Virology Exam 2

-Gene Expression divided into early and late phases.
-Early: Encodes enzymes & regulates proteins needed to start viral replication.
-Late: Encodes structural proteins needed for assembly of he mature virus (ex: Capsid Protein)

-Oncogenic
-Ancient but not prevalent until 1980's
-A human herpes virus (* large DNA)
-<3% of cells within a lesion display evidence of lytic infection. (97% of cells are not undergoing lytic viral replication)

-Transcripts of latent viral genes in cells of tumors exist as proviruses & are being transcribed.
-Viral genome contains genes that are implicated in growth deregulation
-165 kb pairs

D Cyclin: cell cycle checkpoint
-Binds to CDK's
Interleukin 6 Homolog: Stimulates immune response

Bcl2 Homolog: apoptosis cascade
~Don't see Kaposi's Sarcoma unless person is immunocompromised
~Saw a rise in 1980's due to emergence of HIV

~ -ss DS DNA genome that replicates via reverse transcriptase
~Integrate its viral DNA into host DNA
~Transmitted via sex contact & exchange of bodily fluids
~May cause liver cancer

~RNA virus that replicates in cytoplasm
~No obvious oncogene
~No integration event
~Possible genomic instability
~Transmitted via body fluids (also liver cancer)

-Small, naked, icosahedral, DS DNA, Circular (8,000 bp)
Early and Late Overlap-HPV 16
-L1&2 are capsid proteins (structural)
-E5-7 are transcribed in the oncogenic transformation

~2nd most common cancer worldwide for women
~It can become an episome (not tumorgenic)
-Most papilloma virus cause warts in skin or mucous membrane
-Multiple risk groups from low to high

-Infects stratifying basal epithelial cells at bottom and are actively (mitotic) dividing.
-Virion replication, synthesis, & maturation occurs in nucleus
-Can have a 20 year latency period

~The virus times its replication along the differentiation of the cell.
~Virus enters skin cells
~Virus expresses early genes that induce cell to replicate DNA more frequently than uninfected cells.

~Remains as an episome
~As cells divide, they differentiate change function, & express keratin (this induces formation of wort)
~Viruses are released during cell death

-Viral proteins (E6, E7) inhibit p53 AND Rb proteins-> TSG's
-E6 &7 are the primary genes responsible for oncogenesis
-Transformation occurs upon integration

~Virus not produced from transformed cells
-p53: Recognizes uv light damage & halts cell cycle
-Rb: retinoblastoma gene inhibits movements into S phase; if Rb is produced, movement is halted. (inhibits when phosphorylated)

~Benign warts of the skin either have less severe inhibition of p53 or Rb or the cells are close to death in their differentiated state and they cannot become cancerous