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Virology > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Sporadic

A

occasional cases

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2
Q

Endemic

A

Present in a community at all times but in relatively low frequency

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3
Q

Epidemic

A

Sudden severe outbreak in a region or group

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4
Q

Pandemic

A

Widespread epidemic affecting whole region, continent, world

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5
Q

Stages of transmission

A
  1. agent only in humans - no further transmission to humans
  2. Primary infection –> from animals
  3. limited outbreak –> few animals or few cycles humans
  4. long outbreak –> animals or many cycles humans
  5. exclusive human agent –> only from humans
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6
Q

Endemic diseases

A

Seasonality, ongoing activity
Reports in excess –> epidemic
Age incidence determined by immunity duration

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7
Q

Pandemic

A

Novelty, susceptibility (20-40 yrs old over represented), transmissibility

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8
Q

Epidemiologic modelling

A

Considers causal processes involved in infection & transmission, recognises interdependence of observations –> scenario analysis and prediction

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9
Q

SIR paradigm

A

Susceptible (number of people)–> infectious –> recovered

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10
Q

Host susceptibility

A

Age, immune status, underlying risk conditions, pregnancy, ethnicity - confounded by socioeconomic determinants

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11
Q

Virus determines natural history

A

Latency - can’t be quarantined, alter behaviour
Infectiousness - asymptomatic, duration, mode of transmission
Induction of immune response - temporary (strain specific) or permanent (strain transcending)

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12
Q

Population determinants of spread

A 
Birth rate
Household size & crowding - influenza in a house, people 4x more likely to catch influenza
Social and employment networks
Population density and connectedness
Population mobility
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13
Q

Environmental risk determinants

A

Seasonality
Sanitation
Proximity to vector and reservoir animal populations
Natural disasters

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14
Q

Syndromic surveillance

A 
Not constrained by individual disease diagnosis
Year on year comparison
Identification of unseasonal activity
Threshold detection algorithms
Need astute clinician detection
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15
Q

Non-pharmaceutical measures

A

Environmental & personal hygiene
Case and contact quarantine
PPE
Social distancing - school closure, banning of mass gatherings

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16
Q

Pharmaceutical measures

A

Vaccines and antivirals

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17
Q

Ebola

A

Incubation period: 2-21 days

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18
Q

Containment

A

Only feasible when low transmissibility, high visibility

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19
Q

Cancer initiation

A

Appears to be genetic alteration

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20
Q

3 classes of cancer-causing agents

A
  1. chemical carcinogens - ethidium bromide
  2. UV and ionising radiation - sun exposure, nuclear bombing
  3. viruses - induction of cancer does not benefit viruses
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21
Q

Tumour

A

Growth produced by abnormal cell proliferation, most benign - remain localised
Some malignant - invasive = cancer
Metastatic - spread by lymph or blood

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22
Q

Carcinoma

A

Tumour of epithelial origin

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23
Q

Sarcoma

A

Tumour of fibroblast

24
Q

Lymphoma

A

Solid- leukocyte

25
Q

Leukemia

A

Circulating cells

26
Q

Carcinogenesis

A

Multistage process by which cancer develops

27
Q

Cancers are clonal

A

Arise from single cell

Transformed

28
Q

Transformation

A

Introduction of inheritable changes in a cell –> change in growth phenotype and immortalization of cell line
~ first step of cancer in humans

29
Q

Transformed cells differ from normal cells

A
  1. lack contact inhibition of growth
  2. lack of dependence on exogenous growth factors
  3. Lack of anchorage dependence of some cell types
30
Q

Cell cycle

A

G1 - synthesis of proteins required for DNA synthesis, regulated by extracellular stimuli (mitogen, adhesion)
S: replication of DNA
G2: synthesis of proteins for daughter cells
M: cell division

31
Q

GO regulator

A

Growth factors, oncogenes, cyclins and CDKs

32
Q

STOP regulators

A

Tumour suppressor genes, CDK inhibitors

33
Q

Oncogenes

A

Genes encoding proteins that give GO signal = proto-oncogenes = cellular oncogens = c-onc

34
Q

V-onc

A

Virus version of oncogene

35
Q

Tumour suppressor gene

A

Cellular genes encoding proteins that negatively regulate cell cycle e.g. p53 and Rb

36
Q

4 classes of oncogenes

A
  1. growth factors
  2. growth factor receptors
  3. intracellular signal transducers
  4. transcription factors
37
Q

____% of human cancers associated with 1 of 5 viruses

A

20%

38
Q

RNA viruses

A

Human T cell leukemia virus

Hep C

39
Q

DNA viruses

A

Papilloma, Epstein Barr, Hep B

40
Q

Retroviruses (RNA tumour) vs DNA tumour virus

A

RNA:

  • not lytic, integration essential
  • If v-onc involved is not unique –> c-onc counterpart
  • Transformation involves stimulating c-onc

DNA:

  • Can be lytic, integration not essential
  • V-onc unique viral product, no c-onc
  • Transformation involves inactivation of inhibitors
41
Q

Endogenous retrovirus

A

Integrated provirus
Transmitted in germline to every cell
In response to certain stimuli –> virus produced

42
Q

Exogenous retrovirus

A

Typical infectious virus

43
Q

Defective virus

A

Needs helper virus to produce progeny (coinfection with virus that has missing part)
Carries oncogene instead of gag, pol, env

44
Q

Replication competent

A

e.g. Rous sarcoma virus
Hasn’t swapped gene for retroviral genes, but in addition
- gag, pol, env + SRC

45
Q

Mechanisms of tumour production by exogenous retroviruses

A
  1. transducing
  2. cis-activating
  3. trans-activating
46
Q

Transducing

A

Acute transforming e.g. Rous sarcoma in chickens
Introduce v-onc under LTR transcriptional control into host genome
Doesn’t need helper virus
Never isolated from humans
Tumours can be polyclonal - infecting different cells and introducing its v-onc

47
Q

Cis-acting

A

Non-acute transforming retorviruses
No v-onc, but LTR drives expression of c-onc (insertional mutagenesis)
1. Longer message that includes cellular oncogene (constantly read off)
2. Provirus incorporated more distantly but acts to unwind DNA (enhancer) at proto-oncogene –> normal transcript read off

Not seen in humans
E.g. Koala retrovirus

48
Q

Trans-activating retrovirus

A

HTLV-1
exogenous containing gene regulation protein
Asociated with adult T cell leukemia-lymphoma
Prevalent in Japan, Caribbean, central Africa , (Indigenous Australians - no link to cancer)
Can be transmitted across placenta, sexually transmitted, needles
Persists for life
Target CD4 receptor
Tax - acts on LTR, upregulate gag, pol rev and acts on c-onc genes, acts on IL2 (T cell growth factor) and its receptor –> T cell proliferation

49
Q

Overexpression of Tax

A

–> expression on MHC I –> killed by CD8

Levels downregulated by HBZ protein

50
Q

Tumour induction by DNA viruses

A

Most undergo lytic growth
Require host enzymes to replicate DNA
Escape cell cycle: encode early proteins that stimulate cells to enter S phase
Tumours: early genes mostly, show integration

51
Q

Rb protein

A

Controls transition from G1 –>S, hypophosphorylated form associated with E2F family of transcription factors, sequestering them –> break in cell cycle

52
Q

p53

A

Transcription factor –> arrest growth of cell and initiate response to DNA damage
50% cancers have mutations of p53

Hep C binds p53 –> p53 can’t bind DNA –> replication

Papilloma protein –> degrades p53 –> replication

53
Q

Papillomavirus

A

Epithelial layers
Benign skin tumours - can spontaneously clear, HPV genome kept as episome
HPV 16 & 18 –> cervical carcinoma, most common women cancer in developing world
E6 and E7 interacts with p53 and pRb
In malignant cells: HPV randomly integrated
Loss of E2 during integration –> not able to repress transcription of E6 and E7

54
Q

Hep B virus genome

A

Most integrated genomes retain X and its promoter
X encodes transactivating gene which may deregulate nearby c-onc
Indirect role: destruction and regeneration of cells lead to accumulation of chromosomal mutations

55
Q

Epstein-Barr virus

A

Herpes - most strongly associated with cancer
Burkitt’s lymphoma
Nasopharyngeal cancer
B cell lymphomas in immune suppressed
Hodgkins (EBV detected in 40% of patients)

56
Q

Burkitt’s lymphoma

A

Transforms B cells –> clonal expansion
Malaria furhter expand B cells and decrease T cells
Enhances chances of genetic accidents –> chromosomal translocation of c-myc
Chromosome break: c-myc becomes under control of heavy chain enhancer region –> produces c-myc instead of Ig heavy chain
c-myc encodes transcription factor –> GO signal

Virology (9 decks)

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