virus infection Flashcards

1
Q

what are the methods of transmission in plant viruses?

A
  • mechanical
  • vegetative propagation
  • vectors
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2
Q

what is required for viruses to infect plants?

A

a mechanical breach of the integrity of the cell wall in order to directly introduce a virus particle into the cell

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3
Q

how do some viruses utilise the plasmodesmata?

A

normal plasmodesmata are too small to allow passage of virus particles and genomic nucleic acids, but many plant viruses have evolved specialised movement proteins to modify the plasmodesmata

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4
Q

give an example of a virus which utilises the plasmodesmata to infect plants

A

TMV - produces 30-K protein which causes the plasmodesmata to begin to transport genomic RNA from infected cells to neighbouring cells

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5
Q

what are the symptoms of virus infection in plants?

A
  • growth retardation
  • distortion
  • mosaic patterning on leaves
  • yellowing
  • wilting
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6
Q

what do the symptoms of virus infection in plants result from?

A

necrosis
hypoplasia
hyperplasia

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7
Q

what is hypoplasia? (plants)

A

localised retarded growth that frequently leads to mosaicism

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8
Q

what is hyperplasia? (plants)

A

excessive cell division or growth of abnormally large cells, resulting in the production of swollen or distorted areas of the plant

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9
Q

what does the hypersensitive response refer to?

A
  • the synthesis of a range of new proteins - in response to virus
  • increase in production of cell wall phenolic substances
  • release of active oxygen species
  • production of phytoalexins
  • accumulation of salicylic acid
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10
Q

what are the characteristics of systemic resistance to virus infection in plants?

A

these plants have a tendency to increase local necrosis, producing substances such as proteases and peroxides to prevent systemic spread

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11
Q

how is Tobacco N gene an example of how a plant may have systemic resistance to viral infection?

A
  • this gene encodes a cytoplasmic protein with a nucleotide binding site that interferes with TMV replicase
  • when present in plants, this gene causes TMV to produce a localised necrotic infection rather than systemic mosaicism
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12
Q

how are virus-resistant plants created?

A

by production of transgenic plants expressing recombinant virus proteins or nucleic acids that interfere with virus replication without producing the pathogenic consequences of infection

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13
Q

which virus components can be used to create a virus-resistant plant?

A
  • virus coat proteins
  • intact or partial virus replicase that interfere with genome replication
  • antisense RNAs
  • defective virus genomes
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14
Q

what is the importance of the humoral immune response to virus infection?

A

permits clearance of the virus from the body

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15
Q

what is the importance of serum neutralisation in the humoral immune response?

A

stops the spread of virus to uninfected cells and allows other defence mechanisms to mop up infection

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16
Q

which three classes of antibody are induced by viral infection?

A

IgM
IgG
IgA

17
Q

what is IgM?

A

a large, multivalent molecule that is effective at cross-linking large targets such as bacterial cell walls

18
Q

what is the importance of IgA?

A

important for initial protection from viral infection

-secretory IgA is produced at mucosal surfaces and results in ‘mucosal immunity’

19
Q

give examples of the mechanisms which may cause direct neutralisation of viruses by antibodies

A
  • conformational changes in the virus capsid

- blocking of virus receptor binding by steric hindrance

20
Q

what is meant by ‘opsonisation’?

A

the secondary consequence of antibody binding where there is phagocytosis of antibody coated target molecules by mononuclear cells or polymorphonuclear cells

21
Q

give an example of where opsonisation of virus may actually enhance virus uptake

A

HIV - causes increase in uptake of virus by macrophage

22
Q

how do observations made on cogenital defects in cell-mediated immunity provide evidence of the importance of cell-mediated immunity in the control of virus infection?

A

-congenital defects result in predisposition to viral infections rather than bacterial infection

23
Q

which three effects does cell-mediated immunity rely on?

A
  • non-specific killing by NK cells
  • specific cell killing (mediated by cytotoxic T lymphocytes)
  • antibody dependent cellular cytotoxicity
24
Q

what is the role of natural killer cells?

A

provide a rapid first line of defence in the early stages of infection

25
Q

what is the distinguishing feature of antibody-dependent cellular cytotoxicity?

A

the mechanism is dependent on the recognition of antigen on the surface of the target celery means of an antibody on the surface of the effector cell

26
Q

what is necrosis marked by?

A

non-specific changes such as disruption of the plasma membrane and nuclear envelope, rupture of membrane bound organelles e.g. mitochondria and lysosomes, cell swelling, fragmentation of DNA/RNA etc.

27
Q

by which routes can viruses enter the body?

A
  • skin
  • mucosal membranes
  • alimentary canal
  • respiratory tract
28
Q

what is the advantage to the virus of using a secondary vector?

A

the natural environment is a barrier to infection as most viruses are sensitive to heat, drying and UV light

29
Q

what is horizontal transmission?

A

host-host transmission

direct, relies on high rate of infection to maintain virus population

30
Q

what is vertical transmission?

A

the transmission virus from one generation of hosts to the next, can occur by infection of the foetus before, during or after birth. relies on long term persistence of the virus in the host rather than rapid propagation and dissemination of the virus

31
Q

what is the significance of local infection?

A

virus must initiate an infection by entering a susceptible cell. this initial interaction determines whether an infection will remain localised or become systemic

32
Q

by which ways can infection spread via the bloodstream?

A
  • direct inoculation via arthropod vectors, blood transfusions/IV drug use
  • free travel of virus in the plasma (togavirus, enterovirus)
  • association with blood cells
33
Q

what is the importance of tissue tropism and what dictates it?

A

controls spread.
tissue tropism is controlled by route of infection, but also interaction of a virus attachment protein with a specific receptor molecule on the surface of the cell

34
Q

what is antigenic drift?

A

gradual accumulation of minor mutations (e.g. nucleotide substitutions) in the virus genome, which results in subtly altered coding potential and antigenicity

35
Q

what is antigenic shift?

A

a sudden and dramatic change in the antigenicity of a virus due to reassortment of the segmented virus genome with another virus genome of a different antigenic type

36
Q

what are the two main requirements for long term persistence of virus infections?

A
  • regulation of lytic potential

- evasion of immune surveillance

37
Q

what is abortive infection?

A

when a virus infects the cell but cannot complete the full replication cycle

38
Q

what is meant by the term ‘latent infection’?

A

when the virus down regulates its gene expression and enters an inactive state with strictly limited gene expression and without ongoing replication