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CELL MICRO S1 > Viruses respiratory > Flashcards

Viruses respiratory Flashcards

1
Q

how many people in the US become infected with influenza?

A

29-59 million

36,000 die

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2
Q

give 2 examples of negative strand RNA viruses?

A
  • respiratory syncytical virus (RSV)

- influenza virus (IV)

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3
Q

herpes virus and adenovirus B, C and E are examples of what kind of virus?

A

Double stranded DNA virus

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4
Q

giva an example of a positive strand RNA virus?

A

Coronavirus (CoV)

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5
Q

what can cause the common cold?

A

RHINOVIRUS, RSV, PIV (parainfluenza virus), flu, adeno, coronaviruses

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6
Q

what can cause Tonsilopharyngitis?

A

RHINOVIRUS, RSV, PIV (parainfluenza virus), flu, adeno, coronaviruses, HSV, CMV (Cytomegalovirus), EBV (Epstein–Barr virus)

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7
Q

what can cause bronchitis?

A

RSV, PIV, Adeno, HSV

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8
Q

what can cause Pneumonia?

A

Adeno, PIV, RSV, VZV, Measles, CMV, HSV, Hantavirus

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9
Q

are there vaccines against viral resp infections?

A

trials are currently in progress

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10
Q

what family of viruses is influenza from?

A

Orthomyoxviridae

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11
Q

what is the shape of influenza?

A

pleomorphic

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12
Q

how is RNA packaged in influenza?

what is found on the envelope of influenza?

A
  • individual segments of RNA packaged as separate NUCLEOCAPSIDS
  • PROMINENT PEPLOMERS
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13
Q

what does Type A influenza cause? who does it affect?

A

causes WORLDWIDE PANDEMICS

infects man and animals

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14
Q

what does Type B influenza cause? who does it affect?

A

localised outbreaks

infects man

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15
Q

who does Type C influenza affect? what type of symptoms?

A

infects HUMANS AND PIGS

mainly asymptomatic

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16
Q

what is classification of the influenza virus based on?

A

antigenic properties of surface glycoproteins: Haemagglutinin and Neuraminidase

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17
Q

what recognises N-acetyl neuraminic acid?

A

carbohydrate binding proteins

Alpha linked terminal carbohydrate of upper respiratory tract and lung associated glycoconjugate

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18
Q

what is the role of Neuraminidase (NA)?

A

Tetramer-Particle dispersal: assist movement along the upper respiratory tract and virus release

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19
Q

what is the role of Haemagglutinin (HA)?

A

Trimer-Attachment and fusion: initial point of contact by binding cell glycoconjugates

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20
Q

where is the receptor binding site located on influenza?

A

on top of haemagglutinin (HA)
HA binds sialic acid
- the TYPE of sialic acid bound is key to determine virus tropism

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21
Q

describe antigenic drift as a factor of evolution?

A
  • accumulation of aa changes that result in subtle changes in ANTIGENS and infections where host immunity is INCOMPLETE
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22
Q

describe antigenic shift as a factor of evolution?

A
  • reassortant viruses (segmented genome) resulting in novel antigenic virus stains
    (this commonly occurs with human and avian viruses)
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23
Q

in influenza, where can antigenic changes occur?
where can aa changes occur?
how can this lead to drift?

A
  • antigenic changes cluster in 5 highly variable regions surrounding the RECEPTOR BINDING POCKET
  • aa changes occur at other sites in HA1 molecule
  • ->DRIFT when mutations ACCUMULATE in 2 or more of the antigenic domains
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24
Q

how are variants in influenza different?

how does spread of the virus occur?

A

they have REDUCED SUSCEPTIBILITY to PRE-EXISTING immunity in the infectable population (i.e they are more likely to infect)
- spread occurs because of the large numbers of SUSCEPTIBLE HOSTS and the increased liklihood of the virus causing symptomatic infection

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25
Q

why are pigs an important mixing vessel for influenza?

A

they can be infected by HUMAN AND AVIAN viruses

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26
Q

in human lungs, what is the dominant receptor used in influenza?

A

α(2,6)

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27
Q

in bird intestine (enteric inf), what is the dominant receptor used in influenza?

A

α(2,3)

28
Q

in swine lungs (respiratory inf), what is the dominant receptor used in influenza?

A

α(2,6) and α(2,3) abundant

29
Q

what causes antigenic shift in influenza?

A

sult of reassorting between segments of different Influenza, can occur between different human viruses or between human and animal viruses

30
Q

what are the 2 features of an antigenic shift in influenza?

A
  • sudden appearance

- antigenically distinct from Influenza currently circulating in humans

31
Q

what was the cause of the Spanish flu? how many did it kill?

A

H1N1 infection, killed 50m

32
Q

how does neurominidase work?

A

NEUROMINIDASE (enzyme) cleaves SIALIC ACID off, means that virus DOES NOT AGGREGATE and can leave the HOST CELL

33
Q

name 2 drugs used against influenza, how do they work? how are they administered|?

A

1) Zanamivir (Relenza) (inhaled)
2) Oseltamavir(Tamiflu) (oral)
- sits in the binding site of
neurominidase, stops it working, causes clumping of virus

34
Q

when do drugs against influenza oseltamavir and Zanamavir need to be deployed?
what other situations canthey be used in?
what is a concern abut oseltamavir?

A

quickly!

  • can be used prophylactically
  • natural polymorphisms can lead to drug resistance against oseltamavir
35
Q

describe the two influenza vaccines
what are the 3 types of trivalent flu vaccine?
who are they used in

A

1) TRIVALENT vaccine
- STANDARD :made using virus grown in eggs
- RECOMBINANT: egg free, used in 18+ inc pregnant women
- made with ADJUVANT (creates stronger immune response in body) for 65+

2) QUADRIVALENT

36
Q

RSV stands for what?

A

respiratory syncytial virus

37
Q

when was RSV discovered?

A

1956

38
Q

how many deaths p/a caused by RSV?

A

200,000

39
Q

what does RSV cause?

A

acute disease, leads to longer term respiratory conditions

40
Q

describe the seasonal nature of RSV?

A

in temperate zones: late autumn, winter spring
tropical/Arctic: all year round
Europe: winter

41
Q

what is the structure of genetic info in RSV?

A
  • single stranded
  • non segmented NEGATIVE SENSE RNA genome
  • has ‘G’ attachment protein (imp for receptor binding and vaccine development, site of genetic variation)
  • ‘F’ fusion protein
  • 2 subgroups A and B
42
Q

describe the pathogenesis of RSV? how does it infect? incubation period?

A

initial infection: contact of particles w/ nose/eyes
incubation period: 2-8 days
- initial infection of epithelial cells/ upper or lower RT
- extensive inflammation, monocyte and T cell infiltration
- overproduction of mucus
- HIGH virus load associated with more symptoms

43
Q

what are risk factors for severe infection of RSV?

A
  • premature birth
  • co morbidities (cardiac/respiratory disease)
  • genetic predisposition affecting T cell responses
44
Q

what kind of environmental factors are important in RSV?

A

smoke, pollution, crowding

45
Q

if initial exposure to RSV is 6wks – 9 months of age, what happens?
if severe?
if underlying cardiac or respiratory disease?

A

causes mild/ asymptomatic upper resp tract inf
(25-40% involves lower resp tract)
- most cases: recovery after 7-12 days after initial illness
- if severe: coughing and wheezing causes respiratory failure
- if underlying cardiac or respiratory disease, progression can be rapid and fatal

46
Q

what characterises acute RSV inf in nromal adults?
how long does it last?
what about if older patients?

A
  • rhinorrhea
  • pharyngitis (sore throat)
  • cough, fever
  • lasts ~5 days
  • older patients= inf = severe
47
Q

describe the epidemiology of RSV?

A
  • worldwide
  • major paediatric inf esp infants 6 wk-9 months more likely to have LRT inf (esp boys)
  • RE inf = common & ASYMPTOMATIC
48
Q

how is RSV transmitted?

A

via large droplets or fomite contamination and spread requires close contact or contamination of hands between contaminated areas and nasal or conjunctival mucosa

49
Q

how is RSV controlled?

A
  • hand washing

- gloves and gowns

50
Q

what did the early vaccine for RSV cause? how?

A
  • more SEVERE disease on re-exposure to community RSV
    Caused by:
    -Inadequate serum neutralising antibodies
  • Lack of local immunity
  • Excessive induction of Th2 responses with pulmonary eosinophilia and increased production of IL-4 and IL-5
51
Q

how are newborns protected from RSV?

A

Passive immunisation (via placenta) with IgG protects newborns against infection/disease

52
Q

is there a current vaccine for RSV?

A

ongoing study

  • study shows purified F protein = safe and immunogenic
  • 4x inc in RSV neutralising Ab
53
Q

how are RSV inf treated?
how is treatment administered?
how does it work?

A

infant? considerable supportive care
- only RIBAVIRIN (nucleoside analogue)
- administered by SMALL PARTICLE AEROSOL (no systemic toxicity)
- drug causes DEC VIRAL SHEDDING and INC level of oxygenation
but ribavarin may not affect mortality rates

54
Q

give an example of a corona virus?

A

SARS

55
Q

corona viruses cause what?

A

URTI and GI inf infections of mammals and birds

56
Q

what was the major global outbreak of SARS in China in 2002 exacerbated by?

A

extensive global human travel

57
Q

how did SARS-CoV emerge?

A

RECOMBINATION between 2 bat CoVs

58
Q

what % of bats are CoV positive in China?

A

6%

59
Q

how did CoV go from bats to humans?

A

bats transmitted to PALM CIVETS–> humans via live animal markets in China

60
Q

what in CoV increased transmission?

A

rapid adaptation of VIRUS SPIKE PROTEIN

61
Q

what is MERS-CoV?

A

middle east resp syndrome associated coronavirus

62
Q

what does MERS-CoV use as a receptor?

A

dipeptidy peptidase

63
Q

where did MERS orginiate?

A 
zoonotic- bats.
camel inf (URT) = closest link w/ human infections
64
Q

how is MERS transmitted?

A

through contact with camels, BUT human cases have been reproted where there is no contact with camels

65
Q

what specimens are used to make diagnosis?

A

using specimens:

  • nasopharyngeal aspirate/swab
  • throat sawb
  • endo-tracheal aspirate
  • broncho-alveolar lavage

CELL MICRO S1 (16 decks)

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