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48 Cards in this Set

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  • Back
How does RNA tumor viruses "create" oncogenes?
By acquiring, modifying and deregulating cellular genes (proto-oncogenes)
For RNA tumor viruses, are viral oncogenes essential viral genes?
NOT essential
For RNA tumor viruses are viral oncogenes related to its strategy of viral replication?
NOT related
T/F - Replication of RNA virus is cytocidal.
T/F - Replication of RNA virus is required for tumorigenesis.
Once the RNA tumor virus integrates into DNA host chromosome, expression of the provirus is under control of what?

(viral transcription regulatory sequences)
What are the mechanisms of cell transformation for RNA tumor viruses? x3
Retroviral TRANSDUCTION of oncogene

Activation of oncogene by retroviral INSERTION.

Mediation of oncogenesis by essential retrovirus PROTEINS
Transducing retrovirus:

- has capacity to do what?
- options x2 with v-onc?
- why does it need helper virus?
Transform if deregulated

Overexpression of it
Change its structure

B/c secondary loss of viral coding info has made it replication defective
For RNA tumor viruses, acquired genes are components of what?
signaling networks
What are the components of the signaling network that is acquired by the RNA tumor virus?

Name components for each.
External signal molecules

Cellular receptor
(erbB, fms, kit)

Secondary messengers in signaling cascade
(kinases: src, abl, yes, fgr, mos raf)

Transcription factors
(myb, myc, jun, rel, fos, ets)
RNA tumor virus will structurally change the Epidermal Growth Factor Receptor (EGFR or cErb B) into what? how?

How does this altered receptor function?
v-Erb B

Transduced viral gag on it

Constitutively activated receptor
Retroviral Transduction outcome x3
"Single hit" carcinogenesis

Tumors in days

(tumor growth initiated in every cell)
RNA tumor virus Retroviral Transduction is characteristic of what kind of viruses?
ANIMAL retroviruses.
Activation of oncogenes by retroviral insertion:

- random?
- activation by how?
- insertion where?

cis activation by promoter/enhancer

insertion next to proto-oncogenes (encoded by exons 1-3)
Cis-acting oncogenes:

- carry what oncogenes
- retain what viral genes
- replicate?
NO oncogenes

ALL viral genes

Replication competent
Outcome of oncogene activation by retrovirus insertion? x3
1. Slow-induced (months) tumors

2. Transformation of cell (RARE)

3. Monoclonal tumors
Why are cell transformations rare when oncogene is activated by retrovirus insertion.
Because the probability of insertion near a potential oncogene is RARE.
Why are tumors derived from the outcome of oncogene activation by retrovirus INSERTION, so slow (months)?
B/c tumor derived form single cell.
In gene therapy, a retroviral insertion near what gene can cause childhood T-cell leukemia.

What does this do?

How does this cause CA?

Blocks T-cell differentiation

The subsequent insertion of IL-2Receptor (absent in SCID) causes massive cell division.
HTLV-1 is type A B or C

(thus no precursor, central core)
T/F - HTLV-1 carries cellular oncogenes.

Just like cis.
Adult T-cell Leukemia (ATL) has what symptoms?
Skin nodules all over

- envelope?
- central core components? x3

Structural proteins
2 copies of RNA genome
Enzymes (RTase, protease, integrase)
HTLV-1 Transmission routes: x3
Sexual (mostly male to female)


Blood products
For successful transmission of HTLV-1 what must happen cellularly? via?
Cell-to-cell contact transmission

MTOC - with GAG, ICAM, LFAT, Tax
T/F - Cell-free HTLV1 is NONinfectious.
How do you screen for HTLV-1 in donated blood?
ELISA and Western blot
Seroprevalence of HTLV is greater or lesser than HIV?

Which serotype of HTLV is most common and seen in what population group?

What is the oncogenic potential of this?
Greater 3x


IV drug users

NO oncogenic potential
Two major diseases associated with HTLV-1.

HAM (HTLV-1 Associated Myelopathy)
HTLV1 infects what cells?
CD4+ T cells

- onset when
- diagnosis test
- does chemo help?
20-40 years after primary infection

Antibody detection of CD4 and CD25

Minimal improvement of survival

- what are the two types and describe
Fulminant (survival 6 mos)

Indolent (50% 4 year survival)
Pathologic diseases associated with ATL. x3
Skin involvement
Lab tests with ATL would show what? x2

Elevated Serum calcium levels

Lytic bone lesions

(overexpression of PTH-related protein)

- what are the regulatory gene products responsible for pathogenesis? x2

- what ar the regulatory proteins responsible for replication and gene expression?
Tax and HBZ

Tax and Rev
HTLV-1 has HBZ encoded from which part of genome?
MINUS strand of provirus

- regulates expression of
- binds what? why?
- dissociates
- upregulates what?
viral genes

Transcription factors to enhance their binding to cellular PROMOTERS.

NF-kB/IkB complexes

IL-2, IL-2R alpha, IL-1, IL-3,.....
Tax targets cell cycle regulatory proteins (like DNA) how? x2
Inactivates p53

Binds MAD1 (interfering with G2/M phase)
ATL has Atypical "flower cells"

- reflects what?
- found where?
- what are these?
- describe its nuclei x2
Tax expression
(elevated levels of IL-2R)
(perturbed chr segregation - MAD1)

CSF and Blood

Wierd CD4+ T cells

Indented, convoluted
Is Tax continuously expressed in the tumor itself?

Why or why not?
No. simmers down its expression

To avoid antibody detection
How do T-cells proliferate without Tax protein expression?
HBZ protein influences host gene expression (AP1 transcription) to drive replication.

mRNA that has just encoded for HBZ protein will go off and drive proliferation of T-cells via the E2F1 pathway.
What are the bimodal protein functions for HBZ
Influence host gene expression for T-cell proliferation
(via AP1 transcription)

Suprress transcription of viral genes (Tax encoding genes) from the plus trand.

Keep in mind that Tax came from MINUS strand.
HTLV-1 Induced Oncogenesis:

- type of process
- latency duration
Multistep process
(not just caused by virus, but other factors)

LONG -> Decades

Is Tax expressed in tumors?
Although involved in tumor initiation,

OFTEN NOT expressed
What type of tumors do you get with HTLV-1?

BUT integration site VARIES among patients.
(NO cis-activation)
T/F - Tax is a STRUCTURAL protein.

It is NON structural
T/F - In maintenance of ATL transformation, HBZ and Tax are both expressed.

Only HBZ
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