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Foundations of Medicine > Week 3 - Microbiology Tumor Virology > Flashcards

Week 3 - Microbiology Tumor Virology Flashcards

1
Q

Cellular transformation

A

Poor or no control of cellular division

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2
Q

What do DNA tumor viruses do to permissive cells? To non-permissive cells?

A

Lyse permissive cells (kill)

Transform non-permissive cells

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3
Q

Permissive host cell

A

A host cell the virus can completely replicate in

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4
Q

What do RNA tumor viruses do to permissive cells?

A

RNA tumor viruses transform permissive and non-permissive cells

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5
Q

What do RNA tumor genes carry that are responsible for the transformation of permissive cells?

A

Oncogenes

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6
Q

Carcinogenesis

A

A multistep process involving multiple genetic changes

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7
Q

Cellular transofmration

A

A stable, heritable change, resulting in poor or no control of cellular growth

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8
Q

What does cellular transformation result in?

A

In the alteration of cellular processes and properties which can result in altered morphology, growth control, and cellular and biochemical properties

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9
Q

All tumor viruses are DNA viruses OR…

A

Generate a DNA provirus (retrovirus)

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10
Q

Know what virus family and virus causes human cancer

A

Use Association of Viruses with Human Cancers Table

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11
Q

Papovavirdae

A

rr

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12
Q

Herpesvirdae

A

rr

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13
Q

Hepadnavirdae

A

rr

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14
Q

Retroviridae

A

rr

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15
Q

What is P110rb?

A

P110 RB (retno blastoma) - protein that when is phosphorylated, it is master break in cell cycle - so when it is ACTIVE you will NOT have uncontrolled cell growth… It is a break in cell cycle on purpose.. WITHOUT the block you get uncontrolled growth

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16
Q

What is P53?

A

P53 - If active, turns on P21 when regulates cycling kinases (phosphorylates things). The kinases shut P110 RB down. This phosphorylates (inactivates) the P110rb and uncontrolled cell growth will occur

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17
Q

C - Oncogenes

A

Cellular oncogenes

Mutated forms of normal cell genes (proto-oncogenes)
Code for heterogeneous group of proteins that are involved in normal cell division or differention pathways
Abnormal expression or regulation lead to cellular transformation or cancerous growth

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18
Q

V-oncogenes

A

Only occurs from RNA viruses

Are copies of cellular oncogenes which have been acquired by viruses during replication

Present in viral genome

Responsible for cellular transforming activity of those viruses which contain them

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19
Q

Tumor suppressor genes

A

Negative regulators of cellular growth.

Anti-oncogenes or growth suppressor genes

Cause cellular transformation if functional activity of both alleles is lost

Are exemplified by P110rb and P53

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20
Q

Adenoviruses

A

affect rodent cells.. In human cells - can make early proteins but don’t have all enzymes needed. Early cells E1b binds to P53 and E1a binds to P110RB.. So break is eliminated and have uncontrolled growth…….

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21
Q

Do DNA and RNA viruses produce tumors in host cell?

A

No for DNA tumor viruses

Yes for RNA tumor viruses

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22
Q

What host cells do DNA tumor viruses transform?

A

ONLY non-permissive cells

Interaction of specific viral proteins with products of tumor suppressor genes directly lead to or contribute to the transformation process (P110rb, P53)

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23
Q

What viruses are associated with human cancers?

A

EBV, HBV, HSV, HPV

24
Q

Types of adenoviruses

A

Types
Vary in their oncogenic potential from high to not at all
Types 12, 18 and 31 are highly oncogenic
Transformation characteristics
Transform rodent cells
No association with human neoplasms
Transforming proteins
E1a – binds to p110Rb (represses cell proliferation)
E1b – binds to p53 (represses cell proliferation)

25
Q

Papillomaviruses

A

Types

60 different types have been described; types 16 and 18 have a strong association with cervical intraepithelial neoplasia (CIN)

Transformation characteristics

Majority of cervical, penile and vulvular cancers contain HPV DNA
Suspected cofactors include tobacco smoke and coinfection with HSV
Virus multiplies only in differentiating keratinocytes
Type 16 transforms rodent cells
Viral DNA is episomal in normal tissue, but integrated in cancers and CIN

Transforming proteins

E6 – binds to p53
E7 – binds to p110Rb

26
Q

Polyomaviruses

A

Types

BK (renal transplant patient) and JC (PML patient) viruses can transform rodent cells and induce tumors in newborn hamsters
SV-40 replicates in monkey cells, transforms rodent cells and induces tumors in newborn hamsters
Polyoma virus replicates in mouse cells and transforms hamster’s cells

Transforming proteins

SV-40 – large tumor (T) antigen has domains that bind to p110Rb and p53
One or two of the three polyoma virus T antigens have transforming activity

27
Q

EBV

A

Epstein-Bar virus

28
Q

Episome

A

Extra chromosomal piece of DNA

29
Q

Herpesviruses

A

Some are linked to human cancer

Data is most convincing for EBV

EBV
Linked to Burkitt’s lymphoma and nasopharyngeal carcinoma
EBV DNA in Burkitt’s cells
Viral genome is mostly multiple episomes, but some is integrated
Important viral proteins involved in transformation include: EBNA-2 (transcriptional transactivator), LMP 1 and LMP 2a and b (tyrosine kinases)
Possible cofactors involved are malaria and c-myc proto-oncogene translocation (chromosome 8 to 14)

30
Q

HSV-2

A

Implicated in cervical cancer and CIN

DNA fragments, including those containing ribonucleotide reductase, can transform cells

31
Q

CMV

A

Implicated in cervical cancer and CIN

Some DNA segments can transform cells

32
Q

HHV-8

A

Cause of Kaposi’s sarcoma
Implicated in multiple myeloma
Contains 16 cellular genes including C-cyclin and cytokines

33
Q

Pox viruses

A

Skip

34
Q

Hepadnaviruses

A

75-85% of primary human hepatocellular carcinoma cells carry human hepatitis B virus (HBV) genes

Impaired immunity and alcohol-associated hepatic cirrhosis are co-factors

X protein interacts with p53 (X is synthesized by HepB virus)

Hep B virus can cause cancer**

Latency period between infection and primary hepatocellular carcinoma ranges from 9-35 years

35
Q

What hep virus can cause cancer?

A

HEP B

36
Q

RNA tumor virues

A

lk

37
Q

***Viruses cuase transformations by:

A

– introduction of oncogenes
– insertional activation or promoter insertion
– transcriptional activation

38
Q

Sub families of retroviurses

A

s

39
Q

IMportant aspects of retroviridae

A

s

40
Q

Oncovirus morphologica types.. retroviruses

A

l

41
Q

Endogenout tyep c viruses

A

Lots of type C retroviruses in body**

42
Q

Exogenous type C virses

A

Spread horizontally; behave as infectious agents
When oncogenic, mainly cause tumors of reticuloendothelial system and hematopoietic systems (leukemia, lymphomas) or connective tissue (sarcomas)

43
Q

Endogenous Type C viruses

A

Found in all cells of all individuals of a species
Viral information – is a constant part of genetic constitution; not pathogenic for host; can be activated by radiation, chemical carcinogens or metabolic inhibitors

44
Q

What are genes involved in replication of retroviruses?

A

GAG, POL, ENV

Replication is reverse transcription and the integration of DNA into host cell DNA

45
Q

Watch movie on retrovirus replicaton.

A

IMportatn

reverse transcription occurs
get DNA copie of RNA
Stuck into host chromosome by integrate
then make mRNAs from chromosome and make positive sense copies of

46
Q

Protease

A

Cuts polyprotein so make all diff proteins for formation of virus . that s why its a good drug target.

47
Q

If virus was integrated next to oncogene in host

A

When the viral dna comes out of the host, it can accidentaly make copy of onco gene. it then goes to other cell.. and makes product of oncogene. Once onco gene is sitting with virogene it is called v-onc.

48
Q

Viral Oncogenes

A

Viral conpies of cellular oncogenes involved in cellular division

49
Q

What are non-defective viruses?

A

Infectious progeny virus formed

Include most leukemia viruses and Rous sarcoma virus, an acute tumor virus which contains virogenes and an oncogene

50
Q

Defective Viurses

A

Have lost part or an entire virogene which has been replaced by an oncogene
Require a helper virus for replication
Are acute transforming viruses

In order for them to replicate… they need a helper virus (why? because their own replication genes was replaced with onco gene from host.. (it made a mistake))

51
Q

Defective acute transfoming virus

A

Introduce oncogenes into cell. THe gene products are NOT turned off, they are turned on and

52
Q

Mechanisms of Oncogenicity 1

A

Mechanism of transformation by acute transforming viruses utilized by both nondefective viruses (e.g., Rous sarcoma virus) and defective viruses (e.g., many sarcoma and acute leukemia viruses, like Abelson murine leukemia virus) to transform cells

53
Q

Mechanisms of oncogenicity 2nd method

A

Insertional activation or promoter insertion (e.g., chronic leukemia viruses and mouse mammary tumor virus):

Involves viral promoters and transcriptional enhancer in LTR’s in activation of cellular oncogenes
A mechanism of transformation by chronic transforming viruses

This takes much longer for this cancer to appear.. the virus is randomly inserted.. The virus isnt replicating the cell replicates and happens to also make the virus (because it was inserted)

54
Q

3rd mechanism.. Transcriptional activation

A

Involves transactivator proteins to activate cellular oncogenes - go sit on DNA sequences and say ‘make me’

The tax protein of HTLV-1 enhances transcription of viral genes and cellular genes like IL-2, IL-3, GMCSF and IL-2 receptor

Always activated in cells that are about ready to divide.

55
Q

Tax protein

A

Enhances transcription of viral genes and cellular genes

Foundations of Medicine (42 decks)

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