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MICROBIOLOGY: CMOD-Block 2 > Oncoviruses > Flashcards

Oncoviruses Flashcards

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1
Q

T or F: 15-20% of all viruses can be attibuted to viral infection.

A

True.

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2
Q

How long does it take humans to show signs of cancer after getting infected with a virus?
- who is most suceptible?

A
  • Takes YEARS

- Immunocompromised people are most susceptible to these viruses

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3
Q

T or F: for oncoviruses viruses depend on cancer is a step required for replication

A

False, viruses do not need to cause cancer to persist as a virus (no selective advantage?)

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4
Q

What 3 mechanisms do viruses use to cause cancer?

A
  1. Activate Signaling Pathways to Stimulate Constitutive Growth
  2. Release Cell Cycle control - allows for uncontrolled growth
  3. Infected cell destruction/clearance leads to unplanned regeneration
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5
Q

Why is it hard to prove that a virus caused a cancer?

A

Its difficult to prove that your virus wasn’t:

  • a Virus that just took residence in a tumor
  • just be a contaminant
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6
Q

How do you determine if a virus is oncogenic or not?

A
  1. Virus should transform cells in vitro
  2. Virus genome should be present in tumor but not in normal cells
  3. Tumor is induced in experimental animals
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7
Q

What 6 human viruses do we know to be oncogenic?

A
  1. Epstein Barr Virus
  2. Human Herpes Virus - 8 (KSHV)
  3. Human Papilloma virus
  4. Human T-lymphotropic virus type 1 (HTLV-1)
  5. Hepatitis B
  6. Hepatitis C
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8
Q

What is the only retrovirus known to cause cancer?

A

Human T-Lymphotropic Virus type 1

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9
Q

What is the difference between an immortalized cell line and a transformed cell line?

A

Immortalized - RETAIN original cell properties but grow indefinitely

Transformed Cells - Grow Indefinitely but LOSE many growth properties

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10
Q

What growth properties are often lost from transformed cells?

A
  1. Reduced Need for Serum Growth Factors
  2. Loss of Contact Inhibition
  3. Anchorage Independent (don’t have to adhere to anything- they just grow in SOFT AGAR)
  4. Appear Round as opposed to Typical Morphology
  5. May cause tumors when introduced into a suitable Animal
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11
Q

What does it mean to say that ALV (avian leukosis virus) and RSV (Rous Sarcoma virus) are transducing retroviruses?

  • How often are tumors caused?
  • Genome?
A
  • Tumors caused 100% of the time

- V-oncogenes in their genomes that are always active

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12
Q

What is the difference between a transducing Retrovirus and a non-transducing retrovirus?
- speed?

A

Transducing - causes cancer 100% of the time because it carries the ONCOGENE with it.
- this happens quickly

Non-Transducing - causes transformation often times and there is still a High rate of transformation BUT the oncogenic gene IS NOT carried with the virus Instead the virus inserts close to a host oncogene causing its upregulation
- this take week to months usually

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13
Q

Differentiate Non-Transducing and Non-transducing long latency retroviruses?
- What is an example of the latter?

A

Nontransducing Retrovirus
- Doesn’t carry oncogene with it but inserts close to one

Nontransducing, Long Latency Retrovirus
- Doesn’t replicate quickly so tumor formation happens slowly over time (this can take years)

HTLV-1 is a Nontransducing Long Latency Retrovirus

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14
Q

What are v-oncs?

A

Constitutively activated components of a signaling pathway in the host

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15
Q

What disease is caused by HTLV-1?

  • what oncogenes are involved?
  • How does this work?
  • Virus Type?
A

Adult T cell Leukemia and Lymphoma (ATL)
- aka infects and transforms CD4+ T cells

How:

  • TAX (coded for by the virus) constituatively activates IKK which phosphorlyates IkB sending if for Ubiquitination at the 26S proteosome
  • This leaves NFkB free do enter the nucleus and promote constant T cell proliferation

Type:
Nontransducing Long Latency Retrovirus

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16
Q

What diseases are caused by EBV?

- why does it cause these types of cancers?

A

Virus Lays Latent in B-cell and Epithelial cells - this corresponds to the type of cancer it causes in people.

  • Burkitt’s Lymphoma
  • Hodgkin’s Lymphoma
  • Post-transcriptional Lymphoma
  • Nasopharyngeal Carcinoma
17
Q

What Makes EBV oncogenic?

A
  • Encodes Latency Membrane Protein-1 (LMP-1) - a membrane protein that keeps the NFkB pathway on
  • Leads to B cell immoraliztion through the same IKK and NFkB pathways that HTLV-1 does
18
Q

What cancers/tumors are caused by KSHV (aka HHV-8)?

- where does this virus take up residence?

A
  • Latent in B-cells mostly, but also monocytes, T cells, and endothelial Cells

Cancers:

  • Kaposi’s Sarcoma (lymphatic endothelial cancer)
  • Pleural Effusion Lymphoma (non-Hodgkin’s body cavity lymphoma)

Benign:
- Castleman’s Disease (lymph node tumors)

19
Q

What are the underlying mechanisms to the oncogenicity of KSHV (HHV-8)?

A
  1. encodes Constitutively active GPCR = vGPCR, also encodes cytokines, chemokines, and apoptotic inhibitors that are thought to have less of an effect most imp.
  2. Encodes v-cyclin that binds and activates CDK6
    - v-cyclin/CDK6 pathway cannot be inhibited by Cip or INK4
    - Cell cycle stays activated
  • No signal needs to be sent to the molecule for it to turn the disease on
20
Q

How does Simian Virus 40 (SV40) lead to cancer?

- genome structure?

A

Genome:
- Polyoma Virus so genome is Circular RNA

Cancer:
- sT (small transforming protein) binds and INHIBITS protein phosphatase 2A (ser/thr phosphatase)

  • This means signals take a longer time to get turned off and cell division gets disregulated
21
Q

T or F: Replication proteins of DNA tumor viruses can also disrupt the cell cycle during non-lytic replication

A

True, HPV does this

22
Q

What allows HPV to cause cancer?

A

normally HPV enters “Permissive” cells and replicates

sometimes HPV enters “non-permissive” cell

  • when this happens virus can either (1) stay in the episome
    (2) enter the host (human) chromosome
  • IF entry gets messed up E2 (regulatory gene) gets messed up and E7 and E6 get expressed always
  • E7 binds Rb and E6 bins p53 leading to cell proliferation
23
Q

What virus binds to Rb and p53 the same way that HPV does?

A
  • SV40
24
Q

By what mechanism do Hepatitis B and C lead to liver cancer?

A
  • Unplanned Regeneration

**This is the Leading Cause of Liver cancer

25
Q

What is the mechanism underlying how HBV and HCV cause cancer?

A
  • Chronic Inflammation causes the liver cells that don’t really want to replicate to constantly regenerate
  • Since they aren’t made for this many mutations accumulate over many years

***NOTE: NO ONCOGENES are needed (although some think a HBV X antigen may contribute the cancer)

26
Q

Differentiate Unplanned Regeneration to Unplanned Longevity?

A

Unplanned Longevity:

  • EBV can lead to Burkitt’s Lymphoma via t(8,14) with the H chain promoter region ending up beside c-MYC (oncogene)
  • This translocation is because EBV causes B cells to liver longer than they were supposed to

Unplanned Regeneration:
- Is the opposite the Liver cells with HBV liver less time than their supposed to and increased turnover leads to mutation

27
Q

T or F: almost all c-oncs have cellular origins

A

True - they are derived from some host’s onco-genes

28
Q

OF THE 6 KNOWN tumor VIRUSES they account for 1/5 of HUMAN CANCERS

A

OF THE 6 KNOWN tumor VIRUSES they account for 1/5 of HUMAN CANCERS

29
Q

Viruses use cellular pathways identified in non-viral cancers to cause transformation in cell culture and tumors in animals

A

Viruses use cellular pathways identified in non-viral cancers to cause transformation in cell culture and tumors in animals

MICROBIOLOGY: CMOD-Block 2 (5 decks)

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