Medical Virology: Hepatitis, Viral OmpathStudy

MEDICAL VIROLOGY — SECTION 2 (Comprehensive Notes) Covers: Hepatitis Viruses → Oncogenic Viruses → Arboviruses → HIV (everything after the Mid-Term CAT) 1. Hepatitis Viruses General concept : "Hepatitis" = liver inflammation. Several unrelated viruses cause it — they differ completely in genome, transmission, and chronicity potential. This comparison table is one of the most commonly tested areas. Virus Genome/Family Transmission Incubation Chronicity? Key exam points --- --- --- --- --- --- Hep A (+)ssRNA, Picornavirus Faecal-oral (contaminated food/water) 2–6 weeks No chronic state Self-limiting; vaccine available; common in poor sanitation areas Hep B dsDNA-RT (Baltimore class VII), Hepadnavirus Blood, sexual contact, vertical (mother-to-child) 1–6 months Yes — can become chronic, especially if acquired at birth Has surface antigen (HBsAg) used for screening; vaccine available; risk of cirrhosis & hepatocellular carcinoma Hep C (+)ssRNA, Flavivirus Blood (transfusion, needles, IV drug use) 2 weeks–6 months Yes — majority (~75-85%) become chronic NO vaccine available; treated with direct-acting antivirals (DAAs) now, very high cure rates; major cause of liver cirrhosis/HCC globally Hep D (Delta) ssRNA, defective/satellite virus Blood, sexual Variable Yes, worsens disease Requires Hep B co-infection to replicate (uses HBsAg as its own coat) — cannot infect alone Hep E (+)ssRNA, Hepevirus Faecal-oral (contaminated water) 2–8 weeks No (except in immunocompromised) Similar to Hep A clinically, BUT high mortality in pregnant women (can exceed 20% in 3rd trimester) — important exam point Non-A Non-B Historical term — — — Used before Hep C/E were identified as distinct agents; now mostly replaced by these specific diagnoses Clinical course pattern to remember for essays : Acute hepatitis (any cause) → fever, malaise, nausea, jaundice, dark urine, pale stool, raised liver enzymes (ALT/AST) → either resolves (Hep A, E) or can progress to chronic carrier state/cirrhosis/hepatocellular carcinoma (Hep B, C, D). Serological markers — Hep B (commonly examined) : HBsAg – surface antigen; marker of current infection (acute or chronic) Anti-HBs – antibody to surface antigen; marker of immunity (from vaccine OR past cleared infection) HBeAg – marker of active viral replication/high infectivity Anti-HBc IgM – marker of recent/acute infection Anti-HBc IgG – marker of past infection (with or without clearance) --- 2. Oncogenic Viruses (Viral Carcinogenesis) Key terms — distinguish clearly for exam : Carcinogenesis – the overall multi-step process by which normal cells become cancerous Oncogenesis – specifically the development of a tumor through activation of oncogenes/inactivation of tumor suppressor genes Tumorigenesis – the formation and progression of a tumor mass How viruses cause cancer (general mechanisms — important for essay answers) : 1. Insertional mutagenesis – viral genome integrates near a host proto-oncogene, disrupting normal control and activating it 2. Viral oncogenes – virus carries its own cancer-causing genes (e.g. HPV's E6 and E7 proteins) 3. Inactivation of tumor suppressor genes – e.g. HPV E6 degrades p53; E7 inactivates Rb (retinoblastoma protein) — both are critical "brakes" on cell division 4. Chronic inflammation – persistent infection/inflammation (e.g. chronic Hep B/C) damages tissue and promotes cell turnover, increasing mutation risk 5. Immunosuppression – some oncogenic viruses act mainly by suppressing host immunity, allowing other oncogenic processes to proceed unchecked (e.g. EBV in immunocompromised patients) Major human oncogenic viruses — table form : Virus Associated Cancer(s) Mechanism --- --- --- HPV (Human Papillomavirus) types 16, 18 Cervical cancer, also anal/oropharyngeal cancers E6 degrades p53; E7 inactivates Rb HSV / VZV (mentioned in outline re: latent infection) Not strongly oncogenic themselves, but their latency mechanism is the model studied alongside oncogenic herpesviruses Establish lifelong latency in neurons; reactivate under stress/immunosuppression CMV Implicated in some cancers (e.g. glioblastoma) — less definitive than others; well known for congenital infection Possible oncomodulation (alters tumor microenvironment) rather than direct transformation EBV (Epstein-Barr Virus) Burkitt lymphoma, Nasopharyngeal carcinoma, Hodgkin lymphoma Infects B cells; drives them to proliferate continuously (immortalization); associated with c-myc translocation in Burkitt lymphoma Hepatitis B & C Hepatocellular carcinoma (HCC) Chronic inflammation + (for HBV) insertional mutagenesis into host genome HHV-8 Kaposi's sarcoma Drives proliferation of endothelial cells, especially in immunosuppressed (HIV/AIDS) patients HTLV-1 (retrovirus, often grouped here) Adult T-cell leukemia/lymphoma Tax protein interferes with cell cycle control Exam tip : If asked "discuss oncogenic viruses," structure your answer as: (1) define carcinogenesis/oncogenesis/tumorigenesis, (2) explain general mechan