Non-cytocidal changes in virus infected cells Flashcards
cell transformation
changing of normal cell into caner cell
neoplasia
descriptive term that denotes an abnormal tissue overgrowth that may be either localized or disseminated
oncology
study of neoplasia and neoplasms
benign neoplasm
growth produced by abnormal cell proliferation that remains localized and does not invade adjacent tissue
malignant neoplasm
locally invasive and may also spread to other parts of the body (metastasis)
oncogenic viruses
viruses that cause or give rise to tumors
neoplasms
(tumors) arise as a consequence of dysregulated growth of cells derived from a single, genetically altered progenitor cell.
metastasis
spread of cancer cells from the part of the body here it started (the primary site) to other parts of the body
proto-oncogenes
encode proteins that function in normal cellular growth and differentiation
tumor-suppressor gene
plays a role in keeping cell division in check . encodes proteins that regulate and inhibit uncontrolled growth
Rb protein
alternates between the phosphorylated state and unphosphorylated.
what phosphorylates Rb protein
cyclin dependent kinases (CDKs)
E2F
binds to unphosphorylated Rb protien= prevents its activity and therefore not allowing cell division to proceed from G1 to S phase
binds to phosphorylated Rb protein= releases E2F from its inhibition and allows the cell cycle to proceed
P16
blocks CDK thereby preventing phosphorylation of Rb protein
p53
activates the DNA repair system and stops the cell cycle at G1 checkpoint (before DNA replication) if it is not repairable it triggers apoptosis
oncogenic viruses
generally have a viral DNA genome integrated into host genome, however some can replicate in sync with host genome but are not integrated
productive infection in permissive cells
the virus completes its replication cycle, resulting in cell lysis
non-productive infection in non-permissive cells
virus transforms the well without completing its replication cycle. viral genome is integrated into the cellular DNA, complete genome persists as an autonomously replicating plasmid (episome). host cell becomes cancerous
papillomavirus-induced malignant cancer
the viral DNA is integrated into that of the host. thus, integration probably is necessary for malignant transformation
E6 &E7
viral oncogenes that remain intact and cause malignant transformation
E6- blocks p53
E7 blocks Rb protein—E2F is free—cells divide
E1A
in adenovirus: inhibits Rb
E1B
in adenovirus: blocks p53
acutely transforming retrovirus
steals proto-oncogene from host. converts proto-oncogene into oncogene, then attacks a new host cell where it can cause cancer. RNA enters host —cDNA by reverse transcriptase, DNA integrated into host genome, steals proto-oncogene from host, no longer under regulatory control—> viral mutation rapidly
slowly transforming retrovirus
sits on the regulatory portion of the gene of the host that regulates the proto-oncogene activity there by disruption the activity of the proto-oncogene causing cell proliferation and cancer
promotor
DNA sequence at which DNA-dep RNA polymerase binds to initiate transcription
enhancer
a transcriptional regulatory sequence located some distance from the promotor; it increases the rate of initiation of transcription
5 types of tumor antigens
- excessive amounts of normal proteins (prostate specific antigens)
- oncogen antigens (FLV, FSV, ex. FOCMA)
- abnormal proteins due to mutation
- onco-fetal antigens (normally regress)
- testis/cancer antigen (specific to male germ-line)
what are tumor antigens
immune system recognizes these abnormal antigens as foreign and tries to destroy the tumor cell, the antigens are not properly presented to cells of the immune system
FOCMA
a tumor antigen; feline oncornavirus membrane- associated antigen; presented on cell surface of these infected cells
