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virology > lecture 9 > Flashcards

lecture 9 Flashcards

1
Q

cytocidal effect of viruses on host cells

A

cell death via lysis or apoptosis

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2
Q

non-cytocidal effect of viruses on host cells

A

persistent infection

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3
Q

cell transformation effect of viruse on host cells

A

tumor cells

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4
Q

cytopathic/cytopathogenic effect

A

damage or morphological changes to host cells during virus invasion

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5
Q

cell fusion (syncytium of polykaryon formation)

A
  • involves fusion of plasma membrane of four or more cells to produce enlarged cell with four or more nuclei, prone to mature cell death
  • result from fusion of infected cell with neighboring infected or uninfected cells
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6
Q

inclusion bodies in host cell during viral infection

A
  • abnormal structure in cell nucleus, cytoplasm, or both such as aggregates of proteins, have characteristic staining properties, associated with certain viral infections
  • help to identify certain viral infection
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7
Q

characteristics of inclusion bodies

A
  • accumulation of viral components
  • result from degenerative changes in cell
  • crystalline aggregates of virions
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8
Q

visible effects of inclusion bodies

A
  • intracytoplasmic, intranuclear or both
  • single or multiple
  • large or small
  • round or irregular
  • eosinophilic/acidophilic or basophilic
  • acidophilic- recognizes affinity for acid dyes such as eosin, appear pinkish
  • basophilic staining- recognizes/affinity for basic dyes such as hematoxylin, purplish blue upon staining
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9
Q

mechanisms of virus-induced cell injury and death

A
  • inhibition of host-cell nucleic acid synthesis
  • inhibition of host-cell RNA transcription (mRNA production and processing)
  • inhibition of host-cell protein synthesis
  • some viruses cause lysosomes to release hydrolytic enzymes, then destroy host cell
  • interference with cell membrane function
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10
Q

apoptosis

A
  • process of programmed cell death, mechanism of cell suicide, host activates as last resort to eliminate viral factories before progeny virus production is complete
  • different from lysis- viral replication is complete, host cell destroyed, new virions released
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11
Q

role of capsases in apoptosis

A
  • activation of host-cell capsases mediates death of cell

- once activated, capsases responsible for degradation of cell’s DNA and proteins

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12
Q

intrinsic (mitochondrial) apoptotic pathway

A

-activated as result of increased permeability of mitochondrial membranes subsequent to cell injury

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13
Q

extrinsic (death receptor) pathway

A

-activated by enlargement of specific cell-membrane receptors which are members of TNF receptor family (TNF, Fas, others), thus binding of cytokine TNF to cell receptor can trigger apoptosis

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14
Q

cytotoxic T lymphocytes and NK cells

A
  • can also initiate apoptosis of virus infected cells

- use perforin and granzymes, which activate capsases inside target cell

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15
Q

antibody-dependent cell mediated cytotoxicity

A
  • resulting from surface membrane fusion of enveloped viruses
  • viral glycoproteins are retained on cell surface, since these are antigenic, the cell can become a target of the immune system of the host
  • antibody binds Ag on surface of target cell
  • Fc receptors on NK cell recognize bound Ab
  • cross linking of Fc receptors signal NK cell to kill target cell
  • target cell dies by apoptosis
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16
Q

cell transformation

A

-changing of normal cell into cancer cell

17
Q

neoplasia

A

-descriptive term that denotes abnormal tissue overgrowth that may be either localized or disseminated, it is the process that leads to the formation of neoplasms (carcinogenesis )

18
Q

oncology

A

study of neoplasia and neoplasms

19
Q

benign neoplasm

A

growth produced by abnormal cell proliferation that remains localized and does not invade adjacent tissue

20
Q

malignant neoplasm (cancer)

A

locally invasive and may also be spread to other parts of the body (metastasis)

21
Q

oncogenic viruses

A

-cause or give rise to tumors

22
Q

metastasis

A

-spread of cancer cells from part of body where it started (primary site) to other parts of the body

23
Q

proto-oncogenes

A

encode proteins that function in normal cell growth and differentiation

24
Q

tumor suppression genes

A
  • Rb and p53

- plays a role in keeping cell division in check, encodes proteins that regulates and inhibits uncontrolled growth

25
Q

oncogenes

A

-mutated forms of proto-oncogenes or aberrantlye xpressed proto-oncogenes

26
Q

retinoblast protein (Rb)

A
  • important tumor suppressor gene/protein that blocks E2F and keeps cell division in check
  • E2F facilitates cell division
27
Q

p53 protein

A
  • important tumor supressor gene/protein that prevents cells with damaged DNA from entering cell division
  • tries to mediate repairing of damaged host cell DNA
  • if damaged DNA cannot be repaired, p53 mediates apoptosis of cell with damaged DNA
28
Q

tumor viruses/oncogenic viruses

A
  • cause cancer

- oncogenic viruses generally have DNA genome, or generate DNA provirus after infection (retrovirus)

29
Q

oncogenic DNA viruses

A
  • have viral oncogenes in the viral DNA (oncogenes are natural part of viral DNA)
  • oncogenes cause cancer in host cells, may also help in virus replication process
  • when oncogenic DNA viruses infect permissive cells, they can replicate successfully (no cancer)
  • when oncogenic DNA viruses infect non-permissive cells, they cannot replicated, viral DNA integrates into host DNA or may remain episomal (like plasmid) results in cancer
30
Q

productive infection in permissive cell

A
  • virus completes its replication cycle, resulting in cell lysis
  • no cancer
31
Q

non-productive infection in non-permissive cell

A
  • virus transforms cell without completing its replication cycle
  • cancer
  • viral genome, or truncated version of it is integrated into cellular DNA, alternatively the complete genome persists as an autonomously replicating plasmid (episome)
32
Q

actively transforming retrovirus

A

viruses steal proto-oncogene from infected host cell DNA, then converts proto-oncogene into oncogene

33
Q

slow/chronic transforming retrovirus

A
  • virus genome gets inserted into the regulatory (enhancer region) gene of host cell DNA
  • as result of this insertion, regulatory gene cannot function properly
  • no control on proto-oncogene of host DNA
  • excessive cell division/cancer
34
Q

tumor antigens

A

-new antigens appear on the surface of tumor cells that may provoke immune response

35
Q

expression of tumor antigens

A

FOCMA

virology (12 decks)

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