Potential Questions on the Final.docx

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MICR 3330
Azad K Kaushik Bonnie Mallard

Potential Questions on the Final Properties of movement proteins: bind nucleic acids to form long and thin RNPs, increases size exclusion limit from plasmodesma, phosphorylation by cellular kinases lower binding affinity Old model vs. new model of cellular movement in TMV: Old model utilizes a fusion of viral Membrane protein with the viral RNA to form a thread like structure which threads and transverses through the small pore of plasmodesma, therefore limiting the size of particles allowed to pass through New Model illustrates TMV moving as a Viral Replication Complex (VRC). Helicase domains interlink to form ring-like hexameric structure, MTR anchors at the ER and the VRC moves on actin filaments (Talin binds actin filaments). Talin links integrase molecules to the actin cytoskeleton by interacting with viniculin and alpha-actinin Describe Influenza’s mechanism for viral replication in the host cells genome: PB1 protein contains endonuclease activity therefore cleaves 5’ capped host mRNA which allows it to synthesize viral mRNA using oligonucleotides from host mRNAs. The ability for influenza viruses to hijack the host machinery and able to synthesize +ve sense mRNA by utilizing host machinery RNA splicing of segments 7 & 8 produce M1 and M2 proteins involved in forming matrix (most expressed protein) and making Ion channels in the envelope membrane. Replication of the viral genome involves the binding of Nuclear protein to cRNA switching off the synthesis of host mRNA. From there M1 binds to RNAP and inhibits RNA synthesis. NEP binds to M1-RNP complex and this initiates export of this complex into the cytosol. Difference between antigenic drift and shift: Antigenic shift involves the switching of surface antigens, evades host immunity, while Antigenic drift involves the major switching of surface antigens due to re-assortment of genome segments in cells. Antigenic drift is the cause for periodical pandemics. Describe the Replication Cycle Papillomavirus Via alternative splicing. Three stages of viral genome replication: i) Initial DNA replication ~50-100 copies in basal stem cells via an unknown mechanism ii) Genome maintenance, ~ 1 division per cell cycle as an episome (closed circular DNA with that are not replicated in the nucleus; characteristic of herpesvirus, polyomavirus, adenoviruses iii) Proliferative DNA replication: in differentiated cells, burst in genome DNA synthesis, union assembly and egress Two viral proteins encoded by Papillomaviruses force cell to enter S phase which is required for the replication of viruses. Protein E7 which initiates DNA synthesis: - Rb (retinoblastoma protein)= tumour suppressor - Normally Rb binds to E2F TFs, which causes cell cycle arrest - Phosphorylation of Rb causes the release of E2F from the bound state, causing the cell to enter S phase - E7 protein binds Rb, thus release E2F, cell enters S phase - When the host and HPV genomes integrate, E2 function is disrupted, preventing repression of E6/E7 Protein E6 which prevents Apoptosis: - P53, tumour suppressor protein - P53 also causes cell cycle arrest through interaction with TF’s p21 and Bax - E6 bound with E6AP binds with p53 leading to p53 ubiquitination and degradation into proteasomes. The molecular mechanisms of Adenoviruses to be able to hijack host cellular machinery and turn it into a viral factory: 1. E1A binds to Rb, releasing E2F, activating an E2F response gene which induces the cell to enter the S phase. 2. E1A stabilizes p53, inducing apoptosis via two mechanisms: binding of p53 to Mdm-2 and binding of p53 to p14Arf 3. E1B blocks apoptosis via binding to bax and p53 4. VA (virus assistance) RNAs help suppress PKR which allow the maintenance of cellular replication while inside the host 5. VA RNAs bind to the ds RBM of PKR, blocking its binding site to dsRNA, therefore no activation and allowance of translation to occur ** Normal function of PKR: activated by dsRNA which in turn PKR phosphorylates eIF2-alpha which blocks translation DNA replication in Adenoviruses: Unique mechanism of genome replication in adenoviruses, involves using the use of the terminal protein as a primer. Requires DNAP and ss-binding protein, both encoded by the virus: i) Serine in TP forms phosphodiester bond within dCMP; DNAP extends nascent strand displacing the parental strand ii) Displaced strand circularizes to form panhandle structure, TP bonds with C and primes synthe
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