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Viruses respiratory Flashcards

(65 cards)

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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
why are pigs an important mixing vessel for influenza?
they can be infected by HUMAN AND AVIAN viruses
26
in human lungs, what is the dominant receptor used in influenza?
α(2,6)
27
in bird intestine (enteric inf), what is the dominant receptor used in influenza?
α(2,3)
28
in swine lungs (respiratory inf), what is the dominant receptor used in influenza?
α(2,6) and α(2,3) abundant
29
what causes antigenic shift in influenza?
sult of reassorting between segments of different Influenza, can occur between different human viruses or between human and animal viruses
30
what are the 2 features of an antigenic shift in influenza?
- sudden appearance | - antigenically distinct from Influenza currently circulating in humans
31
what was the cause of the Spanish flu? how many did it kill?
H1N1 infection, killed 50m
32
how does neurominidase work?
NEUROMINIDASE (enzyme) cleaves SIALIC ACID off, means that virus DOES NOT AGGREGATE and can leave the HOST CELL
33
name 2 drugs used against influenza, how do they work? how are they administered|?
1) Zanamivir (Relenza) (inhaled) 2) Oseltamavir(Tamiflu) (oral) - sits in the binding site of neurominidase, stops it working, causes clumping of virus
34
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?
quickly! - can be used prophylactically - natural polymorphisms can lead to drug resistance against oseltamavir
35
describe the two influenza vaccines what are the 3 types of trivalent flu vaccine? who are they used in
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
RSV stands for what?
respiratory syncytial virus
37
when was RSV discovered?
1956
38
how many deaths p/a caused by RSV?
200,000
39
what does RSV cause?
acute disease, leads to longer term respiratory conditions
40
describe the seasonal nature of RSV?
in temperate zones: late autumn, winter spring tropical/Arctic: all year round Europe: winter
41
what is the structure of genetic info in RSV?
- 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
describe the pathogenesis of RSV? how does it infect? incubation period?
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
what are risk factors for severe infection of RSV?
- premature birth - co morbidities (cardiac/respiratory disease) - genetic predisposition affecting T cell responses
44
what kind of environmental factors are important in RSV?
smoke, pollution, crowding
45
if initial exposure to RSV is 6wks – 9 months of age, what happens? if severe? if underlying cardiac or respiratory disease?
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
what characterises acute RSV inf in nromal adults? how long does it last? what about if older patients?
- rhinorrhea - pharyngitis (sore throat) - cough, fever - lasts ~5 days - older patients= inf = severe
47
describe the epidemiology of RSV?
- worldwide - major paediatric inf esp infants 6 wk-9 months more likely to have LRT inf (esp boys) - RE inf = common & ASYMPTOMATIC
48
how is RSV transmitted?
via large droplets or fomite contamination and spread requires close contact or contamination of hands between contaminated areas and nasal or conjunctival mucosa
49
how is RSV controlled?
- hand washing | - gloves and gowns
50
what did the early vaccine for RSV cause? how?
- 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
how are newborns protected from RSV?
Passive immunisation (via placenta) with IgG protects newborns against infection/disease
52
is there a current vaccine for RSV?
ongoing study - study shows purified F protein = safe and immunogenic - 4x inc in RSV neutralising Ab
53
how are RSV inf treated? how is treatment administered? how does it work?
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
give an example of a corona virus?
SARS
55
corona viruses cause what?
URTI and GI inf infections of mammals and birds
56
what was the major global outbreak of SARS in China in 2002 exacerbated by?
extensive global human travel
57
how did SARS-CoV emerge?
RECOMBINATION between 2 bat CoVs
58
what % of bats are CoV positive in China?
6%
59
how did CoV go from bats to humans?
bats transmitted to PALM CIVETS--> humans via live animal markets in China
60
what in CoV increased transmission?
rapid adaptation of VIRUS SPIKE PROTEIN
61
what is MERS-CoV?
middle east resp syndrome associated coronavirus
62
what does MERS-CoV use as a receptor?
dipeptidy peptidase
63
where did MERS orginiate?
``` zoonotic- bats. camel inf (URT) = closest link w/ human infections ```
64
how is MERS transmitted?
through contact with camels, BUT human cases have been reproted where there is no contact with camels
65
what specimens are used to make diagnosis?
using specimens: - nasopharyngeal aspirate/swab - throat sawb - endo-tracheal aspirate - broncho-alveolar lavage

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