Medical Virology: Parvovirus B19 & Adenovirus Exam Guide

#VIROGY EXAM NOTES — PART 1 OF 2 --- 1. PARVOVIRUS B19 Structure: Smallest DNA virus. Non-enveloped, icosahedral, ssDNA (linear). Only one serotype. Only B19 causes human disease. Epidemiology: 65% adults infected by age 40. Peak: late winter/spring. Children 4–15 yrs = main reservoir/source. Pathogenesis — Two-Stage Disease: Stage 1 (Infectious/Febrile): B19 replicates in nasopharynx → viremia → bone marrow → kills erythroid precursor cells → stops RBC production ~1 week. Patient is CONTAGIOUS here. Flulike symptoms. Large viremia; antibody eventually stops it. Stage 2 (Symptomatic/Immune-mediated): Rash + arthralgia appear WHEN antibody appears + immune complexes form. Patient is NO LONGER contagious during the rash. Clinical Syndromes — must know all four: ERYTHEMA INFECTIOSUM (Fifth Disease): Prodrome 7–10 days (fever, sore throat, malaise, myalgia, mild drop in Hb) → "slapped cheek" facial rash → spreads to arms/legs → resolves 1–2 weeks. Relapses common. Fifth of the classic exanthems; first four = varicella, rubella, roseola, measles. APLASTIC CRISIS: In patients with chronic hemolytic anemia (sickle cell disease, thalassemia). Transient reticulocytopenia lasting 7–10 days + drop in Hb. Most serious complication. Normal people tolerate the 1-week RBC pause; sickle cell patients cannot. ACUTE POLYARTHRITIS: Adults. Arthritis of hands, wrists, knees, ankles. HYDROPS FETALIS: Seronegative pregnant woman infected → B19 crosses placenta → kills fetal erythroid precursors → fetal anemia → congestive heart failure → fetal death. No congenital abnormalities (this distinction matters). Seropositive mothers = usually safe. CHRONIC INFECTION: In immunocompromised patients. Diagnosis: PCR = most sensitive (detects B19 genome). ELISA for IgM (recent infection) and IgG (past/immunity). IgM or viral DNA needed to distinguish B19 rash from rubella in pregnancy. Treatment: No antiviral. No human vaccine. (Vaccines exist for dogs/cats — classic trick question.) Exam traps: Contagious BEFORE the rash, not during Aplastic crisis = sickle cell, not normal hosts No congenital malformations — only fetal death via hydrops Only ONE serotype of B19 --- 2. ADENOVIRUSES Structure: dsDNA, 30–38 kbp. Non-enveloped, icosahedral, 65–80 nm. Replicate in the NUCLEUS. ~100 serotypes; ≥47 infect humans. Six subgroups A–F. Types 1–7 most common. Encodes 25–30 proteins (15 structural). Key structural feature: Fiber = attachment protein + hemagglutinin. Pentons + fibers = type-specific antigens. Epidemiology: Fecal-oral + respiratory droplets + hand-to-eye + venereal. Close contact settings: classrooms, military barracks. Most infections ASYMPTOMATIC. Self-limiting ~2 weeks. Endemic in children. Pathogenesis: Local replication → viremia → visceral spread. Becomes LATENT in adenoids, tonsils, Peyer's patches → reactivates in immunosuppressed. Oncogenic in rodents but NEVER in humans. Clinical Syndromes: Syndrome Key Detail --- --- Acute febrile pharyngitis Children <3 yrs; mimics strep throat Pharyngoconjunctival fever Pharyngitis + conjunctivitis together Acute respiratory disease Serotypes 4 & 7; military recruits; fever + cough + pharyngitis + cervical adenitis Epidemic keratoconjunctivitis Swimming pool conjunctivitis; foreign body = risk factor Gastroenteritis Serotypes 40–42; 15% of hospitalised gastroenteritis cases Hemorrhagic cystitis — Pertussis-like illness — Diagnosis: PCR, fluorescent antibody assay. Culture on HeLa (epithelial) cells → lytic infection with inclusion bodies. Must distinguish inclusions from CMV inclusions. Serology for epidemiology only. Treatment/Prevention: No approved antiviral. Live oral vaccine for types 4 and 7 used in MILITARY RECRUITS only. Exam traps: First isolated 1953 from human adenoids Oncogenic in RODENTS, not humans Military recruits → types 4 and 7 → oral live vaccine Gastroenteritis = types 40–42 Latency in lymphoid tissue → reactivation in HIV/transplant patients --- 3. INFLUENZA VIRUS Classification: Family Orthomyxoviridae. (−)ssRNA, 8 segments, Baltimore Group V. Three types: A, B, C. Structure: Lipid envelope (host-derived) with two surface glycoproteins: HA (Hemagglutinin) — attaches to host cell sialic acid receptors NA (Neuraminidase) — cleaves sialic acid to release new virions M1 matrix protein (structural) M2 ion channel (target of amantadine) 8 RNA segments coding for different proteins Types Compared: Type A Type B Type C --- --- --- --- Severity Highest Moderate Mild Animal reservoir Swine, birds, horses None None Outbreaks Pandemics + epidemics Epidemics Rare Chemotherapy Amantadine, Rimantadine, Oseltamivir, Zanamivir Oseltamivir, Zanamivir only None Naming: A / Place / Isolate number / Year (H-subtype N-subtype). Example: A/California/7/2009 (H1N1). Type B omits H/N subtypes. Influenza A Subtypes: H1–H16 (hemagglutinins), N1–N9 (neuraminidases) --- ANTIGENIC VARIATION — Most Exam-Heavy Topic Antigenic DRIFT Antigenic SHIFT --- --- --- Mechanism Gradual point mutations in HA/N