1.explain two mechanisms of how integration of proviral DNA from a simple retrov

Question

1.explain two mechanisms of how integration of proviral DNA from a simple retrovirus can induce oncogenesis

2. Adenovirus, SV-40, and human papillomavirus (HPV) oncoproteins dysregulate p53 and retinoblastoma. explain how this contributes to cellular transformation.

3.list 3 goals in designing oncolytic viruses

.4 what role does VPg protein have in the poliovirus replication cycle?

5. explain the mechanisms used by poliovirus to deactivate host protein translation while still allowing viral protein translation.

Explanation / Answer

1. Reverse transcription takes place in the cytoplasm; the viral DNA is translocated into the nucleus where the linear copy of the retroviral genome is inserted into chromosomal DNA with the aid of the virion integrase to form a stable provirus. Integration does not permute the linear order of the proviral sequences, LTR-gag-pol-env-LTR. The number of possible sites of integration into the cellular genome is very large and very widely distributed. With integration, the provirus achieves the status of a cellular gene and is expressed through the agency of cellular RNA polymerase II and replicated by cellular enzymes in concert with chromosomal DNA. Control of proviral transcription remains largely with the noncoding sequences of the viral LTR. Transcription of the provirus generates spliced and unspliced mRNAs and full-length progeny RNA genomes. In infection with simple retroviruses, control of transcription is mediated solely by interaction of cellular factors with the DNA of the LTR. Complex viruses, in contrast, take a more active role, encodingtrans-activating factors that affect the levels of transcripts and the relative amounts of the products of the various genes. This strategy allows these viruses a measure of control of gene expression not seen with the simple viruses.

2.

Viral oncogenes are responsible for oncogenesis resulting from persistent virus infection. Although different human tumor viruses express different viral oncogenes and induce different tumors, their oncoproteins often target similar sets of cellular tumor suppressors or signal pathways to immortalize and/or transform infected cells. Expression of the viral E6 and E7 oncogenes in papillomavirus, E1A and E1B oncogenes in adenovirus, large T and small t antigen in polyomavirus, and Tax oncogene in HTLV-1 are regulated by alternative RNA splicing. However, this regulation is only partially understood. DNA tumor viruses also encode noncoding RNAs, including viral microRNAs, that disturb normal cell functions. Among the determined viral microRNA precursors, EBV encodes 25 from two major clusters (BART and BHRF1), KSHV encodes 12 from a latent region, human polyomavirus MCV produce only one microRNA from the late region antisense to early transcripts, but HPVs appears to produce no viral microRNAs.

4. VPg , a small protein that binds viral RNA and is necessary for synthesis of viral positive and negative strand RNA.

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