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microbiology > Paramyxo-Rabies-Influenza > Flashcards

Paramyxo-Rabies-Influenza Flashcards

1
Q

negative strand RNA viruses genuses

A

paramyxoviruses
rhabdoviruses
orthomyxoviruses

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2
Q

paramyxoviruses spp

A

measles
mumps
respiratory syncytial
parainfluenza

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3
Q

rhabdovirus spp

A

rabies

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4
Q

othromyxovirus spp

A

influenza A, B, and C

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5
Q

Paramyxoviruses structure

A 
Helical nucleocapsid
Pleomorphic envelope (variable shape)
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6
Q

surface adhesin of paramyxoviruses

A

hemagglutin

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7
Q

hemagglutin of paramyxoviruses

measles?

A

on envelope, will bind sailic acid on cell surface glycoproteins
on measels will bind CD46 protein

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8
Q

paramyxoviruses genome

A

negative single strand RNA

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9
Q

Paramyxovirus replication

A

minus strand RNA injected into host cell
Viral RNA poly used to produce + strands for protein synthesis and - strand replication
both proteins and -RNA are packaged to nucleocapsid and bud from the host cell membrane for envelope
REPLICATION IS ENTIRELY CYTOPLASMIC

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10
Q

measles virus
genus
surface proteins

A

paramyxovirus
hemagglutins
F protein

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11
Q

hemagglutin for measles

A 
envelope glycoproteins
attachment proteins (bind virus to host cells)
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12
Q

F protein of measles

A
  • causes membranes to fuse together: role in viral entry into cells
    expression on infected cells causes cell-cell fusion= Giant cells (syncytia)
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13
Q

paramyxoviruses and syncytia

A

All paramyxoviruses can induce syncytia formation

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14
Q

Measles (Rubeola)
caused by?
enters thru?
contagious?

A
  • caused by measles virus
  • enters body through respiratory tract
  • extremely contagious
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15
Q

measles spread thru body

A
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16
Q

skin involvment of measles due to?

A 
skin involvement (partly, inflammation due to host response)
humoral and cellular immune responses modulate outcome
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17
Q

symptoms of measles

A

3 C’s = cough, coryza, conjunctivitis
Also morbilliform appearance (rash = exanthem)

Early sign of Koplik spots in oral cavity

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18
Q

complcaitions asscoiated with measles infection

A

Pneumonia (giant cell pneumonitis)
Bacterial superinfections of middle ear and lung
subacute sclerosing panencephalitis

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19
Q

bacterial infection associated with measles

spp?

A

– Bacterial superinfections of middle ear and lung

– pneumococci, staphylococci, and meningococci

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20
Q

subacute sclerosing panencephalitis

A

rare progressive degeneration of central nervous system caused by a type of measles virus

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21
Q

treatment, prevention, and control of measles

A

– symptomatic/supportive therapy
– attenuated measles vaccine
• MMR vaccine (measles, mumps, rubella)
• Live Measles vaccine - 1993

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22
Q 
Mumps
caused by? 
genus?
shape? 
envelope? 
geometry? 
Genome?
A 
caused by mumps virus
Paramyxovirus
pleomorphic
enveloped virus
helical nucleocapsid
negative strand RNA
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23
Q

mumps spread thru the body

A
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24
Q

clinical manifestations of mumps
occur when?
complications?

A

– develop 16-18 days after infection
– fever, and swelling and tenderness of salivary glands
– complications include meningitis and orchitis (inflammation of testis)

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25
Q

mumps prevention

A

live attenuated vax (MMR)

26
Q

respiratory syncytial virus (RSV)
genome
envelope

A

-RNA

enveloped

27
Q

RSV surface proteins/ functions

A

G protein binds host cell not hemagglutinin

F protein causes membrane fusion and syncytia formation

28
Q

RSV F protein

A
29
Q

RSV entry/spread in body
enters what cells? spreads down what?
spread to distant sites?
effects in lungs?

A

virus enter respiratory epithelial cells, then spreads downward along the respiratory mucosa

no clinically significant spread to distant sites

in lungs:
necrosis of epithelial cells
infiltration of lymphocytes
increased mucous production

30
Q

RSV and kids

A

considered to be most dangerous respiratory infections

in young children

31
Q

RSV spreads by?

A

spread by hand contact and respiratory secretions

32
Q

RSV clinical manifestations

what may account for more serious symptoms?

A

clinical manifestations
– acute onset of fever, cough, rhinitis, and nasal congestion
– often progresses quickly to severe bronchiolitis and pneumonia

• bronchiolitis - bronchiole obstruction that can lead to respiratory failure

host response may account for most serious symptoms

33
Q

test for RSV

A

rapid immunological tests

34
Q

rabies
caused by?
target?

A

rabies virus

highly neurotrophic= CNS target

35
Q

rabies genome

A

-RNA

36
Q

rabies transmitted by

A

– bites of infected animals
– aerosols in caves where bats roost
– contamination of scratches, abrasions, open wounds, or mucous membranes with saliva of infected animals

37
Q

rabies
envelope?
shape?

A

enveloped

characteristic bullet shape

38
Q

where does rabies replication occur in host cell?

RNA poly?

A

entirely cytoplasmic, brings its own RNA poly

39
Q

main source of rabies

A

wild animals, less common in domesticated animals due to vax

40
Q

incubation period of rabies

depends on?

A

incubation can be up to 12 months after virus enters body
depends on size of inoculum and location of bite
face bite has shorter incubation

41
Q

Negri bodies

A

masses of nucleocapsids of rabies in cytoplasm seen in brain tissue of 70-90% of infected
humans

42
Q

rabies spread thru body

A
43
Q 
rabies clinical manifestations 
begin? 
symptoms? 
hydrophobia?
death from?
A

– begin 2 to 16 weeks after exposure
– pain or paresthesia at wound site, anxiety, irritability, depression, fatigue, loss of appetite, fever, and sensitivity to light and sound
– Hydrophobia: contractions of muscles involved in swallowing (sometimes sight of water elicits this)
– quickly progresses to paralysis
– death results from destruction of regions of brain that regulate breathing

44
Q

treatment, prevention, and control of rabies

A

– Passive administration of antibody (antiserum or immunoglobulin) (human rabies immune globulin = HRIG collected from immunized persons)
– postexposure vaccination
– preexposure vaccination of individuals with high risk of exposure, dogs, and cats

45
Q

Orthomyxoviruses
genome
envelope

A

-RNA

enveloped

46
Q

Orthomyxoviruses spp

A

flu A, B and C

47
Q

Orthomyxoviruses genome

A

8 segments of RNA (for influenza viruses A and B)

7 segments of RNA (for influenza virus C)

48
Q

Orthomyxoviruses replication

A

bind cell via hemagglutinin: entry
nucleocapsid uncoats with the drop in pH at endosome, releasing -RNA
RNA may enter nucleus for transcription to + via viral RNA poly
+RNA exits nuc and is translated to proteins, or remains in nuc to form new -RNA
proteins follow exocytosis route and are assembled with -RNA and bud from host cell mem

49
Q

cap-snatching of Orthomyxoviruses

A

uses 5 end of host mRNA to prime viral mRNA synthesis

50
Q

Orthomyxoviruses random packaging

A

Random packaging of the 8 segments (11 segments packaged per virion)

51
Q

Orthomyxoviruses surface proteins

A

Surface spikes (peplomers)
hemagglutinin (HA)
neuraminidase (NA)

52
Q 
Orthomyxoviruses hemagglutinin
binds?
promotes?
what cells does it aggregate?
eleicits what response?
A

attachment to host cell surface (prior to entry), binds to sialic acid on epithelial cell surface
promotes membrane fusion (viral-cellular)
binds/aggregates RBCs
elicits protective neutralizing antibody response

53
Q

Orthomyxoviruses neuraminidase (NA

A

release of virus from envelope

cleaves sialic acid (NA has enzymatic activity)

54
Q

pathogenesis/ spread of influenza A

A
55
Q

flu symptoms usually due to?

A

interferon induction

56
Q

treatment, prevention, and control of influenza

A

–Treat with amantidine, rimantidine (A strain only); ribavirin (A and B)
–inactivated virus vaccine

57
Q

late complications of the flu

A

Later, pneumonia may result from bacterial
pathogenesis, viral pathogenesis, or
immunopathogenesis.

58
Q

Antigenic shift

A

Antigenic shifts in influenza virus are caused by reassortment of viral genomic fragments during a mixed infection by two different influenza viruses from different spp

59
Q

Antigenic drift

A

Changes in influenza virus surface proteins (hemagglutinin and neuraminidase) due to
point mutations that occur during viral replication is called antigenic drift.

60
Q

antigenic drift and shift prevent what

A

life long immunity from the flu

61
Q

pigs as a “mixing vessel” for the flu

A

Pigs play an important role as a “mixing vessel” for influenza viruses from humans, birds, and pigs. This is because pigs can become infected by these different influenza viruses

In the pig the virus may undergo antigenic shifts to form new genomes, capable of infecting humans

62
Q 
1918 flu pandemic: “spanish influenza”
# killed 
usually what demo 
mechanism of death 
genome
A

killed 50 million world-wide
victims usually young and previously healthy

Likely killed via a “cytokine storm” in victims with strong immune systems unchecked positive feedback loop between cytokines and cellular response
result: too many immune system cells activated in an single space = tissue damage

genome recovered in 1997 from victim in permafrost grave in Alaska
Sequencing showed the virus originated in birds and mutated to be infectious in humans

microbiology (42 decks)

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