9_Respiratory Virus Flashcards
1
Q
Which viruses affect the UPPER respiratory tract?
A
Unique to Upper respiratory:
- Coxsackivirus
- Coronavirus
- Herpesvirus
- Rhinovirus
Others:
- Adenovirus
- Bocavirus
- Influenzairus
- Parainfluenza virus
- Respiratory syncytial virus
2
Q
list the viruses that infect the LOWER respiratory tract?
A
Unique: *Metapnuemovirus
- Adenovirus
- Bocavirus
- Influenzavirus
- Parainfluenza virus
- Respiratory syncytial virus
3
Q
What are the major viral respiratory pathogens?
A
4
Q
Parainfluenza viruses:
- family
- structure
- size
- serotypes
A
- Family: Paramyxoviridae
- Structure: enveloped, ss-RNA, negative, non-segmented
- size: pelomorphic (virions 150-300 nm diameter)
- 4 serotypes (1, 2, 3, 4)
5
Q
parainfluenza viral life cycle:
what is it?
A
- HIV virion binds to cell –> fuses with cell
- uncoats the virion
- genome undergoes transcription, and replication, and translation
- genome –> buds off
- and is released from the cell
6
Q
parainfluenza viruses - epidemiology
- environmental
- season
- age
A
- environmental: parainfluenza type 3 is a serious nosocomial infxn
- season: parainfluenza 1& 2 infections occur in fall/winter, often in alternating years
- age:
- 90-100% of children 5+ y/o, seropositive for parainfluenza type 3
- 75% have Antibodies to parainfluenza types I & 2
7
Q
Parainfluenza:
- transmission
- pathogenesis
- clinical sxs
A
- transmission: close contact w/ infected persons or contaminated surfaces
- through mucous membranes of eyes/mouth/nose
- pathogenesis:
- site of replication: epithelial lining of upper respiratory tract
- causes localized infection: no viremia occurs
- incubation period: 2-3 days
- virus is shed 8-10 days after infxn, up to 30 days
- clinical sxs
- croup (parainfluenza 1& 2)
- bronchiologitis (parainfluenza 3)
- pneumonia (parainfluenza 3)
8
Q
Parainfluenza:
- immunology
- treatment
A
- immunology:
- serum antibodies: questionable value since no viremia occurs
-
secretory antibodies: good correlation experimentally b/w IgA levels and protection against infxn, however protective levels not achieved in young children
- passive immunity in breast fed children significant
- vaccine: no vaccine currently available
9
Q
Respiratory syncytial virus (RSV)
- epidemiology
- at risk populations
A
- primary cause of lower respiratory tract illness in young children
- RSV infxn: 125,000 pediatric hospitalizations in the US
- at risk populations: children
- generally resolves uneventfully
- high risk populations may develop severe (sometimes fatal) illnesses
- annual mortality to RSV in infants/children is 200-2,700
10
Q
Respiratory syncytial virus (RSV)
- structure
- environmental
- season
- age of at risk population
A
- structure:
- family: paramyxoviridae
- enveloped, (negative sense) single stranded, non-segmented RNA
- pleopmorphic, 2 serotypes (A &B)
- environmental: hospitals ,day care, nursing homes
- season: annually every Nov-Mar, later in warmer climates
- age of at risk population: 50% of all children are seropositive by 1 yr of age, 85% by 4 years old
11
Q
Respiratory syncytial virus (RSV):
- morbidity and mortality
- factors contributing to inc. risk
A
- 100,000 hospitalizations; 4,500 deaths per year in US
- Factors contributing to increase risk:
- premature infants, infants <6 weeks old
- infants w/ congenital heart disease
- infants w/ chronic lung conditions; cystic fibrosis
- immunodeficiency
- lower socioeonomic status/ crowded living conditions
- attendance in day care setting
- infants who are not breast fed
- exposure to cigarette smoke
12
Q
Respiratory syncytial virus:
- transmission and
- immunology
A
- transmission: large aeorsolized respiratory droplets, generated by sneezing/coughing/through contact w/ nasal secretions/contaminated surfaces
- enters through eyes/nose and infects epithelial cells of upper respiratory tract
- incubation: 3-4 days
- virus shedding 1-2 days prior to symptoms and can last up to 3 wekks
- immunology: virus transmitted cell-cell fusion
- free virus is not present –> neutralizing antibodies are not formed
- primary infection doesn’t prevent re-infection
- passive immunity - maternal antibodies reduce severity of infxn
- secretory IgA directed against F protein is effective neutralizing antibody
13
Q
Respiratory syncytial virus:
clinical symptoms (childhood infxns, adults)
A
- childhood infxn
- lower respiratory illness
- bronchiolitis - cough
- pneumonia (crackles, repiratory distress)
- adult infections
- upper respiratory infxn resembling the common cold
14
Q
key differences b/w URT and LRTs:
which is more severe?
which viruses start this?
how does infection spread?
A
15
Q
Rhinovirus:
- family
- structure
- size
- causes what illness?
A
- family: Picornaviridae
- structure: positive, ss-RNA (non-segmented)
- non-enveloped
- icosahedral capsid
- size: 30 nM in diameter
- hundreds of serotypes
- causes: “common cold”
16
Q
what are the two unique physical properties of Rhinovirus?
A
-
Temperature stability
- extremely stable at room temp;
- can survive on surfaces at room temp for 18 hr or more
- adapted to replicated better at 33 degrees celsius than 37 degrees
- infect URT due to lower temp.
-
pH lability
- unlike other enteroviruses (+ssRNA viruses), rhinoviruses are not acid-stable
- rhinoviruses are destroyed at low pH
17
Q
Rhinovirus:
epidemiology (Ages it affects, seasonal variations)
A
- age: children are most frequently infected and are major source of adult infections
- seasonal variations:
- rhinoviruses –> cause colds in Fall and Spring
- Coronavirus –> cause winter colds
- (patterns may be due to changes in living w/ the seasons)
18
Q
Rhinovirus:
- transmission
- pathogenesis
- clinical symptoms
A
- transmission:
- *direct contact w/ infectious nasal secretions on skin/contaminated surfaces
- enters via eye or nasal pharynx and attaches via ICAM-1 or LDL receptor to epithelial cells in the posterior nasal pharynx and nasal passages
- pathogenesis
- incubation: 2-3 days
- sxs appear after 3-4 days
- virus shedding begins 1-2 days prior to sxs –> continues for 1 week
- infxn is self-limiting and localized to URT
- clinical symptoms
- ST, stuffy nose, runny nose, sneezing, malaise
25
Q
Influenza virus:
- structure
- types
A
- family: Orthomyxoviridae
- negative stranded ss-RNA virus
- genome has 8 segments
- enveloped virus, w/ haemagglutinin adn neuraminidase spikes
- 3 types based on serotype of ribonucleic protein
- Type A: infects multiple species; undergoes antigenic shift and drift
-
Types B and C infects exclusively humans;
- B: undergoes antigenic drift ONLY
- C: relatively stable
26
Q
Influenza A Virus:
shifts and drifts?
which causes pandemics? what causes epidemics?
A
- Antigenic SHIFTS of haemagglutinin –> pandemics
- Antigenic DRIFTS of H& N proteins –> epidemics
29
Q
do type A, B, and C influenza virus vary based on the following criteria?
A
30
Q
Influenza virus:
pandemic
epidemics
A
32
Q
antigenic drift:
define
A
- gradual accumulation of mutations that allow the virus to escape neutralizing antibodies
- can result from changes in amino acids
- can involved any antigenic protein
- can occur every year
- epidemic strains thought to have changes in 3 or more antigenic sites
34
Q
Mechanisms of influenza virus antigenic “shift”?
A
- DIRECT: non-humans –> humans
- indirect:
- non-human virus –> animal –> reassortment virus –> humans
- human virus –> animal –> reassortment virus –> humans
39
Q
What is the immunity to influenza?
A
41
Q
how does diagnosis hemagglutination inhibition function?
A
and near patients or rapid tests which detects rise in antibodies to influenza or NA activity
43
Q
describe the types of vaccines for influenza
A
Types of vaccines:
- Killed whole virus
- Live virus
- Virus subunit
- Synthetic
