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11 Cards in this Set

  • Front
  • Back
DNA Viruses

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

RNA Viruses

RNAviruses

1. Influenza

2. Retroviruses

3. Picornavirus: Poliovirus •Beta: Cytomegalovirus


4. Paramyxo viruses

5. Rubella virus

6. Arboviruses

7. Coronaviruses

8. Rabies viruses


HepatitisViruses


HepatitisA (ssRNA;Positive)

HepatitisB (dsDNA)


Hepatitis C(ssRNA;Positive)

Hepatitis D(RNA)


Hepatitis B

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







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










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


Influenza


Influenza



= ssRNA; Negative


Pathogenesis


•InfectsRespiratorytract cells


Treatment/ Management


•DoNOT give aspirin to children (Reye syndrome)


•Live,inactivated virus (egg!)





PolioVirus


PolioVirus = ssRNA; Positive




Pathogenesis


1. Replicates in GIMucosa +Peyer’sPatches


2. Disseminates to CNShaematogenously




Treatment/ Management


•Attenuatedor Formalin-inactivated vaccines






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

Vaccinations - Passive


Passiveimmunisation


= Transfer of Ig(IgG)to an individual


•Immediatetherapeutic effect


Examples


•HepB


•Rabies


•Tetanus


•Diphtheria





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)