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20 Cards in this Set
- Front
- Back
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3 Basic shapes
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- helical
- polyhedral - complex |
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Icosahedral capsid
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- 20 triangles
- Capsomeres--> pentons: 5 protomers vertices l--> hexons: 6 protomers face |
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Cell entry
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- Membrane fusion: HIV
- Phagocytosis: flu - Direct penetration: polio--> punch a hole then inject genetic materials |
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RNA-dependent RNA-Pol
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- specific to virus
- produced from (+) RNA |
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Virus exit
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- Fiber: recognizes CAP receptor-->keep lung cells separated
- Free fibers: attached to cell epithelium-->open up cell adhesion |
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Acute
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- rapid onset of symptoms
- norwalk, rota, influenza |
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Chronic
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- low grade clinical symptoms, cirus replication
- HBV, HIV |
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Latent
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- no symptoms, no viral replication
- herpes |
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Slow virus
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- no symptoms for many years
- HTLV-1 |
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Antiviral mechanisms
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- inhibits translation
- PKR (Protein Kinase R): recognizes viral RNA-->phosphorylate eiF2alpha (elongation factor) to inhibit translation |
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Pandemics
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- many countries/regions effected
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- epidemics
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- few regions effected
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Influenza Envelope Proteins
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- Hemagglutinin
- Neuraminidase |
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Antigenic drift
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- HA, NA accumulate mutations from RNA pol (no repair mechanism)
- limited out breaks |
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Antigenic shift
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- "NEW" HA/NA
-->reassortment of RNA segments - immune system cannot recognize at all - pandemics - only with Type A Flu virus not B, C |
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Origin of 2009 Swine H1N1 flu
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- reassortment involving avian, swine and human over 20 yrs
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Human Origin of HIV
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- first :+" lymph node biopsies from Congo
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HIV membrane
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- gp120env: CD4 receptor-->depletion of T-cells
- MHC class I, II--> taken from T-cells when exocytosed |
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HIV early proteins
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- GAG: produces large proteins which then cut by protease into smaller ones
- TAT: enhance transcription - REV: inhibit splicing-->late RNA undergoes less splicing - NEF |
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Anti-HIV
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- RT, protease, and integrase targeted
- GP120 -->some people have protective antibody that blocks CD4 from binding to GP120 - Provirus -->drugs cannot target provirus-->stimulates transcription to make infected cells recognizable |
