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INF: Infections > Block II: General > Flashcards

Block II: General Flashcards

1
Q

inhibition of apoptosis

((method of virus transforming cells)

A

cells must choose between proliferation, quiescene or dapoptosis

(inactivation of Rb stimualtes cell growth; inactivation of p53 inhibits apoptosis)

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2
Q

examples of enveloped viruses

A

influenza

ebola

hepatitis B

vaccinia (small pox vaccine)

rabies

HIV

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3
Q

HPV and cervical carcinoma

A

HPV is necessary, but not sufficient, to cause cerviical carcinoma

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4
Q

3 types of influenza viruses

A

Influenza A: pandemics & epidemics

-broad hosts (humans, pigs, birds, seals0

INfluenza B: epidemics (no pandemics)

-human only host

Influenza C: endemics

-human only host

**classification based on NP and M1 proteins

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5
Q

viruses causing cancer..

A

cancer is not a goal but rather a mistake of viruses

(viruses can’t replicate in cancerous state so cancer is not a selective force for viruses)

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6
Q

important proteins in apoptosis & transformation

A

MYC: enfocred expression of myc induces apoptosis, providing p53 functoin is normal

(if p53 is lacking: myc –> transformation)

E2F: family of transcription factors acting on promoters of myc, thymidine kinase, DNA polyermase, DHF reductase

(released at R point in cell cycle –> DNA synthesis)

Rb: tumor suppressor protein that binds to E2F and sequesters it

(Rb-E2F –> Rb-P + E2F –> DNA synthesis)

*most solid tumors hav RB mutations

p53: tumor suppressor protein that can inhibit cell division or induce apoptosis (p53 activates a CDK inhibitor)

*most solid tumors have p53 mutations

BCL-2: overexpression of BCL-2 blocks apoptosis, allowing for transformation (overexpressed in B cell leukemia)

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7
Q

serotype definition

A

-serotype defined by neutralizing antibody

(all viruses inhibited by anti-A are the same serotype)

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8
Q

classification of influenza B viruses

A

no subtypes (all B viruses have the same HA and NA)

-BUT have many antigenic variants/serotypes

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9
Q

SRC

A

oncogene whos product regulates the focal adhesion kinase that regulates actin cables

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10
Q

virus-like particles (VLP) vaccine

A

noninfectious particles (no genome) but otherwise resemble virions

ex- HPV vaccine

advantages: VLPs are similar in size & shape of virus and present antigens in an array; antigenically like virus, ; do not require inactivation, do not containa genome (no danger of reversion or recombination)

disadvantages: immune responses may not be as durable as those stimulated by infectious virus

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11
Q

inactivated virus vaccine

A

-virulent virus is inactivated (formaldehyde) – virus is noninfectious

advantages: safe

disadvantages: immune responses can be weak; immunity short lived; potential for incomplete inactivation; portential for contaminating pathogens

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12
Q

Multistage Carcinogenesis

A

oncogenic conversion from initial stimulation to a metastasizing tumor

1- viral/chemical/irradiation-induced inititation event acting on host DNA & associated with oncogenes or proto-oncogenes

2-inactivation of tumor-suppressor genes

3- cell cycle promotion caused by chemical agents

4-immune selection (select for less immunogenic tumors)

5-generation of angiogenesis factors by the tumor to bring blood to large tumor masses

6-cell surface changes which promote metastasis

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13
Q

syncytia formation

A

-classic of paramyxoviruses (fusion of cells leading to large multinucleated cells)

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14
Q

Antigenic Drift

A

(occurs in both influenza A and B)

  • results in the emergence of new strains; results from random spontaneous mutation occurring within the influenza virus genome as ir replicates
  • mutations within the genes encoding HA and NA surface glycooproteins
  • (within epitopes, causing amino acid differences- need to occur in each of 5 sites)

**appear between pandemics; and cause of epidemics

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15
Q

mechanism of HPV-associated cervical carcinoma

A

-integration of HPV genome into host genome

(appears to be random & unintentional; ends up being terminal for virus)

-E2 gene is inactivated (normally functions to limit E6, E7 expression– so in cancers, E6 & E7 are highly expressed)

E6: binds to p53, promotes its degradation (prevent apoptosis)

E7: binds to Rb and releases E2F (stimulating cell cycle)

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16
Q

genetics involved in cancer

A
  • genetic predisposition to cancer (allelic variants)
  • acquisition of somatic mutations
  • epigenetics
  • virus
  • (1/5 cancers have viral contribution)*
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17
Q

epidemiology cycle of vector born viruses

A

sylvan cycle?

epidemiolody of arboviruses: mosquitos infected for life, bite a small brid/rodent, causing viremia, other mosquitos become infected from biting birds/rodents, then infect others & mammals (maintaining the virus in nature)

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18
Q

what is the target for antiviral influenza drugs?

A

NA

(zanamivir; oseltamivir; peramivir)

  • analogues of sialic acid
  • NA inhibitors block the release of virions
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19
Q

ways that human encounter viruses (transmission)

A
  • respiratory/salivary
  • fecal-oral
  • venereal (sexxually transmitted)
  • vector-mediated (biting arthropod)
  • vertebrate reservoir
  • vector-verebrate reservoir
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20
Q

Steps in infection of single cells

A

1-encounter (virus in proximitiy of susceptible cells)

2-attachment (virus binding to cell surface)

3-entry (insertion of viral genome into cell)

4-replication (synthesis of components of virions)

5-assembly (formation of progeny virions)

6-release (release of progeny virus from infected cells, resulting in spread of infection through an organ, host, or into the environment)

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21
Q

most common cancer-causing viruses

A

HPV, MCV, EBV HepB, HepC

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22
Q

3 forms of viral entry into cell

(viral genome ends up on interior of cell)

A

1- [enveloped] surface fusion: virus directly fused to cell membrane; viral membrane becomes contiguous with cell membran, allowing viral genome inside

2- [enveloped] receptor-mediated endocytosis: fusion in endosome: virion is taken in by endocytosis and membrane fusion event occurs between viral membrane & vesicle membrane

3-[nonenveloped] receptor-mediated endocytosis: lysis of endosome: virion taken in by endocytosis, then acidifies/lyses endosome

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23
Q
A
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24
Q

what shape do nonenveloped viruses usually have?

A

icosahedral

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25
Q

proto-oncogene mutation (insertional mutagenesis)

(method of virus transforming cells)

A

-retroviruses may integrate into the regulatory region or coding region of protooncogene & cause transcriptional activaiton or change the activity of the proto-oncogene encoded protein

(relevant to gene therapy trials)

26
Q

what are the 2 components (+1 potential component) of all viruses?

A

1- genome

2- protein surrounding genome (capsid or nucleocapsid)

SOME:

-lipid membrane (envelope)/glycoproteins surrounding the capsid

27
Q

protooncogene activation

(method of virus transforming cells))

A

-transcriptional activation: viruses can encode proteins that are transcriptional activators

28
Q

assembly of nonenveloped viruses

A

capsid is used to insert progeny genome, then mature virus is able to be assembled

29
Q

what does one virus infecting one cell result in?

A

multiple virus progeny (100-10,000)

30
Q

implications of different serotypes of a virus

A
  • significant variability of amino acids on the surfaces of virions
  • infection due to one serotype will not protect against subsequent infection with another serotype

(ex individuals may be infected with rhinovirus many times since there are multiple serotypes)

31
Q

live, attenuated virus vaccine

A

-live virus that is avirulent (through many passages/generation)

advantages: stimulates long-lived protective immune responses; stimulation of humoral and cellular immune responses

disadvantages: reversion to virulence (low frequency); disease in immunosuppressed individuals

32
Q

examples of nonenveloped viruses

A

rotavirus

adenovirus

hepatitis A

33
Q

tumor suppressor inactivation

(method of virus transforming cells)

A

many viruses encode proteins that bind to & inactivate Rb and p53

(examples: adenovirus, EBV, papilloma virus, polyomavirus)

34
Q

vector transmitted viruses

A

-viruses acquired from nonhuman sources

Vectors:

arthropods: trasnmit arboviruses (togavirsues, flaviviruses, reoviruses)

rodents: transmit bynaviruses

small animals: transmit rabies

35
Q

transduction of an oncogene

(method of virus transforming cells)

A
  • retroviruses may encode oncogenes genetically related to host proto-oncogenes & deliver them directly into cells
  • currently no human example
36
Q

transformation

A

-considered to be any part of the multistep process by which a normal cell becomes cancerous

DNA transforming viruses: adenovirus, hepadnavirus, herpes, polymomavirus, papillomavirus

Rna transforming viruses: retroviruses (reverse transcribe RNA to make DNA)

37
Q

steps of replication of single stranded RNA viruses with positive polarity

A

1-translation into polyprotein

2-proteolytic cleavage into viral proteins (one is likely a RNA dependent RNA polymerase)

3-polymerase copies positive strand (original) to make complementary negative strand

4-negative strand used as template to make more positive strands

–>translation, replication, amplification of virions

38
Q

effects of viral infection on cells

A

aka cytopathic effect (CPE)

1-none/subtle efects

2-cell death

-overwhelm cell metabolism; shut down translation/transcription; affect membranes; induce apoptosis

3-cell transformation

39
Q

attachment of virus to cell

A

-VERY SPECIFIC interaction between VAP (virus attachment protein) and cell receptor

40
Q

ways that virsues can transform cells

A

1-transduction of an oncogene

2-protooncogene mutation (to an oncogene; often RAS)

3-protooncogene activation (to oncogene)

4-tumor suppressor inactivation

5-inhibition of apoptosis

41
Q

properties of transformed cells

A

0unlimited life spans in cell cultures

  • decreased contact inhibition of movement, alignment, growth
  • grow on a confluent monolayer, piling up in transformed foci (clumps)
  • decreased anchorage dependence (grow in agarose)
  • cytoskeletal changes (fewer actin cables)
  • chromosomal alterations
  • different growth factor requirements (perhaps autocrine stimulation or mutation in growth factor pathway)
  • may be sensitivie to complete removal of growth factors and undergo apoptopsis instead of G0 in starvaition
42
Q

how viruses spread systemically

A
  • entry into cells of an organ
  • replication cycles in cells at point of entry
  • progeny virus drains to local lymph nodes

–> primary viremia

-replication of virus in susceptible organs

—>secondary viremia

-infection & damage to target organ (disease manifestation)

43
Q

VAP

A

virus attachment protein

  • protein of virus that interacts (specific interaction) with cell receptor so that the virus can attach
  • in non-enveloped virus: VAP is part of capsid
  • in enveloped virus: VAP is spike structure (glycoprotein) in envelope
44
Q

recombinant-antigen expressed from cloned gene

A

purified protein

advantages: safety

disadvantages: responses are often weak & short lived; requires combination with an adjuvant

45
Q

Classification of Influenza A viruses

A

-based on HA and Na

(subtypes designated by which HA and NA are present)

-each subtype contains antigenic variants or serotypes

46
Q

Types of Vaccines

A
  • inactivated virus
  • live, attenuated virus
  • subunit- purified virion component
  • recombinant-antigen expressed from cloned gene
  • virus-like particles (VLPs)
  • DNA vaccines
47
Q

Steps of replication of double stranded DNA virus

A

1-transcription to early mRNA

2-translated into early proteins

3-DNA replication

4-late mRNA

5-translated into late proteins –> assembly of viruses

(DNA –>mRNA –> replicaiton –> translation –> proteins–>virions)

48
Q

DNA vaccine

A

currently none licensed

-immune responses are often weak

49
Q

genome types of viruses

A

DNA genomes: double stranded or single stranded

RNA genomes:

  • single stranded- positive stranded (same as mRNA) or negative stranded (complementary to mRNA)
  • double stranded
  • may be segmented or nonsegmented*
50
Q

encounter of host cell by virus

A
  • RANDOM
  • virus comes in contact with susceptible cell
51
Q

steps of replication of single stranded RNA virus, negative polarity

A

1-RNA transcribed to mRNA

2-mRNA translated into proteins (one is RNA dependent RNA polymerase)

3-polymerase copies negative strand to make a positive strand

4-positive strand is template to make more negative strands

–>replication, tranlsation, amplification of virus

52
Q

how do neutralizing antibodies affect viruses?

A

they block attachment

(ab binds to surface structure of virus, preventing it from binding cell receptor)

53
Q

transformed cells (cancerous) may express tumor-associated antigens

A

-viral proteins are strong antigens

54
Q

Antigenic Shift

A

(occurs ONLY in influenza A virus)

-generates new pandemic straines

2 underlying mechanisms:

1-direct transfer of avian influenza A virus into humans

2-genetic reassortment of human & avian viruses within a co-infected host

55
Q

2 types of viral infections in animal

A
  • localized: virus remains in original infected organ
  • sytemic: virus spreads to many organs
56
Q

what is a virus?

A

obligate intracellular parasite

(obligate intracellular: requires host metabolism to reproduce)

57
Q

release of nonenveloped viruses

A

Principle pathway: progeny virions accumulate inside of cell, often killing cell, then the cell lyses to release to progeny to the environment

Newer pathway: virions assemble within autophagosomes (membrane fusion), using the autophagosomes for release

58
Q

ways that DNA viruses affect apoptosis/transformation

A

1-some can deliver, mutation or transactivate MYC-like oncogenes

2-some sequester Rb, allowing E2F to activate the cell cycle

3-many bind p53, preventing apoptosis

4-some induce or encode BCL-2-like proteins (preventing apoptosis)

59
Q

HPVs that are high risk

A

HPV16, 18,31, 45

60
Q

subunit–purified virion component vaccine

A

advantage: safety

disadvantage: responses are often weak & short lived; requires combination with adjuvant

61
Q

assembly & release of enveloped viruses

A
  • all component parts of virion are assembled/inserted on cell membrane
  • intact virus buds from cell membrane, releasing the virions

**this does not require cell death

INF: Infections (5 decks)

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