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HIV Pathogenesis and Clinical Findings

Human Immunodeficiency Virus: Pathogenesis and clinical findings Blood transfusion with contaminated blood product Intravenous use of HIV contaminated needles Sexual intercourse with HIV positive partner (with sufficient viral load) Perinatal transmission during pregnancy, childbirth or breast feeding Direct contact of patient bloodstream or mucous membranes with HIV-1 infected blood, semen, rectal fluids, vaginal discharge or breast milk (HIV-2 is transmitted in similar fashion but is less common & more likely to be seen in West Africa) Authors: Taylor Krawec Ishjot Litt, Naima Riaz Reviewers: Candace Chan, Shahab Marzoughi Emily J. Doucette, Sarah Smith* * MD at time of publication Glycoproteins in HIV viral envelope bind to CD4 & chemokine receptors on CD4+ T-cells & other immune cells Viral & host cell membranes fuse Viral single-stranded RNA (ssRNA) genome & enzymes are released into the host cell Host CD4+ cells are destroyed via direct cytotoxic effects & immune cell-mediated cytotoxicity CD4+ cell count ↓ Virions are disseminated throughout host ↑ Viral load Viral proteins are transcribed & assembled into virions Virions bud off host cell membrane ssRNA is transcribed into proviral DNA by viral reverse transcriptase using host nucleotides Infected cells revert to memory state & establish latent HIV reservoir Chronic HIV infection Host is unable to keep up with loss of CD4+ cells Proviral DNA enters nucleus & integrates into host DNA Acute HIV infection Infected immune cells release proinflammatory cytokines Antibodies to HIV are generated in attempt to control infection (2-12 weeks post infection) Positive antibody-antigen immunoassay Cytokines disrupt hypothalamic temperature regulation Systemic immune system activation results in ↑ metabolic demand Cytokines extravasate to the dermis Fever Maculopapular Chills Fatigue rash Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Viral load ↓ & stabilizes around set-point viral load Oral hairy leukoplakia (oral infection with Epstein-Barr Virus) Complications Viral load ↑ & CD4+ cell count ↓ steadily over several years without treatment CD4+ cell count ↓ to 200-500 cells/μL Impaired host immune response ↑ risk of opportunistic infections Oropharyngeal or vulvovaginal candidiasis Severe manifestations of common infections (ex. herpes simplex, HPV) Published April 22, 2025 on www.thecalgaryguide.com Virus evades immune detection to allow ongoing viral replication, chronic immune activation & ↓ thymic function Vague viral symptoms (ex. fatigue, weight loss, lymphadenopathy) CD4+ count ↓ to < 200 cells/μL Acquired immunodeficiency syndrome (AIDS)