Influenza Variation β Drift=gradual point mutations in HA/NA (seasonal epidemics) Β· Shift=segment reassortment between two strains (pandemic potential)
Why the flu vaccine changes every year β and how pandemics arise
Influenza A: 18 HA subtypes, 11 NA subtypes (H1N1, H3N2). Drift: gradual mutations β evades existing antibodies β seasonal epidemics β annual vaccine reformulation needed. Shift: two strains coinfect same cell, exchange RNA segments β novel HA/NA β pandemic (1918 Spanish flu, 2009 H1N1). Only influenza A (not B or C) undergoes antigenic shift.
Interferons: Type I (IFN-Ξ±/Ξ²): antiviral. Infected cell secretes β neighboring cells activate antiviral state.
Type I Interferons β IFN-Ξ± (from leukocytes) and IFN-Ξ² (from fibroblasts); induce antiviral state via JAK-STAT pathway β degrade viral mRNA, halt translation
The body's first-line rapid response to viral infection
Bacteriophage Life Cycles β Lytic (active viral replication β cell lysis) vs Lysogenic (viral DNA integrates as prophage β dormant until induced)
Why lysogeny matters in medicine β prophages carry toxin genes
Lytic: phage injects DNA β hijacks cell β makes copies β lyses cell. Lysogenic: phage DNA integrates as prophage β replicates with host, can persist for generations. Induction (UV, SOS response): prophage excises β lytic cycle. Medical relevance: toxin genes encoded in prophages (cholera toxin, diphtheria toxin, Shiga toxin, Staph toxin superantigens) β lysogenic conversion makes bacteria virulent.
Common Respiratory Viruses β RSV=bronchiolitis in infants Β· Influenza=antigenic drift/shift Β· Parainfluenza=croup (steeple sign) Β· Rhinovirus=common cold (picornavirus)
Match the respiratory virus to its classic clinical presentation
RSV: bronchiolitis in infants under 2 β treat with supportive care, ribavirin for severe; palivizumab prophylaxis for high-risk infants. Parainfluenza: croup (barking cough, steeple sign on X-ray) in children. Rhinovirus: most common cold β 100+ serotypes, no vaccine. Adenovirus: conjunctivitis + pharyngitis + fever. Metapneumovirus: RSV-like in elderly/immunocompromised.
Five childhood rash illnesses β different viruses, different patterns
Measles: 3Cs (cough, coryza, conjunctivitis) + Koplik spots (buccal mucosa) β maculopapular rash head-to-toe. Rubella: mild, posterior lymphadenopathy, 3-day rash, dangerous in pregnancy. Roseola (HHV-6): high fever for 3-5 days β defervescence β rash (rose-colored macules trunk). Varicella: pruritic "dewdrop on rose petal" vesicles β all stages simultaneously. Parvovirus B19: slapped-cheek appearance + arthropathy in adults.
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π Common Exam Questions
Q: Explain Baltimore classification β what is the basis of the system and give two clinical examples per major group?
A: Baltimore classifies viruses by genome type and how they generate mRNA. Group I (dsDNA): herpes simplex (cold sores, encephalitis), adenovirus (conjunctivitis + URI), smallpox/vaccinia. Group II (ssDNA): parvovirus B19 (fifth disease, aplastic crisis in sickle cell, hydrops fetalis). Group III (dsRNA): rotavirus (leading cause of viral gastroenteritis in children worldwide), reovirus. Group IV (+ssRNA, acts as mRNA): poliovirus, HAV, HCV, rhinovirus, dengue, Zika β can be directly translated after entry. Group V (-ssRNA, needs RdRp in virion): influenza, RSV, measles, mumps, rabies, Ebola β must first make +strand copy. Group VI (ssRNA retrovirus): HIV, HTLV-1 β RNAβDNA via RT β integrates. Group VII (dsDNA retrovirus): HBV β replicates via reverse transcription from RNA intermediate. Clinical key: +ssRNA viruses are faster (no need for polymerase) β explains some acute rapid presentations.
Q: Explain antigenic drift vs shift and why influenza A is uniquely capable of shift.
A: Antigenic drift: gradual accumulation of point mutations in the hemagglutinin (HA) and neuraminidase (NA) genes during replication β RNA polymerase lacks proofreading. Result: slightly altered surface proteins that partially evade pre-existing antibodies β seasonal epidemics. Requires annual vaccine reformulation. Occurs in influenza A, B, and C. Antigenic shift: occurs when two different influenza A strains simultaneously infect the same cell (usually in pigs or birds) β mixing of the 8 segmented RNA genome β a completely novel HA and/or NA combination emerges. Results in a strain with no pre-existing population immunity β pandemic potential (1918 H1N1 killed 50 million; 1957 H2N2; 1968 H3N2; 2009 novel H1N1). Only influenza A undergoes shift because influenza B lacks animal reservoir strains β no opportunity for co-infection with animal strains.
Q: Describe the hepatitis viruses β transmission, chronicity, HCC risk, and key serological markers for HBV.
A: Hepatitis A (HAV): picornavirus, +ssRNA, fecal-oral (contaminated water/shellfish). Acute only β no chronicity, no carrier state. Vaccine available. Hepatitis B (HBV): hepadnavirus, dsDNA retrovirus (replicates via RT), enveloped. Blood/sexual/vertical (perinatal #1 worldwide). 10% of adults develop chronic infection; 90% of neonates infected at birth. HCC risk. Vaccine. HBV serology: HBsAg = active infection; HBsAb = immunity (vaccination or recovery); HBcAb IgM = acute infection; HBcAb IgG = past infection; HBeAg = high replication/infectivity. Hepatitis C (HCV): flavivirus, +ssRNA, no envelope. Blood-borne (IVDU #1 in US). 80% develop chronic infection β most common indication for liver transplant in US. No vaccine. Direct-acting antivirals (DAAs) now cure >95%. Hepatitis D (HDV): incomplete RNA virus β requires HBV HBsAg for its own envelope. Coinfection (HBV + HDV together) or superinfection (HDV in chronic HBV carrier). Hepatitis E (HEV): fecal-oral. Epidemic in developing countries. Especially dangerous in pregnancy (20% mortality in third trimester).
Q: What are the oncogenic viruses, their mechanisms of carcinogenesis, and the cancers they cause?
A: Human Papillomavirus (HPV) 16/18: E6 oncoprotein binds and degrades p53 (tumor suppressor). E7 oncoprotein binds and inactivates Rb (cell cycle brake). Together: loss of cell cycle control β cervical, anal, vulvar, vaginal, penile, oropharyngeal cancers. Prevent with Gardasil 9. EBV (HHV-4): infects B cells β immortalization. Burkitt's lymphoma (endemic: jaw tumor in Africa, t(8;14) c-myc translocation; sporadic: abdominal mass). Hodgkin's lymphoma (Reed-Sternberg cells often EBV+). Nasopharyngeal carcinoma. Post-transplant lymphoproliferative disorder. Diagnose mononucleosis with Monospot (heterophile Ab). HBV/HCV: chronic inflammation β cirrhosis β hepatocellular carcinoma. Risk proportional to viral load and duration. HTLV-1: ssRNA retrovirus, blood/sexual/breast milk. Tax protein activates IL-2 receptor and NF-ΞΊB β adult T-cell leukemia/lymphoma (ATLL) after 20-30 year latency. Endemic: Japan, Caribbean. KSHV (HHV-8): Kaposi sarcoma in HIV/AIDS (spindle cell proliferation with slit-like vascular spaces; treat with ART first).
Q: What are prions, and what human diseases do they cause?
A: Prions are infectious misfolded proteins β no nucleic acid (no DNA or RNA). Normal PrPc is rich in Ξ±-helices. Misfolded PrPSc is rich in Ξ²-sheets β insoluble, resists degradation, accumulates in neurons β spongiform vacuolation (holes in brain tissue). PrPSc can TEMPLATE conversion of normal PrPc into PrPSc β how infection spreads. Human prion diseases: Creutzfeldt-Jakob disease (CJD): sporadic (most common, ~1-2 million/yr worldwide), familial (PRNP gene mutation), iatrogenic (contaminated neurosurgical instruments, corneal transplant, growth hormone). Rapidly progressive dementia, myoclonus, EEG triphasic waves, MRI DWI changes. Variant CJD (vCJD): from consuming BSE-infected beef ("mad cow disease"), younger patients, psychiatric onset, florid plaques on pathology. Kuru: from ritualistic cannibalism in Papua New Guinea β ataxia and tremors. Fatal familial insomnia: thalamic degeneration β progressive insomnia β death. Animal prion diseases: scrapie (sheep), BSE (cattle), CWD (chronic wasting disease β deer/elk). Resistant to: autoclaving (standard), UV, formalin, heat. Destroy with: prolonged high-pressure steam sterilization (134Β°C Γ 18 min), NaOH, sodium hypochlorite. No effective treatment.