Virology Flashcards

0
Q

Underlying mechanisms for gender based differences in viral STIs

A
Societal rank
Behavior, sexual practices
Hormone regulation of immune system
Route of infection
Exposure dose
Anatomical differences
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1
Q

Classes of antivirals

A
Attachment - receptor analogue
Entry - 
Reverse transcription - NRTI/NNRTI
DNA replication - nucleoside analogues
Assembly/maturation - protease inhibitors 
Budding off - neuraminidase inhibitors
Other - interferons
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2
Q

Four characteristics to classify viruses

A

Nature of nucleic acid
Symmetry of capsid
Presence of envelope
Dimensions of viron and capsid

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3
Q

Cell functions required for viral propagation

A

Machinery for viral mRNA translation
Energy
Enzymes (replication, assembly)
Transport pathways

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4
Q

Eg of icosahedral virus

A

Adenovirus (no env)
Fandm virus (no env)
HSV

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5
Q

Eg of helical virus

A

Tobacco mosaic virus (no env)
Influenza A
Paramyxovirus

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6
Q

Properties of enveloped viruses

A
Sensitive to:
Heat 
Drying
Acid
Detergents
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7
Q

Non enveloped virus qualities

A
GIT
Fomites
Must kill cell for spread
Only numeral response needed
Infective on drying
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8
Q

Define emerging disease

A

New or reccurance of previously disappeared infection in humans

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9
Q

Modes of spread of zoonoses

A

Direct contact w infected animal
Vector
Asymptomatic animal reservoir eg. Excreta

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10
Q

Clinical syndromes seen in zoonoses

A
Fever and rash
Encephalitis
Viral haemorrhagic fever
ARS
Shock syndrome
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11
Q

Egs of vertebrate host zoonoses

A
Simian herpes virus B
Pox viruses (cow, monkey, orf)
Rabies
Henipavirus
Filoviridae (Marburg, Ebola)
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12
Q

Egs of arthropods

A

Mosquito
Tick
Sandfly

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13
Q

Egs of invertebrate zoonoses

A
Crimean Congo haemorrhagic fever
Yellow fever
Dengue fever
Rift Valley fever 
SARS 
MERS
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14
Q

Factors responsible for zoonoses becoming more common

A
Population density
Invasion of animal habitats
Global travel
Closer contact with reservoir
High density rearing for food
Climate change
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15
Q

Three aspects of host defense to virus

A
  1. Physical/chemical
  2. Intrinsic (cytokines, apoptosis, slow vira replication)
  3. Immunity
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16
Q

Effects of inflammation

A

Inc blood flow
Inc cap permeability
Inc phagocytotic cells
Tissue damage

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17
Q

Five mechanisms for viral evasion of host defenses

A
  1. Sanctuary sites (JC virus, measles)
  2. Latency
  3. Host derived genes modulate IR
  4. CTL evasion
  5. Antigenic variation through mutations
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18
Q

Methods for viruses to persist long term

A

Infect long lived cell
Immortalize cell
Integrate into genome

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19
Q

Factors looked at when assessing epidemiology of virus

A
Mode of transmission
Reservoir/ vector
Infectivity, pathogenicity, virulence
Subclinical disease
Susceptibility and immunogenicity
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20
Q

Ways to assess infectivity

A

Basic reproductive ratio

Attack rate (ill/exposed)

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21
Q

Determinates of infectivity

A

Route of transmission
Viral load
Duration of shed
Host susceptibility

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22
Q

Measure of pathogenicity

A

Illness rate (ill/infected)

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23
Q

Measure of virulence

A

Case fatality rate (deaths/total cases)

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24
Q

Factors that determine immunogenicity

A

Host immune response

Viral immune evasion

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25
Q

Why epidemiology seen as social science

A

Natural hx
Sexual pattern
Globalization

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26
Q

Why are there so few effective viral drugs

A
Intracellular
Need to be given early
Mutate quickly
Must be delivered to site of infection
No natural compound
Cost
27
Q

Levels of disease modification

A

Control
Elimination
Eradication

28
Q

Why surveillance NB

A

Planning
Evaluation
Implementing controls
Assessment

29
Q

Features of type ll epi

A
Stratified squamous (non keratinised)
IgG
No MALT
Langerhans cells
Epithelium make mucous
Sparse sentinel cells
30
Q

Why HPV induces poor immune response

A

Downregulate MHC l
Deplete Langerhans cells
Block type l interferon signaling

31
Q

Current drug being tested for HIV Rx

A

Truvada (tenofovir and emtricitabine)

32
Q

MOA of truvada

A

Nucleoside analogues A and C.

Cause chain termination and inhibit RT

33
Q

Possible reasons why studies show no effect of PrEP in woman

A
Poor adherence
Drug sharing
Poor vaginal []
High HIV [] in partner
STIs and co factors
Chance?
34
Q

Why PrEP not considered solution to HIV

A
Treatment for infected only at 50%
Acute infection = high viral load
Expensive
Dependent on no resistance
Adherence
35
Q

Challenges for HIV vaccine

A
Correlates of protection unknown
Short window to act
High viral diversity 
Hard to induce broad Ab 
No good animal models
Inc safety = dec immunogenicity
36
Q

Four stages of becoming an endogenous virus

A

Colonise
Amplify
Fixation or loss
Inactivation

37
Q

Biological and clinical significance of endogenous viruses

A
Placentation
Evolution
Protection against exogenous viruses
HIV control
Associated diseases (schizophrenia, MS, cancer, autoimmunity)
38
Q

Endogenous viruses associated with cancer

A

MLV - prostate

MMTV - breast

39
Q

Role of endo viruses in HIV

A

APOBEC3 inhibits HERV
HIV Vif block AB3
Therefore increasing HERV
Abs made against HERV also help to control HIV

40
Q

Define basic reproductive ratio

A

The number of secondary cases that will arise following the primary case if the pathogen is introduced into a susceptible population

41
Q

Determinants of susceptibility

A
  • host receptor
  • fitness if the virus in the new host
  • amount of virus exposed
  • immunity to the virus
42
Q

Define immunogenicity

A

Ability to illicit protective immune response

43
Q

Determinants of prevalence

A
  • infectivity
  • population immunity
  • duration if the infection
44
Q

Define an outbreak

A

The occurrence of cases of disease in excess of what would normally be expected in a defined community, geographical area or season

45
Q

General survival strategy of viruses

A
  • viruses package their genome inside a particle for transmission
  • the viral genome contains the info to initiate and complete an infectious cycle within a cell
  • all viral genomes are able to establish themselves in a host population to ensure viral survival
46
Q

Why few antiviral a available

A
  • intracellular
  • need to act fast
  • rapid emergence if drug resistance
  • drug must be delivered to site of disease
  • no natural one
  • need to be cost effective
47
Q

Why acyclovir works as an antiviral

A
  • has thymidine kinase activity
  • needs to be given in 72 hrs
  • drug resistance found in HIV patients on long term treatment
48
Q

Why was smallpox eradicate?

A
  • no secondary host
  • long incubation period
  • no persistent infection
  • low transmissibility
  • easily diagnosed
  • one stable serotypes
  • vaccine cheap
  • severe disease with high mortality
49
Q

Define surveillance e

A

Ongoing systematic collection and analysis of health data

50
Q

General pattern for virus growth

A
  • attachment
  • disassembly
  • replication
  • assembly
51
Q

Example of viral sexually transmitted infections

A

HIV
HPV
HSV
Hep b

52
Q

How HSV enters the cells

A

Multiple cell surface proteins

- heparan sulphate chains on cell surface proteoglycans

53
Q

Sources of IgA in vaginal lumen

A

Secreted from cervix and uterus

Para cellular diffusion

54
Q

Why is Ebola not burning out now

A
  • took too long to recognize
  • desperately poor
  • minimal infrastructure
  • uncooperative population
55
Q

Examples of persistent viruses

A
  • retroviruses
  • herpesviruses
  • polyomaviruses
56
Q

How do viruses avoid recognition

A
  • masking (altering RNA structure)
  • hiding dsRNA
  • block downstream signaling to prevent IFN release
57
Q

2 types of NK receptors

A
  • killer activating (look for self MHC and triggered. Y stress molecules)
  • inhibitory
58
Q

Why is the brain a good sanctuary site?

A
  • no dendritic cells
  • no de novo priming of T cells
  • absent MHC class 1
59
Q

Clinical features of PML

A
Neurocognitive decline
Visual loss
FNS
Chorea
Fatal in months
60
Q

Effects of persistent measles in the brain

A

Measles inclusion body encephalitis

Subacute sclerosing pan encephalitis

61
Q

How does measles replicate in the brain

A
  • partial replication
  • incomplete virus particles
  • spreads from cell to cell
  • fusion via neurokinin
62
Q

Proteins that block key antiviral defense pathways

A
  • interferon synthesis and pathways
  • apoptosis
  • antigen presentation pathway
  • mimic host cytokines/ cytokine receptors
63
Q

How many viral homologous of host proteins does hhv8 have?

A

14

64
Q

Key viral protein in kaposi’s

A

VGPCR (homologue of human IL-8R)

Oncogene that causes release of pro inflammatory and proangiogenic cytokines

65
Q

How does viruses evade ctls

A

Interfere with antigen presentation

  • MHC1 decreased
  • less visible to CTL
  • longer survival