Respiratory Viruses Flashcards

1
Q

rhinovirus type of virus

A
    • ss RNA
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2
Q

importance of rhinovirus infection when young

A
  • may sensitive an individual to early onset asthma
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3
Q

do we have antivirals for RSV

A
  • not specific ones
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4
Q

do we have vaccines for RSV

A
  • no
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5
Q

do we have antivirals for measles

A
  • no
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6
Q

do we have vaccines for measles

A
  • yes
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7
Q

do you normally have a fever during a cold

what about during the flu?

A
  • rare
  • yes
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8
Q

how fast does a cold come on?

A
  • over a few days
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9
Q

how fast does the flu come on?

A
  • sudden
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10
Q

which people are most susceptible to the flu

A
  • the very old and very young
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11
Q

influenza infection often coincides with bacterial superinfection from

A
  • MRSA
  • staph aureus
  • strep pneumo
  • Group A Strep
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12
Q

how long does it take after exposure to flu to develop protective serum antibody?

A
  • about a month
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13
Q

viral infection of respiratory epithelium

A
  • destroys epithelial cells
  • damages mucous membrane
  • membranes are colonized with bacteria
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14
Q

type A influenza virus affects which group

A
  • humans and other animals
  • all age groups
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15
Q

severity of illness for type A influenza

A
  • moderate to severe illness
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16
Q

type B influenza virus affects which group

A
  • humans only
  • primarily children
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17
Q

importance of type C influenza virus

A
  • no neuraminidase activity
  • HA contains esterase activity instead
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18
Q

role of hemagglutinin

A
  • binds the virus to cells with sialic acid on the membrane
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19
Q

role of neuraminidase

A
  • cleaves sialic acid
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20
Q

which type of influenza virus is zoonotic

A
  • type A
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21
Q

what is the process that involves gradual adaptation of zoonotic viruses that allow human infection and transmission

A
  • antigenic drift
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22
Q

what is the process that involves reassortment of the SEGMENTED GENOME that potentially allows swapping of genes between different virus types

A
  • antigenic shift
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23
Q

how does antigenic drift work

A
  • accumulation of point mutations results in amino acid substitutions
  • differences in antigenic sites where host antibody binds to HA and NA glycoproteins
  • prevent binding of antibodies induced by previous infection
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24
Q

how does an antigenic shift work

A
  • HA/NA switch to new chimeric status
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25
antigenic shift only occurs for which type of influenza virus
- type A
26
MOA of amantidine and rimantadine
- M2 ion channel inhibitors that block endosomal release of disassembling virus
27
which type of influenza virus possesses M2 channels
- type A only
28
MOA of zanamivir, oseltamivir, and permavir
- neuraminidase inhibitors
29
how neuraminidase inhibitors work
- interfere with ability of neuraminidase to cleave sialic acid - stops virus from budding
30
how influenza virus uses cap snatching
- flu virus makes its own mRNA - steals 5' cap from host - propagates own life cycle and inhibits host mRNA
31
role of Xoflusa
- inhibits flu cap snatching
32
the most variable antigen on the influenza virus is what?
- HA
33
what is a good target for a universal influenza vaccine
- the stem of HA
34
structure of paramyxovirus
- enveloped, nonsegmented, negative sense RNA
35
what is the life of immunity to RSV
- only 2-3 months
36
who is at the greatest risk of hospitalization as a result of RSV infection
- young infants \< 1 month
37
pathogenesis of RSV
- mucus congests small airways of bronchioles - clogged also by inflammatory cells (macrophages and neutrophils)
38
structure of flu
- enveloped virus with negative sense segmented genome
39
antiviral treatment for RSV
- ribavirin (nonspecific)
40
can the measles virus be transmitted from the host prior to the onset of rash
- yes
41
measles pathogenesis
- inhaled - gets into lung - disseminates out of lung and into lymph and becomes systemic
42
characteristic symptom of measles even before rash comes on
- Koplik's spots - white on mucosa of the oral cavity
43
main target of measles
- alveolar macrophages and dendritic cells THEN - T and B cells
44
complications of measles
- pneumonia - immunosuppression with increased susceptibility to other infections - complications from CNS infection
45
Coronavirus structure
enveloped + ssRNA (non-segmented) RNA packaged in coiled structure composed of nucleocapsid (N) proteins
46
receptor for SARS-CoV-2
ACE2
47
ACE2 receptor expressed where
by epithelial cells in the oral cavity and lung (intestine, kidneys and blood vessels)
48
Comorbidities among patients at risk for serious Covid-19
HTN and diabetes both conditions treated with ACE inhibitors; leads to increased ACE2 expression --\> may promote viral infection
49
Differences between SARS-CoV-2 and Influenza A
SARS-CoV-2: occasional mutations (better proofreading RdRP) lead to sporadic epidemics w/o segment, no potential for shift mediated by reassortment Influenza: continuous drift (small-scale mutations due to error-prone RdRp) shift (large changes in viral HA and NA due to reassortment of viral RNA segments)
50
viruses that infect the HUMAN respiratory tract
Influenza A/B RSV SARS-CoV-2
51
Which virus can lead to SSPE (subacute sclerosing panencephalitis)
Measles Virus
52
For RSV, Influenza and SARS-CoV-2 name the: time of year of infection antivirals vaccines reservoir
RSV: annual/seasonal, no specific antivirals, no licensed vaccines, humans only Influenza: annual/seasonal, specific antivirals, vaccines available, zoonotic SARS-CoV-2: current pandemic, no specific antivirals, vaccines available, zoonotic
53
RSV is in the same family as which virus?
Measles
54
RSV infection in what demographic?
most frequent cause of lower airway disease in infants increasingly associated wth disease in elderly and immunocompromised
55
RSV and children
nearly 100% children infected by 2-3 years of age symptomatic leads to bronchiolitis!!
56
RSV bronchiolitis
mucus and inflammatory material occlude small airways in infants and young children
57
Treatment for RSV
non-specific antiviral (ribavirin) anti-RSV antibody
58
RSV structure for attachment and entry
viral factors: glycoprotein G, fusion protein F host receptors: TLR4, ciliated cell receptors
59
most common causes of bacterial superinfection
staph. aureus and strep. pneumo
60
Pulmonary and Non-pulmonary complications w/ Influenza
Pulmonary → primary influenza viral pneumonia, secondary bacterial pneumonia, Croup, exacerbates lung disease Non-pulmonary → Toxic shock syndrome (S. aureus superinfection), Guillain-Barré syndrome
61
Influenza type C
uncommon, no epidemic potential
62
prevents binding of antibodies
antigenic drift
63
differences in key antigenic sites in HA and NA glycoproteins
antigenic drift
64
accumulation of point mutations results in amino acid substitutions
antigenic drift
65
reassortment of viral segments in Type A viruses
antigenic shift
66
may occur in animals or humans
antigenic shift
67
may result in new H/NN combinations
antigenic shift
68
Responsible for pandemics every 10-40 years
antigenic shift