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INF: Infections > Block II: General > Flashcards

Block II: General Flashcards

(61 cards)

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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
proto-oncogene mutation (insertional mutagenesis) ## Footnote *(method of virus transforming cells)*
-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
what are the 2 components (+1 potential component) of all viruses?
1- genome 2- protein surrounding genome (capsid or nucleocapsid) SOME: -lipid membrane (envelope)/glycoproteins surrounding the capsid
27
protooncogene activation ## Footnote *(method of virus transforming cells))*
-transcriptional activation: viruses can encode proteins that are transcriptional activators
28
assembly of nonenveloped viruses
capsid is used to insert progeny genome, then mature virus is able to be assembled
29
what does one virus infecting one cell result in?
multiple virus progeny (100-10,000)
30
implications of different serotypes of a virus
- 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
live, attenuated virus vaccine
-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
examples of nonenveloped viruses
rotavirus adenovirus hepatitis A
33
tumor suppressor inactivation ## Footnote *(method of virus transforming cells)*
many viruses encode proteins that bind to & inactivate Rb and p53 (examples: adenovirus, EBV, papilloma virus, polyomavirus)
34
vector transmitted viruses
-viruses acquired from nonhuman sources Vectors: **arthropods:** trasnmit arboviruses (togavirsues, flaviviruses, reoviruses) **rodents:** transmit bynaviruses **small animals:** transmit rabies
35
transduction of an oncogene ## Footnote *(method of virus transforming cells)*
- retroviruses may encode oncogenes genetically related to host proto-oncogenes & deliver them directly into cells - currently no human example
36
transformation
-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
steps of replication of single stranded RNA viruses with positive polarity
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
effects of viral infection on cells
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
attachment of virus to cell
-VERY SPECIFIC interaction between VAP (virus attachment protein) and cell receptor
40
ways that virsues can transform cells
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
properties of transformed cells
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
how viruses spread systemically
- 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
VAP
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
recombinant-antigen expressed from cloned gene
purified protein **advantages:** safety **disadvantages:** responses are often weak & short lived; requires combination with an adjuvant
45
Classification of Influenza A viruses
-based on HA and Na (subtypes designated by which HA and NA are present) -each subtype contains antigenic variants or serotypes
46
Types of Vaccines
- inactivated virus - live, attenuated virus - subunit- purified virion component - recombinant-antigen expressed from cloned gene - virus-like particles (VLPs) - DNA vaccines
47
Steps of replication of double stranded DNA virus
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
DNA vaccine
currently none licensed -immune responses are often weak
49
genome types of viruses
**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
encounter of host cell by virus
- RANDOM - virus comes in contact with susceptible cell
51
steps of replication of single stranded RNA virus, negative polarity
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
how do neutralizing antibodies affect viruses?
they block attachment (ab binds to surface structure of virus, preventing it from binding cell receptor)
53
transformed cells (cancerous) may express tumor-associated antigens
-viral proteins are strong antigens
54
Antigenic Shift
(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
2 types of viral infections in animal
- localized: virus remains in original infected organ - sytemic: virus spreads to many organs
56
what is a virus?
obligate intracellular parasite (obligate intracellular: requires host metabolism to reproduce)
57
release of nonenveloped viruses
**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
ways that DNA viruses affect apoptosis/transformation
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
HPVs that are high risk
HPV16, 18,31, 45
60
subunit--purified virion component vaccine
**advantage:** safety **disadvantage:** responses are often weak & short lived; requires combination with adjuvant
61
assembly & release of enveloped viruses
- 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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