EXAM NOTES: VIROLOGY Year 3 — Past Paper OmpathStudy

HIV/AIDS & Herpes Simplex Virus (HSV-1 & HSV-2) High-Yield Revision Notes Institution: Mount Kenya University — School of Medicine & Surgery Unit: MBMM 3300 — Medical Virology and Mycology Level: MBChB Year 3 --- Papers & Examinations Covered These notes are compiled and structured from the following past papers: Exam Date Paper --- --- --- Main Exam January 2022 MBMM 3300 Paper 1 Main Exam February 2021 MBMM 3300 Paper 2 Main Exam July 2019 MBMM 3300 Paper 2 Main Exam January 2023 MBMM 3300 Paper 2 End of Term CAT December 2020 MBMM 3333 Medical Virology CAT II 2018/2019 MBMM 3233 Medical Virology --- Topics Covered HIV/AIDS — structure, pathogenesis, enzymes, clinical staging, diagnosis, antiretroviral therapy, prevention Herpes Simplex Virus (HSV-1 & HSV-2) — structure, portal of entry, pathogenesis, latency, diseases, selective toxicity of acyclovir, diagnosis, treatment --- How to Use These Notes These notes are built around repeat exam questions from MKU past papers. Every section maps directly to an essay or short-answer question that has appeared at least once — most topics have appeared two or more times. Prioritise sections marked as high yield. --- HIV / AIDS — Complete Study Notes 1. The Virus HIV (Human Immunodeficiency Virus) is a retrovirus that progressively destroys the immune system, ultimately leading to Acquired Immunodeficiency Syndrome (AIDS). Family: Retroviridae Genus: Lentivirus Genome: Single-stranded RNA (two identical copies — diploid) Type: Enveloped virus --- 2. Structure Envelope glycoproteins: gp120 — surface unit; binds CD4 receptor on target cells gp41 — transmembrane unit; mediates fusion with host cell membrane Together they form the precursor gp160 Core proteins: p24 — capsid protein; major diagnostic marker detected by ELISA p17 — matrix protein p7/p9 — nucleocapsid proteins Enzymes packaged inside the virion: Reverse transcriptase Integrase Protease --- 3. Transmission Sexual contact — anal, vaginal (most common globally) Blood and blood products — transfusions, sharing needles Mother to child (vertical) — pregnancy, delivery, breastfeeding Needlestick injuries in healthcare workers HIV is NOT transmitted by casual contact, mosquitoes, saliva, tears, or shared utensils. --- 4. Target Cells HIV infects cells that express the CD4 receptor: CD4+ T-helper lymphocytes — primary target Macrophages Dendritic cells Microglial cells (CNS) Co-receptors required for entry: CCR5 — used by macrophage-tropic strains (early infection) CXCR4 — used by T-cell tropic strains (late infection) --- 5. Pathogenesis — The Most Examined Topic Step 1: Attachment and Entry gp120 binds CD4 receptor Co-receptor (CCR5 or CXCR4) binding causes conformational change gp41 inserts into host membrane → fusion → viral core enters cytoplasm Step 2: Reverse Transcription Reverse transcriptase converts viral RNA → single-stranded DNA RNase H activity degrades the original RNA strand Second DNA strand synthesized → double-stranded DNA (dsDNA) High error rate — no proofreading — causes mutations and drug resistance Step 3: Integration dsDNA transported into nucleus Integrase cuts host DNA and inserts viral dsDNA → provirus Provirus remains permanently in host genome This is why HIV infection is lifelong and cannot be cured Step 4: Transcription and Translation Host RNA polymerase transcribes proviral DNA → viral mRNA and genomic RNA Viral proteins synthesized by host ribosomes Protease cleaves large polyprotein precursors into functional proteins Step 5: Assembly and Budding New viral particles assemble at the cell membrane Virus buds off, acquiring its envelope from the host cell membrane Mature, infectious virions released --- 6. The Three Key Enzymes — Highest Yield Reverse Transcriptase Converts RNA → DNA (unique to retroviruses) Has RNase H activity No proofreading → high mutation rate Drug targets: NRTIs (e.g., Zidovudine/AZT, Tenofovir) and NNRTIs (e.g., Nevirapine, Efavirenz) Integrase Integrates viral dsDNA into host chromosome as provirus Provirus is permanent — basis of lifelong infection Drug targets: Integrase strand transfer inhibitors — Raltegravir, Dolutegravir, Elvitegravir (drugs ending in -tegravir) Protease Cleaves Gag and Gag-Pol polyproteins into functional structural proteins and enzymes Required for viral maturation — without it, virions are non-infectious Drug targets: Protease inhibitors — Lopinavir, Ritonavir, Atazanavir (drugs ending in -navir) Why these enzymes make antiretrovirals selectively toxic: These enzymes are unique to HIV and have no equivalent in normal human cells. Drugs targeting them therefore kill or inhibit virus-infected cells specifically without harming uninfected human cells — this is the definition of selective toxicity. --- 7. Clinical Stages of HIV Infection Stage 1: Acute HIV Infection (Primary Infection) Occurs 2–4 weeks after exposure High viral load, rapid drop in CD4 count Symptoms: fever, sore throat, lymphadenopathy, rash, myalgia — resembles glandul