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by: Aparna Pal
Aparna Pal
GPA 3.025
General Virology
Nathan Sherer, Robert Kalejta, Paul Ahlquist

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About this Document

Here is a study guide for HPV
General Virology
Nathan Sherer, Robert Kalejta, Paul Ahlquist
Study Guide
50 ?




Popular in General Virology

Popular in Microbiology

This 3 page Study Guide was uploaded by Aparna Pal on Monday October 19, 2015. The Study Guide belongs to MICROBIO 640 at University of Wisconsin - Madison taught by Nathan Sherer, Robert Kalejta, Paul Ahlquist in Summer 2015. Since its upload, it has received 63 views. For similar materials see General Virology in Microbiology at University of Wisconsin - Madison.

Similar to MICROBIO 640 at UW


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Date Created: 10/19/15
1 HPV infection infects at basal the closest undifferentiated cell Productive viral replication in above basal layers site of viral DNA amplificationparticle assembly 2 HPV Entry L2 binds to proteoglycan and cellular integrinco receptor binding them causing a conformational change where L2 can be seen where L2 is cleaved off at the N terminus using DNA viruses need to get to the nucleus too large for the nuclear pore it must sneak into nucleus during mitosis nuclear membrane melts brings in with it a protein that makes it last longer L2 3 Human Papillomavirus genome EEarly nonstructural LCR Long control region early promoter ori packaging into capsid 4 Early genes 13 E1binds to DNA replication origin replicator DNA Dependent ATPasehelicase recruits DNA polymerase by binding to alpha primase complex E2transcriptional repressor Episomal maintenence in DNA replication cel polymerase only present in S phase 5 Early genes 46 E4 expressed at late times may facilitate viral egress only in top of stratified epithelia E5cel cycle induction E6 same p53 E7same Rb and immune escape 6 Late genes L1 major capsid protein L2minor capsid protein only occurs in differentiated keratinocytes shed in squamos cells 7 LCR LCR Long control region early promoter ori packaging into capsid The LCR is a weak but constitutive promotor no viral factors needed to turn on E2 represses LCR expression limits immune response 8 How does E6 work E7 E6 degrades p53 E7 binds to RB gt activates E2F 9 E6E7 oncogenes inhibits tumor suppressors 10 Why are E6 and E7 increased 1 in warts E2 is a repressor of E6 and E7 2 ln cancers we have linearization and intrgration into host genome so E2 is missing Leading to higher E6 and E7 3 E6 and E7 inactive tumor suppressor genes 4 E7 inactives Rb only turns off G1 to S phase normally when E7 here G1 to 8 doesn39t stop 5 E6 degrades p53 11 HPV E6E7 E6 inactivates p53 E7 mimics phosphorylation of Rb gt activates E2F abrogate G1S and GZM checkpoints rev up cell cycle 12 DNA Replication E1 E2 increases affinity for polymerase easier to separate the bonds between strands Vira E6 and E7 proteins disrupt normal cell cycle checkpoints allowing DNA replication in suprabasal Abnormal growth and division results in warts or cancers 13 Maintenance vs productive replication Papillomavirus only undergoes productive replication once passing through the epidermal level before hand maintenance replication 1 rep per cell cycle 14 HPV nuclear entry hitches onto cytoplasm microfibers nucleus melts and virus is able to pass through without nuclear pore divide with cell during mitosis genome binds to chromatin and anchors 15 Assembly and egress L1withwithout L2 spontanously forms VLPs 16 P53 genes most often mutated in human cancer activated by DNA damage stress unscheduled DNA syynthesis oncogenes high levels lead to apoptosis usually kept under control by Mdm2


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