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Microbiology > Viral Oncogenesis II > Flashcards

Viral Oncogenesis II Flashcards

1
Q

What is Merkel Cell Carcinoma (MCC)

A

highly aggressive neuroendocrine carcinoma of the skin w/ a high propensity of recurrence and metastasis

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2
Q

5-year disease-specific survival rate for Merkel Cell Carcinoma (MCC)

A

60%

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3
Q

virus associated with Merkel Cell Carcinoma (MCC)

A

Merkel cell polyomavirus (MCV)

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4
Q

how common is the Merkel cell polyomavirus

A

rare but incidence is rapidly increasing

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5
Q

is Merkel Cell Polyomavirus associated with all Merkel Cell Carcinoma

A

it is associated with most of it but not all of it; about 20 - 30% of cases of MCC do not have the MCV virus and have a distinct pathoetiology

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6
Q

genome that Hep B and C are associated with

A

Hep B - DNA

Hep C - RNA

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7
Q

organ that Hep B and Hep C virus infect

A

they infect and damage the liver so you get classical symptoms of jaundice and liver enzyme release

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8
Q

80% of all Primary Hepatocellular Carcinoma (PHC) can be attributed to what virus

A

chronic HBV infection

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9
Q

prognosis if a pt has PHC

A

usually fatal – one of the three most common causes of cancer mortality in the world

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10
Q

what type of virus is HBV

A

Hepadnavirus (class VII)

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11
Q

how is HBV spread

A

blood or needles, sexual contact, and

perinatally

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12
Q

median incubation period of HBV

A

3 months which then icterus symptoms begin

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13
Q

what do 5-10% of pts with PHC eventually develop

A

chronic hepatitis

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14
Q

percentage of the world’s population that has been infected with HBV and how many die from it annually

A

1/3 of world infected

1-2 million deaths/year

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15
Q

why has the incidence of HBV gone down

A

vaccination

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16
Q

HBV has a tissue tropism for what organ and what happens when in that organ

A

liver

integrates into the host chromosome and stimulate cell growth

17
Q

oncoprotein associated with HBV

A

HBx

18
Q

type of virus is Hep C

A

flavivirus (Class IV so (+) ssRNA)

19
Q

how long does it take for Hep C to develop into cancer

A

10-50 years (30 years being median)

20
Q

when someone contract HCV acute infection, what are the three fates

A
  • 15%: recovery and clearance
  • 15%: cirrhosis rapid onset
  • 70%: persistent infection with 40% being asymptomatic and other 30% definitely leading to chronic hepatitis
21
Q

of the 30% of those with HCV that eventually become chronic hepatitis, what is their fate

A
  • 6% liver failure
  • 20% cirrhosis
  • 4% hepatocellular carcinoma
22
Q

only known retrovirus known to cause cancer in humans

A

HTLV-1 (RNA tumor virus)

23
Q

what do retroviruses carry with their regular genes

A

they carry oncogenes that they can integrate at particular sites in the host cell

24
Q

example of fast acting and slow/transacting RNA tumor cancer

A

fast: acute leukemia or sarcoma
slow: leukemia

25
Q

what is significant about leukemia virus’ replication (including HTLV-1)

A

replication is competent but they cannot transform cells in vitro

26
Q

how long does it take for HTLV-1 to cause cancer

A

after a long latency period usually about 30 years

27
Q

how does HTLV-1 promote cell growth

A

in more indirect ways than the oncogene encoding viruses

28
Q

what is associated with myelopathy (tropical spastic paraparesis)

A

Adult acute T-cell lymphocytic leukemia (ATLL) and HTLV 1

29
Q

is HTLV-1 only associated with neoplastic diseases

A

no they are also associated with nonneoplastic neurologic disorders

30
Q

what is the importance of HTLV-1 having the tax protein

A

activates promoters in LTR region and specific cellular genes (promote outgrowth of the cell)

31
Q

importance of HTLV-1 integrating near cellular growth controlling genes

A

enhancer and promoter gene sequences can promote expression of growth-stimulating proteins

32
Q

importance of Tax protein being immunogenic

A

eventually cells will evolve and there will be selection for cells that do not have tax hence pushing cells towards having proteins like HBZ that compensates for loss of tax by taking up its function – cells basically become immortal

33
Q

most common among those w/ inherited immune deficiency, autoimmune disease, or HIV

A

Non-Hodgkin’s lymphoma

34
Q

increase the risk of developing non-Hodgkin’s lymphoma

A

Viral infections: HTLV-1, hepatitis C, and EBV

35
Q

mechanism by which cell growth is promoted (viral transformation/ immortalization)

A

either removing the growth suppressors or enhancing growth activators

Microbiology (39 decks)

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