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Respiratory Pharmacology > L7 - acute viral respiratory infections > Flashcards

L7 - acute viral respiratory infections Flashcards

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1
Q

Respiratory tract infections

A

infection of nasal cavities, pharynx or airways

usually viruses over bacteria

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2
Q

Upper RTIs

A

affect nasal cavities and pharynx

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3
Q

Lower RTIs

A

affect airways

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4
Q

upper RTI examples

A

nasopharyngitis, pharyngitis, sinusitis, laryngitis and influenza

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5
Q

Lower RTI examples

A

influenza, bronchitis, bronchiolitis, pneumonia and tuberculosis

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6
Q

RTI diagnosis

A

hemagglutination, blood typing, antibody structure and production, nucleic acid hybridisation, immunoassays, PCR, virus microarrays, qRT-PCR, HTS, VirCapSeq

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7
Q

Respiratory Syncytial Virus

A

major cause of lower RTIs and hospital visits for severe bronchitis during infancy and childhood

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8
Q

?% of infants infected during their first RSV season

A

60%

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9
Q

Respiratory syncytial virus in children

A

nearly all children will have been infected with the virus by 2-3 years old
induces protective immunity which wanes over time therefore people can be infected multiple times

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10
Q

RSV virology

A

enveloped negative sense ssRNA virus of the Paramyxoviridae family

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11
Q

G-protein

A

attachment protein, attaches to Annexin II on airway epithelial cells or L-selectin and CXCR1 on immune cells

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12
Q

TLR4

A

detects fusion protein

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13
Q

TLR3

A

detects dsRNA replication

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14
Q

TLR7

A

detects ssRNA

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15
Q

TLR2/6

A

unknown what it detects

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16
Q

RIG-I

A

detects ssRNA viral genomes bearing 5’-triphosphate, dsRNA

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17
Q

Nod2

A

detects ssRNA

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18
Q

NLRSP/ASC

A

detects small hydrophobic RSV viroporin

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19
Q

RSV prevents an effective host immune response…

A
  1. Non-structural bind RIG-I to prevent signalling
  2. Non-structural proteins bind to IRF3/7 which prevents target binding to the nucleus to produce type I IFNs
  3. Non-structural proteins bind to STAT1 and cause it to degrade, preventing target binding so ISGs are not produced
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20
Q

G protein binds…

A

dendritic and T cells to prevent their activation

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21
Q

RSV disease features

A

cytopathic effect of virus and local inflammatory response

airway epithelial cells highly pervasive to RSV

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22
Q

RSV replication causes…

A

epithelial damage and therefore necrosis

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23
Q

RSV symptoms

A

recruitment of neutrophils and lymphocytes

submucosal oedema, mucus secretion, bronchoconstiction

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24
Q

RSV results in…

A

severe obstruction of airway lumen

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25
Formalin-inactivated vaccine candidate
no protection with higher viral load and 16 fold increase in hospitalisations 2 infant fatalities
26
Anti-RSV F protein MAB
Palizumab | monthly injections successful in high risk infants
27
Liv RSV mechanism
dsRNA leads to RSV replication, enters endosome TLR7 to form RSV ssRNA RIG-I and MDA-5 involved results in TF activation with antibody affinity maturation
28
Formalin-inactivated RSV mechanism
No RSV replication, limited TF activation os no antibody affinity maturation no RIG-I and MDA-5 involvement
29
RSV in wheezing/asthma conception
severe RSV infection in infancy is a firmly established risk factor for subsequent asthma in later childhood
30
Underlying biological mechanisms in RSV and asthma
Chronic epithelial and airway reactivity changes to developing infant lung lung injury altering lung function immunomodulatory changes genetic factors that impact patterns of immune response to infectious agents
31
Infant immune modulation
severe RSV bronchiolitis alters subsequent Th1/2 immune response associated with Th2 polarisation of the lung immune resposnse enhances Th2 sensitisation to aeroallergens and induces development of a chronic asthma phenotypes
32
TLR4 mutations in infants hospitalised for RSV bronchiolitis
ASP299Gly and Thr399Ile
33
TLR4 mutation mechanism
failure to translocate TLR4 to cell surface resulting in reduced NFKB signalling
34
RSV
more inducer than trigger
35
RSV in infants and young children
extensive damage to airways leading to long-lasting bronchial hyperreactivity
36
HRV
more trigger than inducer
37
HRV in infants and young children
atopy as facilitator and recurrent infections, leading to pro-inflammatory cell activation and limited damage
38
Human Rhinovirus
most common cause of upper RTIs
39
HRV causes...
exacerbations of chronic pulmonary diseases, asthma development, severe bronchiolitis in infants and children, fatal pneumonia in elderly and immunocompromised
40
HRVs cause a...
self-limiting syndrome with predominantly upper RTI manifestations in healthy adults
41
airway epithelial cells
respiratory viruses enter and replicate within them, HRV infect nasal epithelial cells but also detected in lower airways
42
cytopathology of AECs
AECs sloughed but airway lining remains structurally intact, disruption to barrier function by dissociation of zone occludens 1 from tight junction complex
43
Macrophages and HRV
predominant lymphocyte in airways, release chemicals to result phagocytosis and modulating immune response
44
HRV prevent macrophages by...
inhibiting antigen presentation, T cell activation and B cell antibody production
45
Neutrophils in HRV
recruited in response to IL-8/CXCL8 | levels in nasal lavage fluid correlate with symptom severity
46
Neutrophils release....
TNFa and produce elastase
47
Eosinophils
recruited in response to RANTES/CCL5 with unclear role
48
T cell responses
recruited in response to RANTES/CCL5 and IP-10/CXCL10 T cells present in nasal lavage and airway epithelium trigger cytotoxic and AB-mediated immune response - Th1 cytokines
49
B cell responses
mucosal IgA, then IgM and finally IgG
50
B cep reformed neutralising IgG
prevents/limits extent of reinfection, elevated serum titers of serotype-specific IgG neutralising antibody correlate with attenuated cold symptoms and reduced viral shedding
51
rhinovirus infection in those with allergic rhinitis
induces rapid increase in serum IgE without evidence of elevation in antigen-specific IgE
52
Bradykinin
in nasal lavage
53
vascular permeability
neutrophil inflex
54
Histamine
unchanged, as no role for mast cells or basophils
55
viral-induced acute exacerbations
further increase in airway inflammation | major cause of morbidity, mortality and accelerates disease progression
56
HRV triggers...
50-85% cause of exacerbations in patients with underlying airway disease
57
experimental HRV infection studies
viral loads higher in asthma and COPD patients than in healthy controls
58
interferons
block viral entry, control viral transcription and translation, cleavage of RNA and induction of apoptosis
59
failure to induce robust IFN response in HRV-induced exacerbations
uncontrolled viral replication and increased inflammatory responses --> possible mechanism
60
Frequent exacerbators
more susceptible to viral infection and/or more severe clinical disease after infection
61
Asthma and exacerbations
deficient IFN production, decreased antiviral Th1 cytokines, increased SOCS1 may link Th2 inflammation with IFN deficiency, increased ICAM-1 expression
62
COPD and exacerbations
deficient IFN production and increased ICAM-1 expression
63
Acute exacerbation mechanism
inadequate IFN response --> increased viral replication --> cell necrosis, release of virus and pro inflammatory mediators --> airway inflammation --> acute exacerbation
64
Allergic sensitisation in HRV infection severity
Il-4 and IL-13 production increased ICAM-1 expression by BEC Increased BEC infection by HRV increased HRV infection severity
65
Th2 bias in HRV infection severity
deficient HRV-induced IFNS and IL-12 production impaired infected BEC apoptosis and killing increased virus replication increased HRV infection severity

Respiratory Pharmacology (17 decks)

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