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🦠 Math · Viruses

Memory tricks for viral structure, HIV, herpes & influenza

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🦠 Memory Tricks
Viruses — 12 Memory Tricks

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🦠 Virology
Virus = nucleic acid + capsid ± envelope. Enveloped = easier to kill. Naked = survives environment.
Viral Structure — capsid protects nucleic acid; enveloped viruses (lipid membrane from host) are destroyed by soap/alcohol; naked viruses resist drying and stomach acid
What every virus is made of — and why it determines transmission route
Enveloped viruses (HIV, influenza, herpes, CMV, EBV, HBV, HCV): lipid membrane from host cell — destroyed by soap and alcohol. Respiratory/blood-borne transmission. Naked/non-enveloped (adenovirus, norovirus, poliovirus, rotavirus, HAV, parvovirus): resist drying, heat, and stomach acid — fecal-oral transmission, harder to kill.
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🃏 🦠 Virology
Enveloped vs naked viruses — which is easier to kill?
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🃏 Answer
Virus = nucleic acid + capsid ± envelope. Enveloped = easier to kill. Naked = survives environment.
Viral Structure — capsid protects nucleic acid; enveloped viruses (lipid membrane from host) are destroyed by soap/alcohol; naked viruses resist drying and stomach acid
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🦠 Virology
Baltimore classification: Groups I-VII based on "How does the virus make mRNA?"
Baltimore Classification — 7 groups by genome type and replication strategy: I=dsDNA · II=ssDNA · III=dsRNA · IV=+ssRNA · V=-ssRNA · VI=ssRNA retrovirus · VII=dsDNA retrovirus
The universal classification system for viruses — based on how they make mRNA
Group I: dsDNA (herpes, adenovirus, poxvirus). Group II: ssDNA (parvovirus). Group III: dsRNA (rotavirus). Group IV: +ssRNA = acts as mRNA directly (poliovirus, HCV, rhinovirus). Group V: −ssRNA = needs RNA-dependent RNA polymerase (influenza, rabies, measles, RSV). Group VI: ssRNA retrovirus (HIV). Group VII: dsDNA retrovirus (HBV).
+ssRNA (Group IV)
Acts as mRNA directly — can be translated immediately after entry; poliovirus, HCV, dengue, Zika
−ssRNA (Group V)
Requires RNA-dependent RNA polymerase (brought in virion); influenza, rabies, measles, RSV, Ebola
Retrovirus (Group VI)
RNA → DNA via reverse transcriptase → integrates into host chromosome; HIV, HTLV
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🃏 🦠 Virology
Baltimore classification — what is it based on?
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🃏 Answer
Baltimore classification: Groups I-VII based on "How does the virus make mRNA?"
+ssRNA (Group IV)Acts as mRNA directly — can be translated immediately after entry; poliovirus, HCV, dengue, Zika
−ssRNA (Group V)Requires RNA-dependent RNA polymerase (brought in virion); influenza, rabies, measles, RSV, Ebola
Retrovirus (Group VI)RNA → DNA via reverse transcriptase → integrates into host chromosome; HIV, HTLV
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🦠 Virology · HIV
HIV: CD4+CCR5/CXCR4 → RT (RNA→DNA) → Integrase (inserts) → Protease (matures). Drug class = step blocked.
HIV Life Cycle — CD4+coreceptor binding → reverse transcription → nuclear integration → polyprotein processing by protease → budding
HIV life cycle and which step each drug class blocks
HIV gp120 binds CD4 + CCR5 or CXCR4 coreceptors → fusion. Reverse transcriptase (error-prone, no proofreading) converts ssRNA → dsDNA. Integrase inserts viral DNA into host chromosome (latency established). Protease cleaves Gag-Pol polyprotein → mature virions. Drug targets: NRTIs/NNRTIs (reverse transcriptase), integrase inhibitors, protease inhibitors, CCR5 antagonists (maraviroc), fusion inhibitors (enfuvirtide).
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🃏 🦠 Virology · HIV
HIV life cycle — the steps drugs block?
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HIV: CD4+CCR5/CXCR4 → RT (RNA→DNA) → Integrase (inserts) → Protease (matures). Drug class = step blocked.
HIV Life Cycle — CD4+coreceptor binding → reverse transcription → nuclear integration → polyprotein processing by protease → budding
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🦠 Virology · Herpes
Herpesviruses: "Herpes never leaves." Establish latency, reactivate when immunity drops.
Herpesvirus Latency — HSV-1/2 (sensory ganglia) · VZV (dorsal root ganglia) · EBV (B lymphocytes) · CMV (myeloid cells) — all latent for life
Why herpes infections recur throughout life — and where each hides
HSV-1/2: latent in trigeminal/sacral sensory ganglia — reactivates as cold sores or genital lesions with stress, UV light, immunosuppression. VZV: primary = chickenpox; latency in dorsal root ganglia; reactivation = shingles (dermatomal). EBV: latent in B lymphocytes — mononucleosis; reactivates → lymphoma in immunocompromised. CMV: latent in myeloid cells — dangerous in transplant recipients.
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🃏 🦠 Virology · Herpes
Herpesviruses — what makes them persist?
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Herpesviruses: "Herpes never leaves." Establish latency, reactivate when immunity drops.
Herpesvirus Latency — HSV-1/2 (sensory ganglia) · VZV (dorsal root ganglia) · EBV (B lymphocytes) · CMV (myeloid cells) — all latent for life
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🦠 Virology · Influenza
Antigenic drift = small mutations (annual flu). Antigenic shift = gene reassortment (pandemic flu).
Influenza Variation — Drift=gradual point mutations in HA/NA (seasonal epidemics) · Shift=segment reassortment between two strains (pandemic potential)
Why the flu vaccine changes every year — and how pandemics arise
Influenza A: 18 HA subtypes, 11 NA subtypes (H1N1, H3N2). Drift: gradual mutations → evades existing antibodies → seasonal epidemics → annual vaccine reformulation needed. Shift: two strains coinfect same cell, exchange RNA segments → novel HA/NA → pandemic (1918 Spanish flu, 2009 H1N1). Only influenza A (not B or C) undergoes antigenic shift.
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🃏 🦠 Virology · Influenza
Antigenic drift vs shift?
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Antigenic drift = small mutations (annual flu). Antigenic shift = gene reassortment (pandemic flu).
Influenza Variation — Drift=gradual point mutations in HA/NA (seasonal epidemics) · Shift=segment reassortment between two strains (pandemic potential)
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🦠 Virology · Oncology
Oncogenic viruses: HPV (cervical) · EBV (Burkitt's) · HBV/HCV (hepatocellular) · HTLV-1 (T-cell leukemia)
Cancer-Causing Viruses — HPV E6 degrades p53/E7 inactivates Rb · EBV c-myc translocation · HBV/HCV chronic inflammation → HCC · HTLV-1 Tax protein activates proliferation
Viruses responsible for ~15% of human cancers worldwide
HPV 16/18: E6 degrades p53, E7 inactivates Rb → cervical, oropharyngeal cancers. Vaccine (Gardasil): prevents HPV 16/18/6/11. EBV: Burkitt's lymphoma (c-myc translocation), Hodgkin's lymphoma, nasopharyngeal carcinoma. HBV/HCV: hepatocellular carcinoma via chronic inflammation and cirrhosis. HTLV-1: adult T-cell leukemia/lymphoma. KSHV (HHV-8): Kaposi sarcoma in AIDS.
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🃏 🦠 Virology · Oncology
Oncogenic viruses — which cancers?
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Oncogenic viruses: HPV (cervical) · EBV (Burkitt's) · HBV/HCV (hepatocellular) · HTLV-1 (T-cell leukemia)
Cancer-Causing Viruses — HPV E6 degrades p53/E7 inactivates Rb · EBV c-myc translocation · HBV/HCV chronic inflammation → HCC · HTLV-1 Tax protein activates proliferation
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🦠 Virology · Innate Immunity
Interferons: Type I (IFN-α/β): antiviral. Infected cell secretes → neighboring cells activate antiviral state.
Type I Interferons — IFN-α (from leukocytes) and IFN-β (from fibroblasts); induce antiviral state via JAK-STAT pathway → degrade viral mRNA, halt translation
The body's first-line rapid response to viral infection
Infected cell detects viral dsRNA (via TLR3/RIG-I) → secretes IFN-α/β. Neighboring cells: IFN binds receptor → JAK-STAT → 2',5'-oligoadenylate synthetase (degrades RNA) + PKR (halts translation). IFN-γ (Type II): activates macrophages. Viruses evade IFN: influenza NS1, HPV E6/E7. Recombinant IFN used: hepatitis B/C, multiple sclerosis.
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🃏 🦠 Virology · Innate Immunity
Interferons — how do they protect cells?
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Interferons: Type I (IFN-α/β): antiviral. Infected cell secretes → neighboring cells activate antiviral state.
Type I Interferons — IFN-α (from leukocytes) and IFN-β (from fibroblasts); induce antiviral state via JAK-STAT pathway → degrade viral mRNA, halt translation
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🦠 Virology
Prions: misfolded PrPSc — no nucleic acid, no treatment, fatal. Convert PrPc (α-helix) → PrPSc (β-sheet).
Prion Diseases — PrPc (normal, α-helix rich) → PrPSc (misfolded, β-sheet rich, insoluble, causes spongiform encephalopathy)
Infectious proteins — not a virus, not a bacterium, but equally deadly
Normal PrPc: α-helix. Misfolded PrPSc: β-sheet — insoluble, aggregates in neurons → spongiform encephalopathy. Human diseases: CJD (sporadic/iatrogenic/familial), vCJD (from BSE/mad cow), kuru (cannibalism), fatal familial insomnia. Resistant to heat, UV, formalin, autoclaving. No effective treatment.
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🃏 🦠 Virology
Prions?
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Prions: misfolded PrPSc — no nucleic acid, no treatment, fatal. Convert PrPc (α-helix) → PrPSc (β-sheet).
Prion Diseases — PrPc (normal, α-helix rich) → PrPSc (misfolded, β-sheet rich, insoluble, causes spongiform encephalopathy)
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🦠 Virology · Hepatitis
Hepatitis: "Vowels (A, E) = fecal-oral. Consonants (B, C, D) = blood/sexual."
Hepatitis Viruses — A and E: fecal-oral (water-borne, acute only, no chronicity) · B, C, D: parenteral/sexual (chronic carrier state possible, HCC risk)
The vowel-consonant rule for hepatitis transmission
HAV: fecal-oral, acute only (no chronicity), vaccine available. HBV: blood/sexual/vertical, dsDNA retrovirus, 10% chronic, HCC risk, vaccine. HCV: blood (IVDU #1), no vaccine, 80% chronic, most common cause of liver transplant in US. HDV: requires HBV coinfection (defective virus). HEV: fecal-oral, deadly in pregnancy. Serologies: HBsAg (active), HBcAb IgM (acute), HBsAb (immune/vaccinated).
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🃏 🦠 Virology · Hepatitis
Hepatitis viruses — how is each spread?
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🃏 Answer
Hepatitis: "Vowels (A, E) = fecal-oral. Consonants (B, C, D) = blood/sexual."
Hepatitis Viruses — A and E: fecal-oral (water-borne, acute only, no chronicity) · B, C, D: parenteral/sexual (chronic carrier state possible, HCC risk)
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🦠 Virology
Lytic: virus destroys cell. Lysogenic: virus hides in chromosome. Stress → lytic switch → toxin release.
Bacteriophage Life Cycles — Lytic (active viral replication → cell lysis) vs Lysogenic (viral DNA integrates as prophage → dormant until induced)
Why lysogeny matters in medicine — prophages carry toxin genes
Lytic: phage injects DNA → hijacks cell → makes copies → lyses cell. Lysogenic: phage DNA integrates as prophage — replicates with host, can persist for generations. Induction (UV, SOS response): prophage excises → lytic cycle. Medical relevance: toxin genes encoded in prophages (cholera toxin, diphtheria toxin, Shiga toxin, Staph toxin superantigens) — lysogenic conversion makes bacteria virulent.
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🃏 🦠 Virology
Lytic vs lysogenic cycle?
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Lytic: virus destroys cell. Lysogenic: virus hides in chromosome. Stress → lytic switch → toxin release.
Bacteriophage Life Cycles — Lytic (active viral replication → cell lysis) vs Lysogenic (viral DNA integrates as prophage → dormant until induced)
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🦠 Virology · Respiratory
Respiratory viruses: "RIPPER" — RSV (infants) · Influenza · Parainfluenza (croup) · Parvovirus · EBV · Rhinovirus (cold)
Common Respiratory Viruses — RSV=bronchiolitis in infants · Influenza=antigenic drift/shift · Parainfluenza=croup (steeple sign) · Rhinovirus=common cold (picornavirus)
Match the respiratory virus to its classic clinical presentation
RSV: bronchiolitis in infants under 2 — 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 — 100+ serotypes, no vaccine. Adenovirus: conjunctivitis + pharyngitis + fever. Metapneumovirus: RSV-like in elderly/immunocompromised.
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🃏 🦠 Virology · Respiratory
Respiratory viruses — RIPPER
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Respiratory viruses: "RIPPER" — RSV (infants) · Influenza · Parainfluenza (croup) · Parvovirus · EBV · Rhinovirus (cold)
Common Respiratory Viruses — RSV=bronchiolitis in infants · Influenza=antigenic drift/shift · Parainfluenza=croup (steeple sign) · Rhinovirus=common cold (picornavirus)
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🦠 Virology · Childhood
Childhood exanthems: Measles (3Cs: Cough+Coryza+Conjunctivitis+Koplik spots) · Rubella (3-day rash) · Roseola (HHV-6)
Childhood Viral Exanthems — Measles (paramyxovirus, Koplik spots) · Rubella (togavirus, lymphadenopathy) · Roseola (HHV-6, fever then rash) · Varicella (VZV, dewdrop vesicles) · Slapped cheek (parvovirus B19)
Five childhood rash illnesses — different viruses, different patterns
Measles: 3Cs (cough, coryza, conjunctivitis) + Koplik spots (buccal mucosa) → maculopapular rash head-to-toe. Rubella: mild, posterior lymphadenopathy, 3-day rash, dangerous in pregnancy. Roseola (HHV-6): high fever for 3-5 days → defervescence → rash (rose-colored macules trunk). Varicella: pruritic "dewdrop on rose petal" vesicles — all stages simultaneously. Parvovirus B19: slapped-cheek appearance + arthropathy in adults.
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🃏 🦠 Virology · Childhood
Childhood rashes — measles vs rubella vs roseola?
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Childhood exanthems: Measles (3Cs: Cough+Coryza+Conjunctivitis+Koplik spots) · Rubella (3-day rash) · Roseola (HHV-6)
Childhood Viral Exanthems — Measles (paramyxovirus, Koplik spots) · Rubella (togavirus, lymphadenopathy) · Roseola (HHV-6, fever then rash) · Varicella (VZV, dewdrop vesicles) · Slapped cheek (parvovirus B19)
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