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Virology Final > Respiratory Infections > Flashcards

Respiratory Infections Flashcards

1
Q

Upper Respiratory Tract (URT)

A

-everything above the larynx

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2
Q

Lower Respiratory Tract (LRT)

A
  • site of bronchitis, bronchiolitis, pneumonia

- everything below the larynx

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3
Q

Common Pathogens of the nasopharynx

A
  • rhinovirus

- coronavirus (except SARS)

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4
Q

Oropharynx

A
  • adeno

- EBV-not a typical respiratory virus but is transmitted by respiratory/oral contact route

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5
Q

Larynx-trachea

A

parainfluenzaviruses

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6
Q

Bronchi

A

-influenzaviruses

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7
Q

Bronchioles

A

-respiratory syncytial viruses (RSV), SARS

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8
Q

alveoli

A

-influenza, parainfluenza, RSV, SARS

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9
Q

LRT pathogens

A

2 major virus families-orthomyxo and paramyxo
Orthomyxo-segmented, H+N surface glycoproteins
paramyxo-HN+F (G+F for RSV)

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10
Q

Antigenic Shift

A
  • reassortment of genome segments

- primarily bird viruses, humans are accidental host

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11
Q

Major Flu pandemics

A 
H1N1-spanish flu: 1918, severe
H2N2-asian flu: 1957, severe
H3N2-hong kong flu: 1968, moderate 
H5N1-hong kong, 1997
H1N1-mexico swine flu, 2009
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12
Q

Antigenic Drift

A

-random mutations affecting antigenicity

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13
Q

Pigs as carrier of flu

A
  • pigs are hosts to both human and avian strains of flu
  • pigs come in contact w/ birds and humans
  • reservoirs for different strains of flu
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14
Q

Influenza Virus Evolution

A
  • H1N1 (spanish)-arose directly from birds
  • H2N2 (asian-1957)-3 of the RNAs derived from new source, antigenic shift
  • H3N2-(hong kong-1968)-PB1, HA derived from new source
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15
Q

Avian Influenza Virus

A

1997-H5N1 strain: found in poultry markets and spread to small numbers of humans w/ high mortality
2007-outbreak from southeast asia westward, virus is endemic in birds
H5N1 transmitted inefficiently from birds to humans

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16
Q

Human and avian influenza virus

A

flu virus receptors are glycoproteins containing sialic acid

  • human flu virus prefer alpha-2,6 gal linkages b/w sialic acid and galactose
  • avian flu viruses prefer alpha-2,3 gal linkages
  • humans possess alpha 2,6 gal in URT, but alpha 2,3 gal in alveoli
  • 10 consistent aa’s implicated in differentiating birds and humans (none in H)
  • fear that new mutations will lead to increased virulence in humans
  • all H5N1 isolates show no more than 1 of these 10 mutations
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17
Q

H1N1 2009 swine flu

A
  • origin in mexico, rapid spread worldwide
  • despite initial rapid spread and virulence, the global epidemic was not severe:
  • vigilant screening
  • voluntary crowd avoidance, quarantines
  • immunization programs
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18
Q

Factors in influenza pathogenesis (4)

A
  • receptor binding (HA and sialic acid)
  • HA proteolytic cleavage
  • virulence/host range aa determinants (esp. HA, PA, PB1, PB2 genes)
  • cytokine storm
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19
Q

HA proteolytic cleavage in flu pathogenesis

A

-cleavage of HA0 to HA1 and HA2 by host protease to activate virus mediated cell fusion
LPA1 (low pathogenic influenza)-proteases localized in respiratory and intestinal organs
HPA1-ubiquitous proteases

20
Q

Cytokine Storm

A
  • potentially fatal immune rxn involving a positive feedback loop b/w cytokines and immune cells
  • highly pathogenic strains trigger higher levels of pro inflammatory cytokines than less pathogenic strains
  • TNF-alpha
  • CCL5 (RANTES)
  • CCL3
  • CCL4
  • CCL2 (MCP-1)
21
Q

Influenza Vaccines (6)

A
  • succesful, formalin inactivated, fertilized egg grown virus trivalent vaccine (A/california/7/2009 H1N1, A/perth/16/ 2009 H3N2, B/Brisbane/60/2008)
  • successful H1N1 immunization program in Canada in 2009
  • live attenuated (nasal) available as of 2003
  • constant surveillance required to detect new strains
  • depends on good growth new strains in embryonated eggs
  • worldwide production-just a few companies in a few countries
22
Q

Immune Modulation of flu

A
  • NS1 (segment 8) has immunomodulatory activities

- antagonism of host immune response

23
Q

Paramyxo Viruses-2 groups

A
  • parainfluenza

- RSV

24
Q

Parainfleunzaviruses (types 1-4)

A
  • types 1-3 major cause of croup (infection of larynx and upper trachea)
  • type 3 assoc. w/ pneumonia and bronchitis
  • type 4 mild upper RT infections
25
Q

Paramyxo C and V proteins in suppression of IFN signalling

A
  • paramyxoviral genome gives rise to multiple mRNAs, one of which is the C/P/V mRNA
  • polycistronic, leaky scanning, atypical mechanisms to access C and V genes
26
Q

Viral Suppression of IFN-activated signalling

A

C, V inhibits Jak-1/Tyk-2
C, V, P (Rabies), VP24 (Ebola) inhibits STAT-1-2
-pathway involved in antiviral response

27
Q

Respiratory Syncytial Virus (RSV) (7)

A
  • most children by age 2 yrs have been infected w/ RSV
  • major LRT pathogen in infants, children, elderly and immunocompromised
  • generally mild cold like symptoms in adults
  • A and B subgroups (differ mostly in G protein)
  • A subgroup more severe
  • envelope glycoproteins F and G induce neutralizing Ab’s
  • occurs every year like flu, never completely protected even though infected over and over again
28
Q

RSV Envelope Spikes (3)

A 
G
-attachment 
-neutralization and protective antigen
-antibody decoy (secreted G)
-fractalkine mimic 
-TLR agonist 
F
-fusion and entry
-neutralization and protective antigen
-TLR4 agonist 
SH
-putative viroporin
-inhibits apoptosis
29
Q

RSV Nucleocapsid-associated proteins (4)

A

N-RNA-binding
P-phosphorylation
L-polymerase
-M2-1-Tc processivity factor

30
Q

RSV Inner Envelope Face proteins (1)

A

M-assembly

31
Q

RSV Regulatory Protein

A

M2-2

  • decreases viral Tc
  • increases RNA rep.
32
Q

RSV Non-structural Protein

A

NS1 and NS2

  • inhibit type 1 IFN induction
  • inhibit type 1 IFN signalling
  • activate P13K and NF-kappaB
  • inhibit apoptosis
  • at 3’ end of genomic RNA
33
Q

The search for a safe and effective RSV vaccine

A
  • formalin killed vaccine
  • non protective and worsened the disease
  • lung inflammation of neutrophils and eosinophils
  • induced non-neutralizing antibodies
  • mouse studies show formalin killed RSV vaccine and RSV G protein primes harmful Th2 response w/ eosinophil recruitment
  • use subunit (F or G protein) or DNA vaccines
  • aim to stimulate Th1 but not Th2 response
34
Q

Immune Evasive Mechanisms Used by RSV (5)

A
  • interference w/ type I IFN signalling (NS1/2 proteins degrade STAT2, block Tc activation)
  • interference w/ TNF signalling (SH protein)
  • tilting Th1/Th2 balance (G protein)
  • TLR4 interaction/signalling (F protein)
  • interference w/ leukocyte chemotaxis (G protein CX3CR-binding motif)
35
Q

Chemokine mimicry by RSV G protein

A
  • G protein has chemokine (CX3CL/fractalkine) activity, allowing binding to CX3CR thereby affecting leukocyte trafficking
  • -> delayed viral clearance, enhanced infectivity of cells
36
Q

RSV and asthma

A
  • correlation b/w severe RSV disease in early childhood and asthma/recurrent wheezing later in life
  • polymorphisms of TLR4 assoc. w/ susceptibility to RSV infection and later development of asthma
37
Q

Emerging Respiratory Virus Pathogens (4)

A
  • new strains of flu
  • hantavirus (member of bunyavirus fam)
  • SARS
  • MERS
38
Q

Hantavirus Structure

A
  • lipid enveloped virion

- 3 ss (-) RNA segments

39
Q

Hantavirus Pulmonary Syndrome

A
  • transmitted by rodents and their droppings, virus spread to humans via inhalation
  • acute respiratory distress syndrome (ARDS)
  • virus remains in interstitial tissue rather than airspaces
40
Q

Hantavirus Pulmonary Syndrome Pathogenesis

A
  • viral antigens within the endothelium of capillaries in various tissues
  • EM confirms infection of endothelial cells and macrophages in the lungs of HPS patients
  • disease severity correlates w/ elevated levels of virus specific CD8+ T cells
  • endothelial cells separate blood vessels from surrounding tissues
41
Q

SARS (coronavirus)

A
  • severe acute respiratory syndrome
  • 1st outbreak in 2003
  • interstitial pneumonia
  • may be spread from animals (bats, civet cats) to humans
42
Q

Mechanism of Immunopathogenesis in SARS

A
  • hyperactive immunopathological response (cytokine storm)
  • virus uses ACE2 (angiotensin converting enzyme 2) as receptor, resulting in its downreg
  • as a result there is accumulation in lung of angiotensin II which is damaging to lung tissue
  • > fluid accumulation in lung tissue
43
Q

SARS interference w/ host immune functions

A
  • most things target IFN response

- nsp-16 disguises the cap of v mRNA to make look like cell mRNA

44
Q

MERS (coronavirus)

A
  • Middle East Respiratory Syndrome
  • emerged 2012 in countries in or near arabian peninsula, also spread by air passenger travel
  • origin unknown
45
Q

RIsks for Severe RSV

A
  • host determined risk factors
  • early age of infection
  • viral factors blocking IFN responses and apoptosis
  • high infectitvity and viral pathogenesis

Virology Final (7 decks)

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