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11 Cards in this Set
- Front
- Back
DNA Viruses
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DNAviruses 1. (HBV) HepatitisB 2. (HPV) H.Papilloma Virus 3. Herpes; ds •Alpha: Herpes Simplex; Varicella Zoster •Beta: Cytomegalovirus •Gamma: (EBV) Epstein-Barr 4. Adenovirus 5. Parvovirus |
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RNA Viruses
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RNAviruses 1. Influenza 2. Retroviruses 3. Picornavirus: Poliovirus •Beta: Cytomegalovirus 4. Paramyxo viruses 5. Rubella virus 6. Arboviruses 7. Coronaviruses 8. Rabies viruses |
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HepatitisViruses |
HepatitisA (ssRNA;Positive) HepatitisB (dsDNA) Hepatitis C(ssRNA;Positive) Hepatitis D(RNA) |
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Hepatitis B
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Pathogenesis Infects Hepatocytes Loves producing loads of decoy, empty capsids sAg (Surface antigen): Viral envelope protein shed by actively infected Hepatocytes; Indie of intact virions cAg (Core antigen): Core protein that is part of virions; NOT detect in serology eAg (E antigen): Nucleocapsid protein; Serologically detectable in active infction Treatment/ Management 1)Vaccinewith recombinant Surface antigen (sAg) 2)Pegylatedinterferon |
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HumanPapilloma virus (HPV) |
dsDNA Oncogenic virus Pathogenesis 1. Infects basal layer of any SquamousEpithelium, 2. Promotes Proliferation +Differentiation of entire epithelium 2 main players that promoteproliferation: •E6–Inactivates p53; Degrades BAX;Activates Telomerase •E7–Binds Rb,releasing E2Fto promote G1 to S-phase Treatment: Gardasil=Vaccine with inactivated HPV |
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EpsteinBarr Virus (aka HHV-4) |
Pathogenesis 1. Infection of Oral+ Pharyngeal Mucosal Epithelial cells 2. Spread to blood and B-lymphocytes Replication •Viralnucleocapsid transported to nucleus, docks @ nuclear pore •InfectionofB-cell causes them to proliferate.•CytotoxicT-cellskill infected B-cells •ButEBVremains latent within B-lymphocytes |
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Influenza |
Influenza = ssRNA; Negative Pathogenesis •InfectsRespiratorytract cells Treatment/ Management •DoNOT give aspirin to children (Reye syndrome) •Live,inactivated virus (egg!) |
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PolioVirus |
PolioVirus = ssRNA; Positive Pathogenesis 1. Replicates in GIMucosa +Peyer’sPatches 2. Disseminates to CNShaematogenously Treatment/ Management •Attenuatedor Formalin-inactivated vaccines |
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HumanImmunodeficiency Virus |
Replication 1. Attachment •Virionattaches to host cell via CD4s; Macrophages; DCs •Entryrequires co-expression of CCR5 CXCR4 2. Penetration + Uncoating •Internationalization into host cytosol •Pre-packagedV-RTasesynthesises V-dsDNA fromV-ssRNA •V-IntegrasesintegrateV-DNAinto Host Genome. 3. Replication •Hostcell machinery transcribes + translates V-Polypeptide precursor•V-Proteaseprocessesinto structural proteins 4. Assembly •HIVvirions are assembled and infected cells migrated to lymphoid tissue |
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Vaccinations - Passive |
Passiveimmunisation = Transfer of Ig(IgG)to an individual •Immediatetherapeutic effect Examples •HepB •Rabies •Tetanus •Diphtheria |
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Vaccinations - Active |
Activeimmunisation = Intentional exposure to anantigen for the purpose of generating an adaptive immune response Can be (i) Viable(ii)Non-Viable(iii)PurifiedPathogen Product These can be: •Toxoid vaccine (Exposure to Endo-/Exo-toxins; TetanusToxoid) •Acellular vaccine (Pertussis) •Dead whole cell (Polio; Salk) |