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BMS 615 Cardiovascular > Test 3: Wk11: 1 Respiratory Viral Infections - Bogomolnaya > Flashcards

Test 3: Wk11: 1 Respiratory Viral Infections - Bogomolnaya Flashcards

1
Q

— are members of the orthomyxovirus group

A

influenza

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2
Q

enveloped, single-stranded negative-sense segmented RNA viruses

A

Influenza

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3
Q

3 major types of influenza viruses

A

A, B, C

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4
Q

influenza types are based on antigenic differences in

A

their ribonucleoprotein (NP) and matrix protein antigens (M)

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5
Q

major influenza epidemics caused by

A

influenza A

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6
Q

— infect a wide variety of species including mammals and birds and have a tendency to undergo significant antigenic changes

A

Influenza A

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7
Q

— are more antigenically stable and are known to infect humans and seals, occur in more localized outbreaks

A

Influenza B

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8
Q

— viruses appear to be relatively minor cause of disease effecting humans and pigs

A

Influenza C

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9
Q

two Influenza virus-specified glycoproteins

A

hemagglutinin (HA or H)

Neuraminidase (NA or N)

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10
Q

ratio of H to N

A

4 or 5 to 1

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11
Q

integral membrane protein in Influenza A known as —

A

M2 ion channel protein

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12
Q

integral membrane protein in Influenza B known as —

A

NB, functions as ion channel

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13
Q

how does influenza C differ from A and B

A

posses only 7 RNA segments and has no N

it does have receptor-destroying capability

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14
Q

the hemagglutinin of Influenza C does what

A

binds to a different receptor than A and B

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15
Q

Named because of its ability to agglutinate red blood cells from certain species

A

Hemagglutinin

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16
Q

It is the viral attachment protein, responsible for binding to sialic acid on epithelial cell surface receptors, which is a critical first step in initiating infection of the cell

A

Hemagglutinin

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17
Q

Is an antigenic hydrolytic enzyme that acts on the hemagglutinin receptors by splitting off their terminal neuraminic acid

A

Neuraminidase

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18
Q

promotes a smooth passage for the virus in the
respiratory tract by inactivating mucoprotein receptors in respiratory
secretions

A

Neuraminidase

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19
Q

destroys viral receptor, thus preventing aggregation

and superinfection in infected cells

A

Neuraminidase

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20
Q

has a major role in viral release from infected cells

A

Neuraminidase

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21
Q

Influenza gene segments

A

A- 8
B- 8
C- 7

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22
Q

Influenza unique proteins

A

A- M2
B- NB
C- HEF

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23
Q

Influenza A host range

A

humans, swine, birds, equines, marine mammals, bats

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24
Q

Influenza B host range

A

humans and seals

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25
Q

Influenza C host range

A

humans, swine

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26
Q

most unique aspect of Influenza A

A

ability to develop a wide variety of subtypes through the processes of mutation and whole gene “swapping” between strains, called reassortment.

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27
Q

Which influenza virus experiences drifts and shifts

A

a

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28
Q

Antigenic Drift

A

mutations acquired over long period of time

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29
Q

Antigenic drift

A

reassortment of genome segments, rapid and unpredictable

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30
Q

Three hemagglutinins —, —, and — and two neuraminidases — and — appear to be of greatest importance in human
infections.

A

H1, H2, H3

N1, N2

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31
Q

human influenza viruses are — in the environment and sensitive to heat, acid pH, and solvents.

A

in general not stable

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32
Q

— retain infectivity for several weeks outside the host

A

avian influenza viruses H5N1

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33
Q

Influenza viruses most common mode of transmission

A

direct droplet

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34
Q

where do Influenza viruses replicate

A

in upper respiratory tract ciliated epithelial cells causing structural and functional abnormalities.

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35
Q

Influenza viruses block

A

Block in host cell syntheses, release in lysosomal
enzymes, and desquamation of ciliated and mucous
producing cells.

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36
Q

most protective antibody for influenza viruses

A

Anti-hemagglutinin, has the ability to neutralize virus on re-exposure because it is a surface protein easily recognized by the antibody

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37
Q

— is a serious complication of influenza viruses most common in infants and children

A

Reye Syndrome, develops 2-12 days after onset of infection

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38
Q

Influenza bacterial superinfection most commonly caused by

A

Streptococcus pneumoniae,

Haemophilus influenzae, and Staphylococcus aureus.

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39
Q

3 ways influenza viruses can cause death

A
  1. underlying disease with decompensation
  2. Superinfection
  3. Direct rapid progression
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40
Q

Influenza Diagnosis Techniques (5)

A

virus culture
serology
rapid antigen and molecular (viral nucleic acid) assays
immunofluorescence
reverse transcription polymerase chain reaction (RT PCR)

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41
Q

avoid — in influenza

A

aspirin

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42
Q

does antibiotic prophylaxis help preventing superinfections

A

no

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43
Q

Neuraminidase inhibitors,

— and — , are useful for influenza A and B

A

oseltamivir, zanamivir

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44
Q

— or — blocked virus uncoating and assembly

A

Amantadine or rimantadine

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45
Q

Three types of flu vaccines are produced in the United States:

A

egg based, cell based, and recombinant

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46
Q

— viruses belong to the paramyxovirus group

A

Parainfluenza

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47
Q

Parainfluenza cause

A

mild cold like symptoms but can also cause serious

respiratory tract disease.

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48
Q

There are four serotypes of parainfluenza viruses:

A

1, 2, 3, and 4.

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49
Q

These enveloped viruses contain linear (nonsegmented),

negative sense, single stranded RNA genome.

A

Parainfluenza

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50
Q

Similar to influenza viruses, parainfluenza viruses possess

A

a hemagglutinin and neuraminidase, but on the same spike.

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51
Q

Parainfluenza viruses differ from the influenza viruses in that RNA synthesis occurs in the — rather than in the —.

A

cytoplasm; nucleus

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52
Q

The single stranded, negative sense linear RNA genome is bound to a
nucleoprotein (helical nucleocapsid), and the matrix protein surrounds
the nucleoprotein complex, which is packaged into a lipid bilayer
envelope containing attachment protein (H and N on the same spike)
and the fusion protein (F).

A

Parainfluenza

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53
Q

are parainfluenza viruses stable? do they have antigenic drift or shift?

A

relatively stable with no drift or shift

54
Q

parainfluenza viruses cause serious disease in

A

infants and young children

55
Q

most common parainfluenzas

A

1 and 3

56
Q

— immunity plays an important role in controlling parainfluenza virus infection.

A

Humoral

57
Q

Parainfluenza viruses onset

A

may be abrupt; usually begins as a mild URI and progress over 1-3 days to middle and lower respiratory tract

58
Q

Parainfluenza virus duration

A

4 - 21 days; usually 7 - 10

59
Q

— is the major cause of acute croup (laryngotracheitis) in infants and young children, but also causes less severe diseases such as mild URI, pharyngitis, and tracheobronchitis in individuals of all ages.

A

Parainfluenza 1

60
Q

Parainfluenza 1 outbreaks occur

A

during fall

61
Q

of slightly less significance. It has been associated with croup, primarily in children, with mild URI, and occasionally with acute lower respiratory disease.

A

Parainfluenza 2

62
Q

Parainfluenza 2 outbreaks occur

A

during fall

63
Q

— is a major cause of severe lower respiratory disease in infants and young children.

A

Parainfluenza 3

64
Q

It often causes bronchitis, pneumonia, and croup in children younger than 1 year of age.

A

Parainfluenza 3

65
Q

In older children and adults, it may cause URI or tracheobronchitis.

A

Parainfluenza 3

66
Q

Parainfluenza 3 outbreaks occur

A

during any season

67
Q

It is generally associated with mild upper respiratory illness only.

A

Parainfluenza 4

68
Q

Parainfluenza viruses control and therapy

A

there is none

69
Q

Parainfluenza viruses treatment

A

relieve sx by using OTC medications

70
Q

Parainfluenza viruses diagnosis (3)

A

RT-PCR, antigen Assay, Virus isolation

71
Q

RSV stands for

A

Respiratory Syncytial Virus

72
Q

— belongs to
Pneumovirus of the
Paramyxovirus group.

A

Respiratory syncytial virus (RSV)

73
Q

It is an enveloped, negative
sense linear RNA virus that primarily infects the
bronchi, bronchioles, and alveoli of the lung.

A

RSV

74
Q

does RSV have hemagglutinin or neuraminidase

A

no

75
Q

The RNA genome is linear (

nonsegmented ), negative sense, and single stranded and codes for at least 10 different proteins.

A

RSV

76
Q

The virion structure is similar to parainfluenza virus except that the envelope glycoproteins are an attachment (G) protein and a
fusion (F) protein.

A

RSV

77
Q

nucleoprotein bound to genomic RNA (helical
nucleocapsid), a phosphoprotein and two matrix (M) proteins in
the viral envelope.

A

RSV

78
Q

The virion also contains the viral RNA polymerase enzyme

A

RSV

79
Q

RSV replicates in the — and buds out from the plasma membrane.

A

cytoplasm

80
Q

In RSV Two envelope glycoproteins (spikes), G and F, mediate

A

attachment and syncytium formation, respectively

81
Q

RSV Subtypes

A

A and B

A is more severe

82
Q

is the most important respiratory virus that causes a severe infection in infants

A

RSV

83
Q

is the major cause of bronchiolitis and pneumonia in infants under 1 year of age

A

RSV

84
Q

is the leading cause of hospitalization in US children, with annual hospitalization rates of 6 per 1000 children younger tha n
5 years.

A

RSV

85
Q

RSV Outbreaks

A

community outbreaks occur annually from late fall to early spring
last 8-12 weeks with 50% of families with children

86
Q

RSV duration

A

The usual duration of virus shedding is 5 to 7 days; young infants, however, may shed virus for 9 to 20 days or longer.

87
Q

Nosocomial infection reduced by

A

careful handwashing

masks are not helpful

88
Q

RSV is spread to the upper respiratory tract by

A

contact with infective secretions.

89
Q

The pathologic effect of RSV is mainly caused by — , which is followed by immunologically mediated cell injury.

A

direct viral invasion of the respiratory epithelium

90
Q

RSV Viral surface — protein plays an important role in pathogenesis by forming syncytia and multinucleated giant cells leading to
cell death.

A

F

91
Q

Infection with RSV results in – and — humoral and secretory antibody responses. However, immunity to reinfection is brief.

A

IgG and IgA

92
Q

in RSV Vaccination with killed vaccine appears to

A

enhance the severity of subsequent disease.

93
Q

RSV Leads to

A

bronchiolitis and pneumonitis with cough, wheezing, and respiratory distress

94
Q

RSV Clinical Findings (3)

A

hyperexpansion of lungs, hypoxemia, hypercapnia

95
Q

RSV causes of death

A

Causes of death include respiratory failure, right

sided heart failure, and bacterial superinfection.

96
Q

is there a vaccine for RSV

A

no

97
Q

RSV prophylaxis in high risk infants

A

Monoclonal antibody to protein F

98
Q

HMPV stands for

A

Human Metapneumovirus

99
Q

— is Pneumovirus of paramyxovirus group, was discovered in 2001 and can cause upper and lower respiratory tract infection in people of all age groups.

A

HMPV

100
Q

— is a significant cause of ARD in infants and young children.

A

HMPV

101
Q

Infection with HMPV generally occurs in

A

slightly older children compared to RSV that infects younger children.

102
Q

HMPV incubation period

A

3-6 days

103
Q

HMPV symptoms

A

fever, nasal congestion, cough, and shortness of breath, which may progress to bronchiolitis or pneumonia

104
Q

HMPV diagnosis

A

RTPCR
viral antigen enzyme immunoassay
immunofluorescence
The virus culture is rarely done

105
Q

HMPV treatment

A

no specific treatment available

106
Q

— are naked capsid, icosahedral, and double

stranded DNA viruses.

A

Adenoviruses

107
Q

7 subgroups of Adenovirus

A

A-G

108
Q

The virion size is in the range of 90 to 100 nm and it contains
a linear double stranded DNA genome covered with an
icosahedral capsid.

A

Adenovirus

109
Q

Adenovirus Capsid

A

The capsid is composed of 252 subunits (capsomeres), including 240
hexons and 12 pentons and fibers.

110
Q

Adenoviruses enter cells via
— and replication occurs in the — by using host RNA polymerase for transcription and viral DNA dependent DNA polymerase (viral DNA polymerase) for replication of DNA genomes.

A

viropexis; nucleus

111
Q

How are adenovirus virions released

A

cell destruction

112
Q

Adenovirus infection route

A

Infects by droplet, oral route, or direct inoculation.

113
Q

After the acute phase of illness, the viruses may remain in tissues, particularly lymphoid structures such as tonsils, adenoids, and intestinal Peyer patches, and may become reactivated and shed without producing illness for 6 to 18 months thereafter.

A

adenovirus

114
Q

Integration of — into the host cell genome has been shown to occur; this latent state can persist for years in tonsillar tissue and peripheral blood lymphocytes.

A

adenoviral DNA

115
Q

Penton projections are toxic to cells

A

Adenoviruses

116
Q

adenovirus death protein

A

is considered important

for efficient lysis of infected cells and release of newly formed virions.

117
Q

adenovirus immunity

A

Immunity to adenoviruses after infection is serotype

specific and usually long lasting.

118
Q

adenovirus symptoms

A

Symptoms include fever, rhinitis, pharyngitis, cough, and conjunctivitis.

119
Q

Adenovirus diagnosis

A

Diagnosis by PCR, antigen detection, virus isolation or serology

120
Q

adenovirus treatment

A

there is no specific treatment

121
Q

— may be effective for severe adenovirus infections

A

Cidofovir

122
Q

adenovirus vaccine

A

Live enteric vaccine containing serotypes 4 and 7 is used in military

123
Q

They are small (20
30 nm), naked capsid virus particles containing single
stranded, positive sense RNA genomes.

A

Rhinovirus

124
Q

The receptor for most rhinoviruses (and some coxsackieviruses) is —

A

glycoprotein intercellular adhesion molecule 1 (ICAM-1)

125
Q

most common cold virus

A

Rhinovirus

126
Q

Lower respiratory tract disease caused by rhinoviruses

A

is uncommon.

127
Q

Rhinovirus infections occur when

A

Rhinovirus infections may be seen at any time of the year. Epidemic peaks tend to occur in the early fall or spring months.

128
Q

Rhinovirus transmission

A

Transmission occurs by hand

to hand, hand to eye, or hand to object to hand ( eg , doorknob) contamination.

129
Q

— can survive for hours on contaminated environmental surfaces. Self
inoculation after hand contamination may be a
more important mode of spread than that by airborne particles.

A

Rhinoviruses

130
Q

Rhinovirus incubation period

A

The usual incubation period is 2 to 3 days, and acute symptoms commonly last 3 to 7 days.

131
Q

Rhinoviruses can be diagnosed by

A

viral genome amplification by RTPCR in nasopharyngeal specimens.

132
Q

contain a positive sense single stranded linear RNA genome,
which is surrounded by an envelope that includes a lipid bilayer derived from
intracellular rough endoplasmic reticulum and Golgi membranes of infected
cells.

A

Coronaviruses

BMS 615 Cardiovascular (49 decks)

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