⚕️ Microbiology · Viruses

Microbiology tricks that make viruses stick

Viral structure, replication cycles, and classification — memorized.

🦠 Viruses

Memory tricks

Proven mnemonics — fast to learn, hard to forget.

Viral Structure
Virus = nucleic acid + capsid (± envelope). Naked viruses survive environment better; enveloped are easier to kill.
Viral Structure
What every virus is made of — and why it matters clinically
Capsid: protein coat protecting nucleic acid. Enveloped viruses (HIV, influenza, herpes): lipid membrane from host cell — destroyed by soap/alcohol. Naked (non-enveloped) viruses (adenovirus, norovirus, poliovirus): resistant to drying and stomach acid — fecal-oral transmission.
Baltimore Classification
Baltimore classification: 7 groups by genome type and replication strategy — "How does the virus make mRNA?"
Baltimore Classification
The universal system for classifying viruses by their genetic strategy
Group I: dsDNA (herpes, adenovirus). Group II: ssDNA (parvoviruses). Group III: dsRNA (rotavirus). Group IV: +ssRNA (poliovirus, hepatitis C). Group V: -ssRNA (influenza, rabies). Group VI: ssRNA retroviruses (HIV). Group VII: dsDNA retroviruses (hepatitis B). Key: +strand RNA = can be directly translated as mRNA.
+ssRNA
Acts as mRNA directly — poliovirus, HCV
-ssRNA
Needs RNA-dep RNA polymerase — influenza, rabies
Retrovirus
RNA → DNA via reverse transcriptase — HIV
HIV Replication
HIV targets CD4+ T cells. RT makes DNA from RNA. Integrase inserts into host genome. Protease matures virions.
HIV Replication Steps
HIV life cycle — and which step each drug class blocks
HIV binds CD4 + CCR5/CXCR4 coreceptors. Reverse transcriptase (RT) converts RNA → DNA (error-prone → mutations → resistance). Integrase incorporates DNA into host chromosome (latency). Protease cleaves polyproteins into functional components. Drug targets: NRTIs/NNRTIs (RT), integrase inhibitors, protease inhibitors, fusion inhibitors.
Herpesvirus Latency
Herpesviruses: establish latency, reactivate when immunity drops. "Herpes never leaves."
Herpesvirus Latency
Why herpes infections recur throughout life
HSV-1/2: latent in sensory ganglia — reactivates as cold sores or genital lesions. VZV: primary = chickenpox; latency in dorsal root ganglia; reactivation = shingles (zoster). EBV: latent in B lymphocytes — reactivates in immunocompromised patients (lymphoma). CMV: latent in myeloid cells — dangerous in transplant recipients.
Influenza Antigenic Variation
Antigenic drift = point mutations (annual flu). Antigenic shift = gene reassortment (pandemic flu).
Antigenic Drift vs Shift
Why the flu vaccine changes every year — and how pandemics arise
Influenza A: 18 HA subtypes, 11 NA subtypes (H1N1, H3N2, etc.). Drift: gradual mutations in HA/NA surface proteins — evades existing antibodies → seasonal epidemics. Shift: two strains infect same cell, exchange RNA segments → novel HA/NA combination → pandemic potential (1918, 2009 H1N1). Only influenza A undergoes shift.
Viral Oncogenesis
Oncogenic viruses: HPV (cervical), EBV (Burkitt's), HBV/HCV (hepatocellular), HTLV-1 (T-cell leukemia)
Cancer-Causing Viruses
Viruses responsible for ~15% of human cancers worldwide
HPV 16/18: E6 degrades p53; E7 inactivates Rb — cervical, oropharyngeal cancers. EBV: Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma. HBV/HCV: hepatocellular carcinoma via chronic inflammation. HTLV-1: adult T-cell leukemia/lymphoma. Kaposi sarcoma herpesvirus (HHV-8): in AIDS patients.
Interferon Response
Interferons: antiviral cytokines. Type I (IFN-α/β): block viral replication in neighboring cells.
Innate Antiviral Defense
The body's first-line response to viral infection
Infected cell detects viral dsRNA → secretes IFN-α and IFN-β. Neighboring cells: IFN binds receptor → JAK-STAT pathway → antiviral state (degrade mRNA, halt translation). IFN-γ (Type II): activates macrophages. Viruses evade IFN: influenza NS1 protein, HPV E6/E7. Recombinant IFN used therapeutically (hepatitis C, MS).
Prions
Prions: misfolded PrP protein — no nucleic acid. Convert normal PrPc into PrPSc. Fatal, no treatment.
Prion Diseases
Infectious proteins — not a virus, not a bacterium, but equally deadly
Normal PrPc: α-helix rich. Misfolded PrPSc: β-sheet rich, insoluble, aggregates in neurons. Causes spongiform encephalopathy. Human diseases: Creutzfeldt-Jakob disease (CJD), kuru (cannibalism), fatal familial insomnia. Animal: scrapie (sheep), BSE/mad cow. Resistant to heat, UV, formalin. No effective treatment.
Lytic vs Lysogenic Cycle
Lytic: virus destroys cell. Lysogenic: virus hides in chromosome. Stress triggers lysogenic → lytic switch.
Bacteriophage Life Cycles
Two strategies bacteriophages use — and why lysogeny matters in medicine
Lytic: phage injects DNA → hijacks cell → makes copies → lyses cell. Lysogenic: phage DNA integrates as prophage → replicates with host. Induction (UV, stress): prophage excises → lytic cycle. Medical relevance: prophages carry toxin genes (cholera toxin, diphtheria toxin, Shiga toxin) — lysogenic conversion makes bacteria more virulent.
Antiviral Drug Targets
Antivirals target viral-specific steps: attachment, uncoating, polymerases, proteases, assembly. Spare host cells.
Antiviral Mechanisms
Why antiviral drugs are harder to develop than antibacterial drugs
Viruses use host machinery for most functions — fewer unique targets. Key antivirals: acyclovir/ganciclovir (herpes thymidine kinase activates → chain terminator). Oseltamivir/zanamivir (influenza neuraminidase inhibitors — prevent release). NRTIs/NNRTIs (HIV reverse transcriptase). Protease inhibitors (HIV/HCV). Resistance develops rapidly due to high mutation rates.
Vaccine Types
Vaccine types: Live-attenuated, Killed/inactivated, Subunit, Toxoid, mRNA. "Live Kings Serve Their Masses."
Vaccine Classification
Five vaccine strategies — each with different strengths and risks
Live-attenuated (MMR, varicella, yellow fever): strong immunity, rare reversion risk — avoid in immunocompromised. Inactivated (flu shot, IPV, hepatitis A): safe, requires boosters. Subunit (hepatitis B, HPV/Gardasil): just the antigen, very safe. Toxoid (tetanus, diphtheria): inactivated toxin. mRNA (COVID-19): instructs cells to make antigen — no live virus, rapid production.
Live
MMR, varicella, yellow fever — strong, 1-2 doses
Killed
Flu shot, IPV, hep A — safe, needs boosters
Subunit
Hep B, HPV — just protein antigen
Toxoid
Tetanus, diphtheria — inactivated toxin
mRNA
COVID-19 — instructs cells to make antigen