Chapter 12: Disorders of the Immune Response, Including HIV/AIDS

The HIV replication cycle encompasses several distinct phases: initial viral attachment through interaction with CD4 receptors and coreceptors such as CCR5, followed by membrane fusion and cellular entry, uncoating of the viral core, and reverse transcription that converts the viral RNA genome into DNA complementary strands. The synthesized DNA integrates into the host chromosome as a provirus, establishing persistent latency while remaining capable of reactivation and production of infectious particles when the host cell becomes activated. As CD4+ cell counts decline below critical thresholds, patients experience increasing vulnerability to opportunistic pathogens including Pneumocystis jirovecii, Mycobacterium avium complex, and cytomegalovirus that rarely cause disease in immunocompetent individuals. Beyond viral immunodeficiency, the chapter addresses autoimmune pathology arising from dysregulated self-recognition, including the mechanism of molecular mimicry wherein pathogenic antigens structurally resemble autoantigens and inadvertently activate cross-reactive lymphocytes that attack host tissues. Primary immunodeficiency disorders resulting from genetic mutations affecting lymphocyte development or function may be treated through hematopoietic stem cell transplantation, though this therapeutic approach introduces significant risks including acute graft-versus-host disease wherein donor-derived T lymphocytes recognize recipient tissues as foreign and mount destructive immune responses. The chapter synthesizes understanding of both acquired and inherited immune dysfunction, treatment modalities, and the complex relationship between pathogenic organisms and autoimmune activation.