integrates into host DNA, and commandeers cellular machinery for viral replication, ultimately lysing the host cell. As the CD4 count declines, specific OIs emerge at predictable thresholds reflecting the loss of immune surveillance against particular pathogens. At CD4 <200 cells/mm3 (the AIDS-defining threshold), Pneumocystis jirovecii pneumonia (PCP) becomes the primary risk — this fungal organism causes bilateral interstitial pneumonia with progressive hypoxemia because alveolar macrophages and CD4+ T cells can no longer coordinate the granulomatous response needed to contain it. At CD4 <100, Toxoplasma gondii reactivates from dormant tissue cysts in the brain (ring-enhancing lesions on MRI), and Cryptococcus neoformans causes meningitis (the encapsulated yeast evades weakened opsonization). At CD4 <50, Mycobacterium avium complex (MAC) disseminates through the bloodstream (pancytopenia, hepatosplenomegaly), and cytomegalovirus (CMV) causes retinitis threatening vision. Prophylaxis follows these thresholds: TMP-SMX at CD4 <200 (covers PCP...