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Infection and Immunity > Retroviruses > Flashcards

Retroviruses Flashcards

1
Q

what type of genome does the Rous sarcoma has?

A

RNA genome

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2
Q

what is Crick’ “Central Dogma”?

A

“once information has got into a protein it can’t get out again”

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3
Q

what is the Rous sarcoma virus replication dependent on?

A

DNA

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4
Q

what effects does Actinomycin D has on RNA synthesis?

A

Actinomycin D inhibits transcription and hence RNA synthesis

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5
Q

what inhibits virus growth?

A

Actinomycin D

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6
Q

what route did the effects of actinomycin D in sarcoma suggested?

A

RNA -> DNA -> RNA -> Protein

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7
Q

what is the provirus hypothesis?

A

the provirus of Rous sarcoma is a region of DNA homologous with viral RNA stably integrated into the molecule of cellular DNA in the nucleus

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8
Q

what is used to fight against HIV?

A

reverse transcriptase inhibitors

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9
Q

what is the viral RNA dependent on?

A

DNA polymerase

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10
Q

what does the reverse transcriptase do?

A

turns RNA back to DNA

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11
Q

what are the subfamilies in the family retroviridae?

A

orthoretrovirinae and spumaretrovirinae

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12
Q

how are retroviruses transmitted?

A

transmission typically via close contact (oronasal, sexual, blood-borne)

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13
Q

what protects the retrovirus?

A

a lipid envelope

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14
Q

why does the retrovirus have an envelope?

A

because it is susceptible to desiccation and detergents (that’s why the envelope has lipids)

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15
Q

what are the key features of retroviruses?

A
  • two copies of RNA genome in each viral particle
  • reverse transcribe RNA to DNA
  • DNA “provirus” integrates into cellular DNA
  • establish persistent infections
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16
Q

what does the “gag” gene encode in the retrovirus genome?

A

core structural proteins

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17
Q

what does the “pol” gene encode in the retrovirus genome?

A
  • enzymes for replication
  • reverse transcriptase
  • integrase
  • protease
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18
Q

what does the “env” gene encode in the retrovirus genome?

A

envelope glycoproteins

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19
Q

how do retroviruses infect cells?

A

by binding to a cell surface molecule called the receptor

- it binds to a nuclear pore and once it binds it starts replicating

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20
Q

what is necessary for a productive viral life cycle?

A

integration

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21
Q

where do simple retroviruses (e.g. FeLV) integrate?

A

in dividing cells

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22
Q

where can lentiviruses (e.g. HIV) integrate?

A

in non-dividing cells

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23
Q

what is integration?

A

the retroviral genome integrates into the cellular DNA and becomes part of the host

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24
Q

how much of the human genome is derived from ancestral retrovirus infections?

A

8.3%

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25
Q

what does integration do?

A

maximises the chance of viral transmission

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26
Q

which retroviruses integrate?

A

all

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27
Q

how does the retroviral assembly work?

A
  • RNA makes a poliprotein (single long protein?
  • sticks under membrane
  • bends the membrane
  • becomes more circular
  • protein inserted in this new molecule
  • has to be cut off from membrane
  • forms an immature molecule
  • then matures
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28
Q

where do some of the retroviruses assemble?

A

at the pericentriolar region of the nucleus, the fully assembled particles then migrates to the cell surface

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29
Q

is there any vaccine against retroviruses that is effective?

A

only the feline leukaemia (FeLV) vaccine works

30
Q

what does the FeLV cause?

A

immunosuppression, tumours, anaemia

31
Q

which are the subgroups of FeLV?

A

three subgroups: A, B, C, classified according to the viral envelope glycoprotein

32
Q

from where has the FeLV-A subgroups been isolated?

A

from all infected cats

33
Q

where are the FeLV-B and C subgroups generated?

A

within the host

34
Q

how viral is FeLV?

A

cats may clear the virus or become persistently infected

35
Q

what do retroviruses establish?

A

persistent infections

36
Q

what does the bovine leukaemia virus cause?

A

zoonotic bovine leukosis

37
Q

what does the bovine leukaemia virus infect?

A

B lymphocytes

38
Q

are there free virus in the blood in bovine leukosis?

A

no

39
Q

what doe persistently infected cattle produce?

A

antibodies

40
Q

what does viral tax protein trans activates?

A

cellular genes

41
Q

how is bovine leukaemia virus transmitted?

A

via infected cells e.g. milk, blood

42
Q

how can bovine leukaemia virus be transmitted?

A

vertically or horizontally

43
Q

which are the oncogenic retroviruses?

A
  • alpha avian leukosis viruses (ALV)
  • beta Jaagsiekte sheep retrovirus (JSRV)
  • gamma feline leukaemia virus (FeLV)
  • delta bovine leukaemia virus (BLV)
44
Q

what are the mechanisms of retroviral oncogenesis?

A
  • oncogene capture and transduction
  • insertional activation
  • insertion leading to truncation
  • insertion leading to gene inactivation
  • other mechanisms
45
Q

how can retroviral proteins lead to tumour formation?

A

they can deregulate normal cellular metabolism and lead to tumour formation

46
Q

what are the effects of an infection with oncogenic virus in the cell?

A
  • lossof contact inhibition
  • increased saturation density
  • increased growth rate
  • anchorage-independent growth
  • tumorigenic in appropriate hosts
47
Q

what causes OPA?

A

a retrovirus called JSRV

48
Q

where does JSRV replicate?

A

only in type II pneumocytes and club cells

49
Q

what are club cells?

A

bronchiolar exocrine cells

50
Q

what does replication lead to?

A

to transformation of every cell

51
Q

what does the viral Env switches on?

A

signals for cell division and activates cell signalling pathways

52
Q

what is the incubation period of Maedi-Visna Virus (MVV)?

A

approx. 2 years

53
Q

what does MVV cause?

A

ovine progressive pneumonia

54
Q

how is equine infectious anaemia virus (swamp fever) transmitted?

A

by bitting insects (horseflies)

55
Q

what is associated with the emergence of viral emergents?

A

episodic pyrexia/illness

56
Q

what are the treatments for swamp fever?

A

there are no treatment options

57
Q

what is swamp fever related to?

A

immune complex formation, complement activation

58
Q

what are the immunodeficiency-causing lentiviruses?

A
  • feline immunodeficiency virus
  • human immunodeficiency virus
  • simian immunodeficiency virus
59
Q

how many people are currently infected by HIV?

A

35 million people

60
Q

how many deaths in sub-Saharan Africa are caused by AIDS?

A

76%

61
Q

where do the endogenous retroviruses (ERVs) genome persists?

A

in host DNA

62
Q

what does the integration of the retrovirus into the germ cellular DNA cause?

A

vertical transmission of viral DNA to offspring

63
Q

what are ERVs?

A

transposable (mobile) genetic elements

64
Q

are ERVs defective?

A

most of them, but not all

65
Q

what do ERV-derived genes may provide to the host?

A

useful or essential functions to the host e.g. syncytin in placental morphogenesis

66
Q

what is the fusion of the trophoblast cell layer into the continuous multinucleate syncytiotrophoblast associated with?

A

implantation of the embryo

67
Q

what mediates the trophoblast cell fusion?

A

the expression of the HERV-W Env (envelope)

68
Q

for what have retroviral vectors been developed?

A

gene therapy

69
Q

what may the integration of DNA provirus lead to?

A

development of cancer

70
Q

what is the integration of DNA provirus used for?

A

exploited for gene therapy

Infection and Immunity (23 decks)

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