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Respiratory Pharmacology > L7 - acute viral respiratory infections > Flashcards

L7 - acute viral respiratory infections Flashcards

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
Q

Formalin-inactivated vaccine candidate

A

no protection with higher viral load and 16 fold increase in hospitalisations
2 infant fatalities

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26
Q

Anti-RSV F protein MAB

A

Palizumab

monthly injections successful in high risk infants

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27
Q

Liv RSV mechanism

A

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
Q

Formalin-inactivated RSV mechanism

A

No RSV replication, limited TF activation os no antibody affinity maturation
no RIG-I and MDA-5 involvement

29
Q

RSV in wheezing/asthma conception

A

severe RSV infection in infancy is a firmly established risk factor for subsequent asthma in later childhood

30
Q

Underlying biological mechanisms in RSV and asthma

A

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
Q

Infant immune modulation

A

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
Q

TLR4 mutations in infants hospitalised for RSV bronchiolitis

A

ASP299Gly and Thr399Ile

33
Q

TLR4 mutation mechanism

A

failure to translocate TLR4 to cell surface resulting in reduced NFKB signalling

34
Q

RSV

A

more inducer than trigger

35
Q

RSV in infants and young children

A

extensive damage to airways leading to long-lasting bronchial hyperreactivity

36
Q

HRV

A

more trigger than inducer

37
Q

HRV in infants and young children

A

atopy as facilitator and recurrent infections, leading to pro-inflammatory cell activation and limited damage

38
Q

Human Rhinovirus

A

most common cause of upper RTIs

39
Q

HRV causes…

A

exacerbations of chronic pulmonary diseases, asthma development, severe bronchiolitis in infants and children, fatal pneumonia in elderly and immunocompromised

40
Q

HRVs cause a…

A

self-limiting syndrome with predominantly upper RTI manifestations in healthy adults

41
Q

airway epithelial cells

A

respiratory viruses enter and replicate within them, HRV infect nasal epithelial cells but also detected in lower airways

42
Q

cytopathology of AECs

A

AECs sloughed but airway lining remains structurally intact, disruption to barrier function by dissociation of zone occludens 1 from tight junction complex

43
Q

Macrophages and HRV

A

predominant lymphocyte in airways, release chemicals to result phagocytosis and modulating immune response

44
Q

HRV prevent macrophages by…

A

inhibiting antigen presentation, T cell activation and B cell antibody production

45
Q

Neutrophils in HRV

A

recruited in response to IL-8/CXCL8

levels in nasal lavage fluid correlate with symptom severity

46
Q

Neutrophils release….

A

TNFa and produce elastase

47
Q

Eosinophils

A

recruited in response to RANTES/CCL5 with unclear role

48
Q

T cell responses

A

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
Q

B cell responses

A

mucosal IgA, then IgM and finally IgG

50
Q

B cep reformed neutralising IgG

A

prevents/limits extent of reinfection, elevated serum titers of serotype-specific IgG neutralising antibody correlate with attenuated cold symptoms and reduced viral shedding

51
Q

rhinovirus infection in those with allergic rhinitis

A

induces rapid increase in serum IgE without evidence of elevation in antigen-specific IgE

52
Q

Bradykinin

A

in nasal lavage

53
Q

vascular permeability

A

neutrophil inflex

54
Q

Histamine

A

unchanged, as no role for mast cells or basophils

55
Q

viral-induced acute exacerbations

A

further increase in airway inflammation

major cause of morbidity, mortality and accelerates disease progression

56
Q

HRV triggers…

A

50-85% cause of exacerbations in patients with underlying airway disease

57
Q

experimental HRV infection studies

A

viral loads higher in asthma and COPD patients than in healthy controls

58
Q

interferons

A

block viral entry, control viral transcription and translation, cleavage of RNA and induction of apoptosis

59
Q

failure to induce robust IFN response in HRV-induced exacerbations

A

uncontrolled viral replication and increased inflammatory responses –> possible mechanism

60
Q

Frequent exacerbators

A

more susceptible to viral infection and/or more severe clinical disease after infection

61
Q

Asthma and exacerbations

A

deficient IFN production, decreased antiviral Th1 cytokines, increased SOCS1 may link Th2 inflammation with IFN deficiency, increased ICAM-1 expression

62
Q

COPD and exacerbations

A

deficient IFN production and increased ICAM-1 expression

63
Q

Acute exacerbation mechanism

A

inadequate IFN response –> increased viral replication –> cell necrosis, release of virus and pro inflammatory mediators –> airway inflammation –> acute exacerbation

64
Q

Allergic sensitisation in HRV infection severity

A

Il-4 and IL-13 production
increased ICAM-1 expression by BEC
Increased BEC infection by HRV
increased HRV infection severity

65
Q

Th2 bias in HRV infection severity

A

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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