Retroviruses Flashcards

1
Q

What do normal RNA viruses contain?

A
  • double stranded RNA positive

- single strand RNA negative

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2
Q

What distinguishes retroviruses?

A
  • diploid positive sense RNA

- contain reverse transcriptase which generates DNA which is integrated into host genome

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3
Q

Main example of a retrovirus

A

HIV

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4
Q

What is the life cycle of a retrovirus?

A
  • virus binds to specific receptor on cell surface
  • double strand RNA enters cell
  • changes to DNA by reverse transcriptase
  • DNA in nucleus integrates into host DNA
  • millions of copies of virus can be made, proteins made
  • proteins assemble at cell surface
  • virus efflux picking up coat of bilayer
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5
Q

What is the receptor which HIB binds to?

A

CD4

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6
Q

Features of the retrovirus structure

A
  • surface envelope (binding to target cell surface)
  • matrix (holds virus shape)
  • capsid inside matrix containing RNA to make copies of itself
  • lipid envelope
  • protease
  • reverse transcriptase
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7
Q

What do accessory proteins do?

A

Interact with host innate immune response to viral infections counteracting it

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8
Q

What is the key enzyme!!! What does it do???

A

Reverse transcriptase - transcription of viral RNA to DNA

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9
Q

What does integrase do?

A

Integration of ds DNA into host genome to form provirus

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10
Q

What does protease do?

A

After new virion release, cleaves certain proteins for viral maturation and infectivity

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11
Q

What are the 2 groups of retroviruses?

A

Oncovirinae - induce oncogenesis causing tumours

Lentivirinae

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12
Q

What are some examples of oncovirinae?

A

RSV (rous sarcoma virus)
HTLV-1 (human T cell lymphotropic virus, first to be discovered)
HTLV -2

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13
Q

What does the genome of retroviruses consist of?

A

Gag, Pol, Env (structural genes)
Plus accessory proteins
Regulatory genes

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14
Q

How widespread is HTLV?

A

Southern Japan (via Portuguese explorers who had been in Africa)
Central America (slave trade reached)
South America (slave trade)
Africa where it originated in ancient times
Caribbean
15-20 million people

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15
Q

How is HTLV is transmitted?

A
  • prolonged breast feeding mother to child
  • sexual contact
  • blood transfusion
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16
Q

How common are the different types of HTLV?

A

1 is most common, 4 is least

17
Q

What does HTLV1 cause?

A

Adult T cell leukaemia
HTLV1 associated myelopathy
Tropical Spastic Paraparesis

18
Q

What is the latency period of HTLV1?

A

20-30 years

Long

19
Q

What is TSP? How does it present?

A

Tropic Spastic Paraparesis

  • chronic
  • progressive
  • nervous system disease
  • weakness, stiff muscles, muscle spasms, sensory disturbances, sphincter dysfunction
  • affects adults in equatorial regions
20
Q

How is TSP treated?

A
  • high dose of IV methylprednisolone and daily prednisolone
21
Q

What is adult T cell leukaemia?

A

Clonal aggressive malignancy of CD4+ T lymphocytes

- skin can be involved

22
Q

How is adults T cell leukaemia treated?

A
  • chemotherapy often ineffective

- ongoing trials (IFNalpha)

23
Q

What does HTLV2 cause?

A
  • HAM/TSP

- hairy cell leukaemia

24
Q

What is the long latency of HTLV2?

A

Longer than HTLV1

20-30 years

25
Q

What is hairy cell leukaemia?

A
  • leukaemia cells collect in spleen
  • spleen swells
  • few normal WBCs as leukaemia invades bone marrow
    = reduced infection resistance
26
Q

How is HTLV transmission different from HIV transmission?

A
  • requires cell to cell contact
27
Q

What are some examples of lentivirinae?

A

HIV-1

HIV-2

28
Q

How widespread is HIV?

A
  • over 70 million people infected
  • main epidemic is HIV1 in West Africa
  • from chimpanzees to human
29
Q

How is HIV transmitted?

A
  • unprotected sexual intercourse with infected partner
  • vertical transmission mother to child (in utero, during delivery or via breastmilk)
  • injection drug use
30
Q

What does HIV require to infect cells?

A
  • both CD4 and chemokine receptor (CXCR4 or CCR5)

to be expressed by cells

31
Q

What is the course of HIV infection?

A
  • first 3 weeks virus multiplies lots and CD4 cell target cell decline
  • immune system takes control and increases CD4 and reduces viral load (clinical latency where individual is unaware of infection)
  • CD4 declines further and viral load increases (opportunistic infections)
32
Q

What are the opportunistic infections of HIV?

A
  • oral candidiasis

- interstitial pneumonia

33
Q

What is a clade?

A
  • related virus from a common ancestor (shows how diverse the virus is)
  • HIV has many clades so is very diverse vs. measles for example
  • Clade B in North and South America and Western Europe and Australia
  • Clade C, A and AG are most common
34
Q

What is a recombinant?

A

When clades combine and make a new virus

35
Q

What is the treatment of HIV?

A
  • HAART (immediately)
36
Q

Role of gag

A

Codes for proteins which make up matrix, capsid and nucleoprotein structures

37
Q

Role of pol

A

Codes for reverse transcriptase and integrase and protease enzymes

38
Q

Role of env

A

Codes for surface and transmembrane components of viral envelope protein