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Virology > Effects of Viruses on Host Cells > Flashcards

Effects of Viruses on Host Cells Flashcards

1
Q

What are the cytocidal effects?

A

lysis and apoptosis

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2
Q

What is a non-cytocidal effect?

A

persistent infection

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3
Q

cytopathic effect

A

primary: induced by viral replication and viral proteins toxic to host cell
secondary: metabolic needs of the virus

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4
Q

What is the most severe form of CPE?

A

complete destruction of cells: all cells in monolayer shrink, pyknosis, detach from glass within 72 hours (enteroviruses)

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5
Q

subtotal destruction of cells

A

some detachment and death but not for all cells in the monolayer (togaviruses)

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6
Q

focal destruction of cells

A

localized areas of infection (herpesviruses and poxviruses)

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7
Q

pyknosis

A

degenerative condition of a cell nucleus marked by clumping of the chromosomes, hyperchromatism, shrinking of nucleus

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8
Q

cell fusion

A

aka synctium or polykaryon formation

  • fusion of plasma membranes of 4 or more cells to produce an enlarged cell with multiple nuclei -> premature cell death
  • often a result of insertion of glycoproteins by enveloped viruses during budding
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9
Q

What may be the only detectable CPE of soem paramyxoviruses?

A

synctia formation

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10
Q

mechanism of synctia formation

A

infected cell producing gp120 spikes binds to CD4 of uninfected cell and they fuse membranes -> can continue with multiple cells

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11
Q

Which virus has characteristic Negri bodies?

A

rabies; intracytoplasmic acidophilic

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12
Q

Which virus has Owl’s eye inclusion bodies?

A

herpesvirus; intranuclear acidophilic

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13
Q

Which virus has crystalline aggregates of virions?

A

adenovirus; intranuclear basophilic (multiple inclusions)

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14
Q

T/F inhibition of host-cell RNA transcription is a consequence of viral effects on host-cell protein synthesis.

A

T: they decrease availability of transcription factors required for RNA polymerase activity

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15
Q

What would be the effect of inhibiting polyadenylation and splicing of host cell primary mRNA transcripts?

A

no formation of mature mRNA -> no protein synthesis

*seen with influenza and herpesvirus

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16
Q

inhibition of host-cell protein synthesis

A
  • viral enzymes that degrade cellular mRNAs
  • factors that bind to ribosomes to inhibit cellular mRNA translation
  • alteration of intracellular ionic environment favoring translation of viral mRNAs
  • production of excess viral mRNA that outcompetes cellular mRNA for ribosomes
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17
Q

interference with cellular membrane function

A
  • promotion of syncytium formation
  • affect ion exchange and membrane potential
  • induce synthesis of new intracellular membranes of rearrangement of previously existing ones
  • damage to cytoskeleton
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18
Q

executioner caspases

A

3 and 6

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19
Q

initiator caspases

A

8 and 9

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20
Q

intrinsic (mitochondrial) pathway

A

activated as a result of increased permeability of mitochondrial membranes subsequent to cell injury (e.g. viral infection)

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21
Q

extrinsic (death receptor) pathway

A

activated by engagement of specific cell-membrane receptors which are members of TNF family (includes Fas) -> binds cytokine TNF to cellular receptor to trigger apoptosis
- CD8 cells can bind Fas receptor and trigger this pathway also

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22
Q

T/F non-cytocidal viruses can’t damage specialized functions of differentiated cells and affect homeostatic and metabolic functions

A

F: they can, including CNS, endocrine glands, and immune system

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23
Q

T/F the effects of non-cytocidal changes on the host animal function depends on which tissues are affected

A

T: most organs and tissues can replace cells fast enough so that function isn’t altered; exception: terminally differentiated cells (nerve cells)

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24
Q

cell transformation

A

changing of a normal cell into a cancer cell

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25
Q

neoplasia

A

abnormal tissue overgrowth that may be localized or disseminated; leads to formation of neoplasms (carcinogenesis)

26
Q

oncology

A

study of neoplasia

27
Q

benign neoplasm

A

growth produced by abnormal cell proliferation that remains localized and doesn’t invade adjacent tissue

28
Q

malignant neoplasm

A

aka cancer

locally invasive and may spread (metastasis)

29
Q

oncogenic viruses

A

give rise to tumors

30
Q

Neoplasms are consequences of what?

A

dysregulated growth of cells derived from a single, genetically altered progenitor cell

31
Q

How do cancer cells travel to other areas of the body?

A

via bloodstream or lymph system

32
Q

proto-oncogenes

A

encode proteins that function in normal cellular growth and differentiation

33
Q

tumor suppressor genes

A

play role in keeping cell division in check; encode proteins that regulate and inhibit uncontrolled growth

34
Q

T/F proto-oncogenes often involved in growth signaling and anti-apoptotic pathways

A

T: they encode…

  • growth factor proteins
  • growth factor receptors
  • transcription factors
  • intracellular signaling proteins
  • signal transducers
35
Q

How do proto-oncogenes become oncogenes?

A
  • virus
  • UV rays
  • chemicals
36
Q

abnormal protein synthesis

A
  • increased synthesis
  • synthesis of a protein containing portions encoded by different genes (fusion protein not under normal control)
  • encoded protein with altered structure/function
37
Q

oncogene

A

mutated forms of proto-oncogenes or aberrantly expressed proto-oncogenes; function in an unregulated manner

38
Q

tumor suppressor genes functions

A
  • hold cell cycle at G1 phase
  • connect cell cycle to DNA damage
  • repairs damaged DNA
  • apoptosis if repair fails
39
Q

metastasis suppressors

A

adhesion proteins that prevent spread of cancer cells

40
Q

retinoblastoma protein (Rb)

A
  • alternates between phosphorylated and un-phos state (via CDKs)
  • un-phos -> binds to E2F to prevent activity and not all cell division to proceed to S phase
  • phos -> can’t bind E2F so allows cell cycle to progress from G1 to S
41
Q

E2F transcription factor

A

necessary for expression of a number of cell-cycle specific genes
*when bound, cell cycle can’t proceed to S phase

42
Q

P16

A

tumor suppressor protein that blocks CDK -> can’t phosphorylate Rb -> E2F remains inhibited, no cell division

43
Q

p53

A

activates DNA repair system and stops the cell cycle at G1 checkpoint, before DNA replication; if damage to cell is irreversible -> apoptosis

44
Q

T/F oncogenic viruses generally have an RNA genome

A

F: DNA genome or generate DNA provirus after infection (as in retrovirus)

45
Q

episomal genome

A

genome never integrates into host genome but has autonomous replicating system; seen in B cells infected with Epstein-Barr and cells infected with papillomavirus

46
Q

T/F oncogenes of DNA viruses have no homologue or direct ancestors (c-onc genes/protooncogenes) among cellular genes of the host

A

T

47
Q

2 ways DNA tumor viruses interact with cells

A
  1. productive infection in permissive cell -> virus completes replication cycle resulting in cell lysis
  2. non-productive infection in nonpermissive cell -> virus transforms cell without completing its replication cycle, viral genome integrated into cellular DNA or persists as episome -> transformed cells!
48
Q

Which virus produces warts on the skin and mucous membranes?

A

papillomavirus

49
Q

Are papillomas malignant or benign?

A

usually benign, regress spontaneously *can progress to malignancy

50
Q

With papillomavirus, what is necessary for malignant transformation?

A

Integration of viral DNA into host genome-> disruption of E2 (viral repressor) *in benign it persists as episome

51
Q

adenovirus oncoproteins

A

E1A -> inhibits RB1 -> viral replication

E1B -> inhibits p53 -> viral replication

52
Q

papillomavirus oncoproteins

A

E6: prevents p53 from making damaged cells commit suicide
E7: binds to Rb and prevents it from stopping damaged cells from growing

53
Q

All RNA tumor viruses belong to which family?

A

retroviridae

54
Q

T/F slow transforming retroviruses have a v-onc gene

A

F

55
Q

promoter

A

DNA sequence at which DNA-dependent RNA polymerase binds to initiate transcription

56
Q

enhancer

A

transcriptional regulatory sequence located some distance from the promoter; increases rate of initiation of transcription

57
Q

v-onc

A

present in acutely transforming retroviruses; originates from host c-onc gene that is inserted into virus genome by recombination between provirus DNA and host DNA
*under control of viral LTRs (strong promoters)

58
Q

T/F transformed cells are more spindle-shaped

A

T

59
Q

tumor antigens

A

abnormal proteins on the surface of tumor cells that arise from mutations and are classified into 5 types:

  1. differentiation antigens: associated with specific stages of cell differentiation
  2. excessive amounts of normal proteins: over-production of normal cell products
  3. cancer/testis antigens: unknown function
  4. viral coded proteins: products of genes of oncogenic viruses
  5. mutated proteins: altered forms of normal cellular proteins
60
Q

FOCMA

A

feline oncornavirus membrane-associated antigen = tumor antigen

Virology (16 decks)

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