Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BIO 315 > Module 11: Viral Pathogenesis (Cancer-Causing Viruses) > Flashcards

Module 11: Viral Pathogenesis (Cancer-Causing Viruses) Flashcards

(84 cards)

Start Studying
1
Q

What was the 1st identified cancer-causing retrovirus?

A

RSV (Rous Sarcoma Virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Who discovered RSV + when?

A

Peyton Rous in 1911 (discovered in chickens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 2 main mechanisms by which viruses are associated with cancer?

A

1) Transformation

2) Tumorigenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Transformation

A

Phenotypic changes in a cell that cause the cell to no longer be controlled by normal cell processes

== the changes a cell undergoes as it become malignant (cancer-like)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What cellular changes occur due to transformation?

(8 total)

A

1) Cell morphology changes
2) Loss of differentiation
3) Immortilization
4) Loss of contact inhibition
5) Increased sugar transport
6) Decreased growth factor requirements
7) Loss of anchorage dependence
8) Chromosomal aberrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tumorigenesis

A

The formation of a tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tumor

A

An abnormal growth of tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Members of ALL virus families of what kind of virus have been found to be associated with Cancer?

A

Members of ALL DNA virus families

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Members of ALL DNA virus families have been found to be associated with…

A

1) Tumor formation in animals

2) Transformation of cultured cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Oncogenes

A

Genes capable of transforming cells (“cancer genes”)

–> Altered form of a proto-oncogene that can lead to uncontrollable growth and tumor development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Viruses exhibit extensive diversity BUT the way they ___________ is SIMILAR

A

Viruses exhibit extensive diversity BUT the way they transform host cells is SIMILAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Viral oncogenes are essential for…

A

Viral replication!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are Papillomaviruses?

A

Non-enveloped dsDNA viruses that are associated with abnormal cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are papillomaviruses named after?

A

Papilloma = warts = skin tumors

–> Papillomaviruses cause warts to form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What was the first discovered link between papillomaviruses and Cancer?

Who discovered this?

A

1935: Peyton Rous

–> Discovered papillomaviruses could cause skin cancer in rabbits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 2 main abnormal cell growth conditions that papillomaviruses cause?

A

1) Genital warts
2) Cervical Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What cells do papillomaviruses typically infect?

A

Keratinocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are keratinocytes?

A

Epithelial cells found forming the outer layer of skin and some mucosal membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Keratinocytes are ______ cells

A

Keratinocytes are QUIESCENT cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Quiescent cells

A

Cells that are not actively dividing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Quiescent cells contain limited amounts of what?

Why?

A

Contain limited amounts of dNTPs and enzymes needed for genome replication

Why? –> Because they aren’t actively dividing so they don’t need to waste energy on materials they aren’t using

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the process of normal keratinocyte differentiation in an epithelium?

A

Basal layer of the epithelium = contains STEM CELLS; actively divide to give rise to keratinocytes

–> Keratinocytes differentiate and stop replicating more and more as they approach the epithelial surface

–> At the surface, quiescent cells are sloughed off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

As you move from the basal layer to the surface of an epithelium, what changes in the cells?

A

Replication activity and differentiation!

–> Replication decreases while differentiation increases as cells move up from the basal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What occurs during keratinocyte differentiation?

A

High molecular weight keratin is synthesized and nuclear degradation occurs

== puts cells into quiescent state!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What does a papillomavirus infected epithelium "look like"? (its progression)
1) Papillomavirus infects basal layer stem cells 2) Viral DNA is replicated and distributed to daughter cells (now transformed cells) 3) Viral gene products force transformed cells into S-phase 4) Daughter cells continuously replicate and DO NOT differentiate 5) A wart forms 6) Virions are released from the epithelial surface of the wart
26
What problem do keratinocytes present to papillomavirus? What is the virus's "solution"?
Their quiescent state is NOT good for viral replication! (limited replication machinery) **Solution** = Forces cell replication by stimulating the cells to enter S-phase of the cell cycle
27
Stimulation of s-phase in quiescent host cells by papillomavirus occurs in what ways?
Via TWO pathways involving viral proteins that interfere with 2 critical cell cycle regulatory proteins of host cells: Rb + p53
28
Rb =
Retinoblastoma
29
Rb + p53 are what kinds of proteins?
Tumor suppressors!
30
Tumor Suppressors
Cellular proteins that inhibit cellular replication
31
How does Rb NORMALLY function?
Rb binds to E2f transcription factors == Blocks their function == RNA polymerase cannot bind and transcribe S-phase genes --> Cell is STALLED in the end of G1! (cannot pass checkpoint to get into S-phase)
32
E2f TFs do what?
E2f TFs promote transcription of S-phase genes!
33
In NORMAL cells, how is S-phase initiated with Rb?
By phosphorylating Rb it dissociates from E2f allowing for transcription of S-phase genes
34
Generally, how does Rb prevent S-phase initiation?
By blocking the transcription of S-phase genes which produce the products needed for S-phase initiation
35
What is the NORMAL p53 tumor suppressor pathway?
1) p53 is phosphorylated in response to DNA damage or cell stress = activates p53 2) Activated p53-P binds to p21 promoter (acts as a TF) 3) p53-P binding allows for RNA polymerase to bind and transcribe p21 mRNA 4) p21 protein is synthesized 5) p21 goes and BLOCKS S-phase initiation
36
What does an accumulation of phosphorylated p53 lead to? Why does this make sense?
Apoptosis --> Makes sense because p53 is phosphorylated usually in response to DNA damage or cell stress so an excess of p53-P means greater cell damage that may be too extensive for cell to continue on
37
What HPV proteins interfere with Rb and p53 function?
E7 interferes with Rb E6 (+ needed E6AP) interferes with p53
38
What does HPV encoded E7 do to Rb?
E7 binds to Rb, inhibiting it from binding to E2f == E2f is unblocked, RNApol can bind, and transcription of S-phase genes occurs == cell enters S-phase!
39
What does HPV encoded E6 do to p53?
1) E6/E6AP complex binds to p53 2) E6/E6AP-p53 is targeted by proteasome for destruction == cleaves p53! 3) Cleaved p53 CANT bind to p21 promoter = no transcription of p21 4) No production of p21 = S-phase is NOT blocked and can therefore be initiated
40
What happens if intact HPV E6 and E7 genes integrate into host genome?
Viral replication would STOP BUT the host cells would still be transformed as E6 + E7 would still be produced == cells not producing any virus BUT still dividing uncontrollably (cannot undergo apoptosis due to p53 inhibition) = acquire mutations overtime = CANCER
41
HPV oncogenesis is a result of what?
Random viral DNA integration; E6 + E7 genes integrating into host cell genome
42
Are all HPV strains oncogenic?
NO --> Not all strains have the "optimal" E6 and E7 genes!
43
How are oncogenic HPV strains different from regular strains?
**Oncogenic HPV:** 1) Produce E7 proteins that bind with greater affinity to Rb = drives infected cells more strongly to mitosis 2) Produce E6 proteins that effectively target p53 to proteasome for degradation = cells cannot undergo apoptosis **Non-Oncogenic HPV**: 1) Produce E7 has lower binding affinity for Rb 2) Produced E6 protein DO NOT effectively target p53 to proteasome for degradation = cells are able to undergo apoptosis
44
How does HPV transformation cause cancer?
HPV-transformed cells continuously divide without being able to undergo apoptosis -----> Overtime continuously dividing cells acquire mutations -----> CANCER
45
How do Adenoviruses cause Cancer?
Just like HPV does, by inhibiting Rb + p53 pathways but just with Adenovirus-specific proteins: E7 analog = E1A (inhibits Rb) E6 analog = E1B (inhibits p53)
46
Most tumorigenic RNA viruses are....
Retroviruses
47
What is the only non-retrovirus RNA virus associates with Cancer?
Hepatitis C
48
Why is Hepatitis C associated with Cancer?
Associated with increased risk of Liver Cancer but **NOT due to viral transformation**, instead due to the constant attempts to replace damaged hepatocytes
49
How are tumorigenic retroviruses different from tumorigenic DNA viruses?
Tumorigenic retroviruses DO NOT cause cancer through GENE PRODUCTS (like DNA viruses do)
50
How do tumorigenic viruses cause tumor formation?
By altering host genome either through introduction of oncogenes or alteration of already exsiting proto-oncogenes!
51
Proto-oncogene
Genes that encode for proteins involved in cell growth
52
How do proto-oncogenes become oncogenes?
When expression or sequence of a proto-oncogene is altered
53
How does proto-oncogene --> oncogene conversion happen due to retroviral integration?
1) By integration causing alterations to proto-oncogene expression 2) By integration introducing an oncogene into the host cell!
54
Cis-acting Retroviruses
Retroviruses that activate a cellular proto-oncogene by integration NEAR a proto-oncogene
55
Transducing Retroviruses
Retroviruses that have acquired a cellular gene + can transfer it to a new cell ( Can introduce an oncogene to a host cell!)
56
How can retrovirus integration alter expression of a proto-oncogene?
If the integration happens NEAR a proto-oncogene, then certain regulatory elements of the retrovirus DNA may alter the expression of the adjacent proto-oncogene!
57
If a proviral DNA of a retrovirus integrates near a proto-oncogene...
The insertion could alter the expression of the adjacent proto-oncogene, potentially causing aberrant cellular replication leading to tumor formation
58
What does "cis-acting" refer to in cis-acting retroviruses?
Refers to how the proviral DNA insertion only impacts an ADJOINING piece of host DNA
59
What is the best studied cis-acting retrovirus?
MMTV = Mouse mammary tumor virus
60
MMTV causes tumorigensis by _____________, its genome does NOT contain ___________
MMTV causes tumorigensis by **integrating near a proto-oncogene**, its genome does NOT contain **an oncogene**
61
What does the MMTV genome contain?
Two terminal LTRs + 3 genes (pol, gag, env)
62
LTR
Long Terminal Repeats
63
What do MMTV LTRs contain?
Contain ENHANCER ELEMENTS!
64
Enhancer Element
DNA sequences that increase transcription of a gene on the same DNA molecule
65
Where does MMTV genome typically integrate in host cell genome?
Near Wnt1 (a proto-oncogene)
66
Wnt1
A proto-oncogene of the Wnt family which encodes for products involved in cell-signalling processes
67
How does MMTV genome impact host cell proto-oncogene?
The LTR enhancer elements of the MMTV integrated genome drives increased expression of downstream adjacent proto-oncogene == increased cell replication
68
What does increased expression of Wnt1 do?
Increased cell replication
69
What is an example of a transducing retrovirus?
RSV
70
What do transducing retroviruses contain in their genomes?
An oncogene! Obtained from a previous cell infection!
71
Transducing retroviruses are RARE and therefore...
are NOT major contributors of Cancer
72
How do transducing retroviruses obtain an oncogene in the first place?
1) Regular retrovirus integrates near a proto-oncogene in a host cell genome 2) During viral production, incorrect transcription of proviral DNA creates an RNA viral genome copy that contains the adjacent cellular proto-oncogene sequence 3) Viral assembly occurs with the proto-oncogene-containing viral RNA genome copy == Transducing retrovirus
73
In the acquisition of a cellular proto-oncogene to form a transducing retrovirus, the proto-oncogene can end up where in the viral genome?
1) ADDED onto an otherwise normal viral genome 2) REPLACING parts of the viral genome
74
RSV + Avian Myelocytoma Virus are transducing retroviruses derived from what "normal" retrovirus?
Avian Leukosis Virus
75
How is Avian Leukosis Virus genome altered to form: RSV + Avian Myelocytoma Virus
**RSV** = Complete Avian Leukosis Virus genome with proto-oncogene ADDED **Avian Myelocytoma Virus** = Incomplete Avian Leukosis Virus genome with proto-oncogene REPLACING parts of the genome
76
In what 2 ways can a transducing retro-virus convert its proto-oncogene into an oncogene?
1) Overexpression of the transduced gene (in the host cell once integrated) 2) Alteration to the acquired proto-oncogene (upon integration)
77
How may transduced proto-oncogenes be overexpressed once integrated into host cell?
Elements like strong viral promoters or enhancers within the retrovirus integrated genome may lead to increased expression of the proto-oncogene within the cell
78
What alteration to the acquired proto-oncogene (from transducing retrovirus) upon integration can convert it to an oncogene?
Truncation! --> Oftenly the proto-oncogene that gets transduced in missing 5' and/or 3' end sequences that may alter the sequence to produce proteins that function aberrantly
79
eRB
A proto-oncogene = Gene encoding for epidermal growth factor (EGFR)
80
EGFR
Transmembrane protein that binds to EGF (epidermal growth factor) triggering a cascade that leads to cell proliferation
81
How does EGFR normally function?
1) EGF ligand binds to EGFR 2) Binding causes conformational change that causes autophosphorylation of the EGFR 3) Signal transduction pathway initiated leading to cell proliferation
82
What does mutated eRB gene do?
Produces an altered form of EGFR that LACKS the extracellular EGF ligand binding domain
83
In what virus is mutated eRB gene found?
Avian Erythroblastius Virus-H
84
How does mutated (truncated) EGFR function?
Modified structure causes EGFR to not be able to bind to EGF AND causes it to constitutively autophosphorylate == constantly stimulating cell proliferation = uncontrolled cell division = Cancer

BIO 315 (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions