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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
neoplasia
abnormal tissue overgrowth that may be localized or disseminated; leads to formation of neoplasms (carcinogenesis)
26
oncology
study of neoplasia
27
benign neoplasm
growth produced by abnormal cell proliferation that remains localized and doesn't invade adjacent tissue
28
malignant neoplasm
aka cancer | locally invasive and may spread (metastasis)
29
oncogenic viruses
give rise to tumors
30
Neoplasms are consequences of what?
dysregulated growth of cells derived from a single, genetically altered progenitor cell
31
How do cancer cells travel to other areas of the body?
via bloodstream or lymph system
32
proto-oncogenes
encode proteins that function in normal cellular growth and differentiation
33
tumor suppressor genes
play role in keeping cell division in check; encode proteins that regulate and inhibit uncontrolled growth
34
T/F proto-oncogenes often involved in growth signaling and anti-apoptotic pathways
T: they encode... - growth factor proteins - growth factor receptors - transcription factors - intracellular signaling proteins - signal transducers
35
How do proto-oncogenes become oncogenes?
- virus - UV rays - chemicals
36
abnormal protein synthesis
- 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
oncogene
mutated forms of proto-oncogenes or aberrantly expressed proto-oncogenes; function in an unregulated manner
38
tumor suppressor genes functions
- hold cell cycle at G1 phase - connect cell cycle to DNA damage - repairs damaged DNA - apoptosis if repair fails
39
metastasis suppressors
adhesion proteins that prevent spread of cancer cells
40
retinoblastoma protein (Rb)
- 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
E2F transcription factor
necessary for expression of a number of cell-cycle specific genes *when bound, cell cycle can't proceed to S phase
42
P16
tumor suppressor protein that blocks CDK -> can't phosphorylate Rb -> E2F remains inhibited, no cell division
43
p53
activates DNA repair system and stops the cell cycle at G1 checkpoint, before DNA replication; if damage to cell is irreversible -> apoptosis
44
T/F oncogenic viruses generally have an RNA genome
F: DNA genome or generate DNA provirus after infection (as in retrovirus)
45
episomal genome
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
T/F oncogenes of DNA viruses have no homologue or direct ancestors (c-onc genes/protooncogenes) among cellular genes of the host
T
47
2 ways DNA tumor viruses interact with cells
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
Which virus produces warts on the skin and mucous membranes?
papillomavirus
49
Are papillomas malignant or benign?
usually benign, regress spontaneously *can progress to malignancy
50
With papillomavirus, what is necessary for malignant transformation?
Integration of viral DNA into host genome-> disruption of E2 (viral repressor) *in benign it persists as episome
51
adenovirus oncoproteins
E1A -> inhibits RB1 -> viral replication | E1B -> inhibits p53 -> viral replication
52
papillomavirus oncoproteins
E6: prevents p53 from making damaged cells commit suicide E7: binds to Rb and prevents it from stopping damaged cells from growing
53
All RNA tumor viruses belong to which family?
retroviridae
54
T/F slow transforming retroviruses have a v-onc gene
F
55
promoter
DNA sequence at which DNA-dependent RNA polymerase binds to initiate transcription
56
enhancer
transcriptional regulatory sequence located some distance from the promoter; increases rate of initiation of transcription
57
v-onc
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
T/F transformed cells are more spindle-shaped
T
59
tumor antigens
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
FOCMA
feline oncornavirus membrane-associated antigen = tumor antigen

Virology (16 decks)

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