Virology Flashcards
(66 cards)
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
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
2
Q
Four characteristics to classify viruses
A
Nature of nucleic acid
Symmetry of capsid
Presence of envelope
Dimensions of viron and capsid
3
Q
Cell functions required for viral propagation
A
Machinery for viral mRNA translation
Energy
Enzymes (replication, assembly)
Transport pathways
4
Q
Eg of icosahedral virus
A
Adenovirus (no env)
Fandm virus (no env)
HSV
5
Q
Eg of helical virus
A
Tobacco mosaic virus (no env)
Influenza A
Paramyxovirus
6
Q
Properties of enveloped viruses
A
Sensitive to: Heat Drying Acid Detergents
7
Q
Non enveloped virus qualities
A
GIT Fomites Must kill cell for spread Only numeral response needed Infective on drying
8
Q
Define emerging disease
A
New or reccurance of previously disappeared infection in humans
9
Q
Modes of spread of zoonoses
A
Direct contact w infected animal
Vector
Asymptomatic animal reservoir eg. Excreta
10
Q
Clinical syndromes seen in zoonoses
A
Fever and rash Encephalitis Viral haemorrhagic fever ARS Shock syndrome
11
Q
Egs of vertebrate host zoonoses
A
Simian herpes virus B Pox viruses (cow, monkey, orf) Rabies Henipavirus Filoviridae (Marburg, Ebola)
12
Q
Egs of arthropods
A
Mosquito
Tick
Sandfly
13
Q
Egs of invertebrate zoonoses
A
Crimean Congo haemorrhagic fever Yellow fever Dengue fever Rift Valley fever SARS MERS
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
15
Q
Three aspects of host defense to virus
A
- Physical/chemical
- Intrinsic (cytokines, apoptosis, slow vira replication)
- Immunity
16
Q
Effects of inflammation
A
Inc blood flow
Inc cap permeability
Inc phagocytotic cells
Tissue damage
17
Q
Five mechanisms for viral evasion of host defenses
A
- Sanctuary sites (JC virus, measles)
- Latency
- Host derived genes modulate IR
- CTL evasion
- Antigenic variation through mutations
18
Q
Methods for viruses to persist long term
A
Infect long lived cell
Immortalize cell
Integrate into genome
19
Q
Factors looked at when assessing epidemiology of virus
A
Mode of transmission Reservoir/ vector Infectivity, pathogenicity, virulence Subclinical disease Susceptibility and immunogenicity
20
Q
Ways to assess infectivity
A
Basic reproductive ratio
Attack rate (ill/exposed)
21
Q
Determinates of infectivity
A
Route of transmission
Viral load
Duration of shed
Host susceptibility
22
Q
Measure of pathogenicity
A
Illness rate (ill/infected)
23
Q
Measure of virulence
A
Case fatality rate (deaths/total cases)
24
Factors that determine immunogenicity
Host immune response
| Viral immune evasion
25
Why epidemiology seen as social science
Natural hx
Sexual pattern
Globalization
26
Why are there so few effective viral drugs
```
Intracellular
Need to be given early
Mutate quickly
Must be delivered to site of infection
No natural compound
Cost
```
27
Levels of disease modification
Control
Elimination
Eradication
28
Why surveillance NB
Planning
Evaluation
Implementing controls
Assessment
29
Features of type ll epi
```
Stratified squamous (non keratinised)
IgG
No MALT
Langerhans cells
Epithelium make mucous
Sparse sentinel cells
```
30
Why HPV induces poor immune response
Downregulate MHC l
Deplete Langerhans cells
Block type l interferon signaling
31
Current drug being tested for HIV Rx
Truvada (tenofovir and emtricitabine)
32
MOA of truvada
Nucleoside analogues A and C.
Cause chain termination and inhibit RT
33
Possible reasons why studies show no effect of PrEP in woman
```
Poor adherence
Drug sharing
Poor vaginal []
High HIV [] in partner
STIs and co factors
Chance?
```
34
Why PrEP not considered solution to HIV
```
Treatment for infected only at 50%
Acute infection = high viral load
Expensive
Dependent on no resistance
Adherence
```
35
Challenges for HIV vaccine
```
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
Four stages of becoming an endogenous virus
Colonise
Amplify
Fixation or loss
Inactivation
37
Biological and clinical significance of endogenous viruses
```
Placentation
Evolution
Protection against exogenous viruses
HIV control
Associated diseases (schizophrenia, MS, cancer, autoimmunity)
```
38
Endogenous viruses associated with cancer
MLV - prostate
| MMTV - breast
39
Role of endo viruses in HIV
APOBEC3 inhibits HERV
HIV Vif block AB3
Therefore increasing HERV
Abs made against HERV also help to control HIV
40
Define basic reproductive ratio
The number of secondary cases that will arise following the primary case if the pathogen is introduced into a susceptible population
41
Determinants of susceptibility
- host receptor
- fitness if the virus in the new host
- amount of virus exposed
- immunity to the virus
42
Define immunogenicity
Ability to illicit protective immune response
43
Determinants of prevalence
- infectivity
- population immunity
- duration if the infection
44
Define an outbreak
The occurrence of cases of disease in excess of what would normally be expected in a defined community, geographical area or season
45
General survival strategy of viruses
- 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
Why few antiviral a available
- 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
Why acyclovir works as an antiviral
- has thymidine kinase activity
- needs to be given in 72 hrs
- drug resistance found in HIV patients on long term treatment
48
Why was smallpox eradicate?
- no secondary host
- long incubation period
- no persistent infection
- low transmissibility
- easily diagnosed
- one stable serotypes
- vaccine cheap
- severe disease with high mortality
49
Define surveillance e
Ongoing systematic collection and analysis of health data
50
General pattern for virus growth
- attachment
- disassembly
- replication
- assembly
51
Example of viral sexually transmitted infections
HIV
HPV
HSV
Hep b
52
How HSV enters the cells
Multiple cell surface proteins
| - heparan sulphate chains on cell surface proteoglycans
53
Sources of IgA in vaginal lumen
Secreted from cervix and uterus
| Para cellular diffusion
54
Why is Ebola not burning out now
- took too long to recognize
- desperately poor
- minimal infrastructure
- uncooperative population
55
Examples of persistent viruses
- retroviruses
- herpesviruses
- polyomaviruses
56
How do viruses avoid recognition
- masking (altering RNA structure)
- hiding dsRNA
- block downstream signaling to prevent IFN release
57
2 types of NK receptors
- killer activating (look for self MHC and triggered. Y stress molecules)
- inhibitory
58
Why is the brain a good sanctuary site?
- no dendritic cells
- no de novo priming of T cells
- absent MHC class 1
59
Clinical features of PML
```
Neurocognitive decline
Visual loss
FNS
Chorea
Fatal in months
```
60
Effects of persistent measles in the brain
Measles inclusion body encephalitis
| Subacute sclerosing pan encephalitis
61
How does measles replicate in the brain
- partial replication
- incomplete virus particles
- spreads from cell to cell
- fusion via neurokinin
62
Proteins that block key antiviral defense pathways
- interferon synthesis and pathways
- apoptosis
- antigen presentation pathway
- mimic host cytokines/ cytokine receptors
63
How many viral homologous of host proteins does hhv8 have?
14
64
Key viral protein in kaposi's
VGPCR (homologue of human IL-8R)
| Oncogene that causes release of pro inflammatory and proangiogenic cytokines
65
How does viruses evade ctls
Interfere with antigen presentation
- MHC1 decreased
- less visible to CTL
- longer survival
