Master Rhinoviruses & RVFV: Common Cold & Zoonotic Fever

--- VIROLOGY EXAM NOTES — PART 2 OF 2 --- 4. RHINOVIRUSES Classification: Family Picornaviridae. (+)ssRNA, non-enveloped, 27–30 nm. Ether-resistant (no lipid envelope). 100 serotypes. Infect only humans and chimpanzees. Grow best at 33°C (nasal cavity temperature — this is why they don't infect lower respiratory tract). Epidemiology: Worldwide. Highest attack rates early fall and winter. Spread by large droplets AND hand contamination/self-inoculation (hand-to-nose/eye). Children spread more efficiently than adults. Adults with school-age children have twice as many colds as those without. Pathogenesis: Enters upper respiratory tract → attaches to ICAM-1 receptors on nasal ciliated epithelial cells Replicates → damages cilia and epithelium → secondary bacterial infection possible Peak viral titers in nasal secretions at 2–4 days post-exposure Viral titers then fall but illness persists (immune-mediated component) Histology: vascular engorgement, edema, mild cellular infiltration, epithelial desquamation complete by day 3 Nasal secretions increase in quantity and protein concentration Clinical Features: Incubation: 2–4 days. Illness: ~7 days. Non-productive cough may persist 2–3 weeks Adults average 1–2 colds per year Symptoms: nasal discharge, headache, mild cough, malaise, chilly sensation, minimal or no fever , reduced sense of smell, mild hoarseness Complications (especially children): otitis media, sinusitis, bronchitis, pneumonitis Diagnosis: RT-PCR = gold standard. Culture possible but not clinically useful. Treatment: No antiviral. Supportive only — rest, rehydration, decongestants, cough suppressants. Exam traps: Grows at 33°C not 37°C → confined to upper airway 100 serotypes → no vaccine feasible No fever or minimal fever (differentiates from influenza) Non-enveloped = ether resistant Most common cause of the common cold worldwide Viremia does NOT occur --- 5. RIFT VALLEY FEVER VIRUS (RVFV) Classification: Family Bunyaviridae. RNA virus. Zoonosis. History/Epidemiology: First identified in Rift Valley Province, Kenya, 1930. Re-emerged 1997/98 following El Niño rains. Reported following heavy rains and floods. Causes abortion storms in cattle — key agricultural clue. Transmission: Mosquito bite — Aedes or Culex species Direct contact with body fluids or tissues of infected animals High-risk: farmers, abattoir workers, veterinarians Pathogenesis: Initial targets = antigen-presenting cells and macrophages Virus AVOIDS presentation to regional lymph nodes (immune evasion) Replicates locally → viremia → systemic spread targeting vascularised organs (liver, spleen, brain) Clinical Features — Three Distinct Syndromes: MILD FORM (majority): Incubation 2–6 days. Influenza-like illness — fever, headache, muscle pains, backache. Self-limiting. SEVERE FORM: Haemorrhagic fever: liver damage + jaundice + spontaneous bleeding (DIC) Retinitis/Ocular disease: photophobia, inflammation of retina, may cause permanent vision loss Meningoencephalitis: stiff neck, confusion, seizures — can occur weeks after initial illness Diagnosis: Serology — anti-RVF IgG and IgM ELISA. Virus isolation in BSL-3 facility. Management: Supportive — analgesics, fluid and electrolyte management, oxygenation. No specific antiviral licensed. Prevention and Control: Animal vaccination (most important intervention) Personal protective equipment when handling sick animals or tissues Universal precautions for specimen collection Proper meat inspection and cooking Isolation of infected patients Vector control (mosquito control) Exam traps: Zoonosis — animal reservoir, NOT human-to-human spread Aedes AND Culex (not just one) Three syndromes: mild flu-like, haemorrhagic, meningoencephalitis + retinitis Abortion in cattle = classic epidemiological clue Re-emergence linked to El Niño/flooding = vector breeding conditions --- 6. VIRAL HEPATITIS — OVERVIEW Hepatitis = liver inflammation. Causes: viral, bacterial, fungal, parasitic, drugs (anti-TBs, ARVs, NSAIDs), alcohol, aflatoxin, metabolic, autoimmune. Comparison Table — All Five Hepatitis Viruses: Feature HAV HBV HCV HDV HEV --- --- --- --- --- --- Family Picornaviridae Hepadnaviridae Flaviviridae Unassigned Hepeviridae Genome RNA DNA RNA RNA RNA Transmission Fecal-oral Blood/body fluids Blood/body fluids Blood/body fluids Fecal-oral Chronic infection No Yes (5–10%) Yes (70%) Yes No Vaccine Yes Yes No No (HBV vaccine protective) Yes Antiviral No Yes Yes No None Memory hook for transmission: HAV and HEV = fecal-oral (both vowels, both gut route). HBV, HCV, HDV = blood/body fluids. Memory hook for chronicity: HCV = most likely to go chronic (70%). HBV = 5–10% adults, 90% infants. HAV and HEV = never chronic. --- 7. HEPATITIS B VIRUS — DETAILED Classification: Family Hepadnaviridae. Circular, partially double-stranded DNA. Enveloped. 10 genotypes (A–J). Hardy virus — survives on surfaces. Epidemiology: 1/3 of global population infected 400 million (5%) have chronic HBV 1 million deaths per year HBV cau