Test 3: Wk11: 1 Respiratory Viral Infections - Bogomolnaya Flashcards
— are members of the orthomyxovirus group
influenza
enveloped, single-stranded negative-sense segmented RNA viruses
Influenza
3 major types of influenza viruses
A, B, C
influenza types are based on antigenic differences in
their ribonucleoprotein (NP) and matrix protein antigens (M)
major influenza epidemics caused by
influenza A
— infect a wide variety of species including mammals and birds and have a tendency to undergo significant antigenic changes
Influenza A
— are more antigenically stable and are known to infect humans and seals, occur in more localized outbreaks
Influenza B
— viruses appear to be relatively minor cause of disease effecting humans and pigs
Influenza C
two Influenza virus-specified glycoproteins
hemagglutinin (HA or H)
Neuraminidase (NA or N)
ratio of H to N
4 or 5 to 1
integral membrane protein in Influenza A known as —
M2 ion channel protein
integral membrane protein in Influenza B known as —
NB, functions as ion channel
how does influenza C differ from A and B
posses only 7 RNA segments and has no N
it does have receptor-destroying capability
the hemagglutinin of Influenza C does what
binds to a different receptor than A and B
Named because of its ability to agglutinate red blood cells from certain species
Hemagglutinin
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
Hemagglutinin
Is an antigenic hydrolytic enzyme that acts on the hemagglutinin receptors by splitting off their terminal neuraminic acid
Neuraminidase
promotes a smooth passage for the virus in the
respiratory tract by inactivating mucoprotein receptors in respiratory
secretions
Neuraminidase
destroys viral receptor, thus preventing aggregation
and superinfection in infected cells
Neuraminidase
has a major role in viral release from infected cells
Neuraminidase
Influenza gene segments
A- 8
B- 8
C- 7
Influenza unique proteins
A- M2
B- NB
C- HEF
Influenza A host range
humans, swine, birds, equines, marine mammals, bats
Influenza B host range
humans and seals
Influenza C host range
humans, swine
most unique aspect of Influenza A
ability to develop a wide variety of subtypes through the processes of mutation and whole gene “swapping” between strains, called reassortment.
Which influenza virus experiences drifts and shifts
a
Antigenic Drift
mutations acquired over long period of time
Antigenic drift
reassortment of genome segments, rapid and unpredictable
Three hemagglutinins —, —, and — and two neuraminidases — and — appear to be of greatest importance in human
infections.
H1, H2, H3
N1, N2
human influenza viruses are — in the environment and sensitive to heat, acid pH, and solvents.
in general not stable
— retain infectivity for several weeks outside the host
avian influenza viruses H5N1
Influenza viruses most common mode of transmission
direct droplet
where do Influenza viruses replicate
in upper respiratory tract ciliated epithelial cells causing structural and functional abnormalities.
Influenza viruses block
Block in host cell syntheses, release in lysosomal
enzymes, and desquamation of ciliated and mucous
producing cells.
most protective antibody for influenza viruses
Anti-hemagglutinin, has the ability to neutralize virus on re-exposure because it is a surface protein easily recognized by the antibody
— is a serious complication of influenza viruses most common in infants and children
Reye Syndrome, develops 2-12 days after onset of infection
Influenza bacterial superinfection most commonly caused by
Streptococcus pneumoniae,
Haemophilus influenzae, and Staphylococcus aureus.
3 ways influenza viruses can cause death
- underlying disease with decompensation
- Superinfection
- Direct rapid progression
Influenza Diagnosis Techniques (5)
virus culture
serology
rapid antigen and molecular (viral nucleic acid) assays
immunofluorescence
reverse transcription polymerase chain reaction (RT PCR)
avoid — in influenza
aspirin
does antibiotic prophylaxis help preventing superinfections
no
Neuraminidase inhibitors,
— and — , are useful for influenza A and B
oseltamivir, zanamivir
— or — blocked virus uncoating and assembly
Amantadine or rimantadine
Three types of flu vaccines are produced in the United States:
egg based, cell based, and recombinant
— viruses belong to the paramyxovirus group
Parainfluenza
Parainfluenza cause
mild cold like symptoms but can also cause serious
respiratory tract disease.
There are four serotypes of parainfluenza viruses:
1, 2, 3, and 4.
These enveloped viruses contain linear (nonsegmented),
negative sense, single stranded RNA genome.
Parainfluenza
Similar to influenza viruses, parainfluenza viruses possess
a hemagglutinin and neuraminidase, but on the same spike.
Parainfluenza viruses differ from the influenza viruses in that RNA synthesis occurs in the — rather than in the —.
cytoplasm; nucleus
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).
Parainfluenza
are parainfluenza viruses stable? do they have antigenic drift or shift?
relatively stable with no drift or shift
parainfluenza viruses cause serious disease in
infants and young children
most common parainfluenzas
1 and 3
— immunity plays an important role in controlling parainfluenza virus infection.
Humoral
Parainfluenza viruses onset
may be abrupt; usually begins as a mild URI and progress over 1-3 days to middle and lower respiratory tract
Parainfluenza virus duration
4 - 21 days; usually 7 - 10
— 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.
Parainfluenza 1
Parainfluenza 1 outbreaks occur
during fall
of slightly less significance. It has been associated with croup, primarily in children, with mild URI, and occasionally with acute lower respiratory disease.
Parainfluenza 2
Parainfluenza 2 outbreaks occur
during fall
— is a major cause of severe lower respiratory disease in infants and young children.
Parainfluenza 3
It often causes bronchitis, pneumonia, and croup in children younger than 1 year of age.
Parainfluenza 3
In older children and adults, it may cause URI or tracheobronchitis.
Parainfluenza 3
Parainfluenza 3 outbreaks occur
during any season
It is generally associated with mild upper respiratory illness only.
Parainfluenza 4
Parainfluenza viruses control and therapy
there is none
Parainfluenza viruses treatment
relieve sx by using OTC medications
Parainfluenza viruses diagnosis (3)
RT-PCR, antigen Assay, Virus isolation
RSV stands for
Respiratory Syncytial Virus
— belongs to
Pneumovirus of the
Paramyxovirus group.
Respiratory syncytial virus (RSV)
It is an enveloped, negative
sense linear RNA virus that primarily infects the
bronchi, bronchioles, and alveoli of the lung.
RSV
does RSV have hemagglutinin or neuraminidase
no
The RNA genome is linear (
nonsegmented ), negative sense, and single stranded and codes for at least 10 different proteins.
RSV
The virion structure is similar to parainfluenza virus except that the envelope glycoproteins are an attachment (G) protein and a
fusion (F) protein.
RSV
nucleoprotein bound to genomic RNA (helical
nucleocapsid), a phosphoprotein and two matrix (M) proteins in
the viral envelope.
RSV
The virion also contains the viral RNA polymerase enzyme
RSV
RSV replicates in the — and buds out from the plasma membrane.
cytoplasm
In RSV Two envelope glycoproteins (spikes), G and F, mediate
attachment and syncytium formation, respectively
RSV Subtypes
A and B
A is more severe
is the most important respiratory virus that causes a severe infection in infants
RSV
is the major cause of bronchiolitis and pneumonia in infants under 1 year of age
RSV
is the leading cause of hospitalization in US children, with annual hospitalization rates of 6 per 1000 children younger tha n
5 years.
RSV
RSV Outbreaks
community outbreaks occur annually from late fall to early spring
last 8-12 weeks with 50% of families with children
RSV duration
The usual duration of virus shedding is 5 to 7 days; young infants, however, may shed virus for 9 to 20 days or longer.
Nosocomial infection reduced by
careful handwashing
masks are not helpful
RSV is spread to the upper respiratory tract by
contact with infective secretions.
The pathologic effect of RSV is mainly caused by — , which is followed by immunologically mediated cell injury.
direct viral invasion of the respiratory epithelium
RSV Viral surface — protein plays an important role in pathogenesis by forming syncytia and multinucleated giant cells leading to
cell death.
F
Infection with RSV results in – and — humoral and secretory antibody responses. However, immunity to reinfection is brief.
IgG and IgA
in RSV Vaccination with killed vaccine appears to
enhance the severity of subsequent disease.
RSV Leads to
bronchiolitis and pneumonitis with cough, wheezing, and respiratory distress
RSV Clinical Findings (3)
hyperexpansion of lungs, hypoxemia, hypercapnia
RSV causes of death
Causes of death include respiratory failure, right
sided heart failure, and bacterial superinfection.
is there a vaccine for RSV
no
RSV prophylaxis in high risk infants
Monoclonal antibody to protein F
HMPV stands for
Human Metapneumovirus
— is Pneumovirus of paramyxovirus group, was discovered in 2001 and can cause upper and lower respiratory tract infection in people of all age groups.
HMPV
— is a significant cause of ARD in infants and young children.
HMPV
Infection with HMPV generally occurs in
slightly older children compared to RSV that infects younger children.
HMPV incubation period
3-6 days
HMPV symptoms
fever, nasal congestion, cough, and shortness of breath, which may progress to bronchiolitis or pneumonia
HMPV diagnosis
RTPCR
viral antigen enzyme immunoassay
immunofluorescence
The virus culture is rarely done
HMPV treatment
no specific treatment available
— are naked capsid, icosahedral, and double
stranded DNA viruses.
Adenoviruses
7 subgroups of Adenovirus
A-G
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.
Adenovirus
Adenovirus Capsid
The capsid is composed of 252 subunits (capsomeres), including 240
hexons and 12 pentons and fibers.
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.
viropexis; nucleus
How are adenovirus virions released
cell destruction
Adenovirus infection route
Infects by droplet, oral route, or direct inoculation.
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.
adenovirus
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.
adenoviral DNA
Penton projections are toxic to cells
Adenoviruses
adenovirus death protein
is considered important
for efficient lysis of infected cells and release of newly formed virions.
adenovirus immunity
Immunity to adenoviruses after infection is serotype
specific and usually long lasting.
adenovirus symptoms
Symptoms include fever, rhinitis, pharyngitis, cough, and conjunctivitis.
Adenovirus diagnosis
Diagnosis by PCR, antigen detection, virus isolation or serology
adenovirus treatment
there is no specific treatment
— may be effective for severe adenovirus infections
Cidofovir
adenovirus vaccine
Live enteric vaccine containing serotypes 4 and 7 is used in military
They are small (20
30 nm), naked capsid virus particles containing single
stranded, positive sense RNA genomes.
Rhinovirus
The receptor for most rhinoviruses (and some coxsackieviruses) is —
glycoprotein intercellular adhesion molecule 1 (ICAM-1)
most common cold virus
Rhinovirus
Lower respiratory tract disease caused by rhinoviruses
is uncommon.
Rhinovirus infections occur when
Rhinovirus infections may be seen at any time of the year. Epidemic peaks tend to occur in the early fall or spring months.
Rhinovirus transmission
Transmission occurs by hand
to hand, hand to eye, or hand to object to hand ( eg , doorknob) contamination.
— 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.
Rhinoviruses
Rhinovirus incubation period
The usual incubation period is 2 to 3 days, and acute symptoms commonly last 3 to 7 days.
Rhinoviruses can be diagnosed by
viral genome amplification by RTPCR in nasopharyngeal specimens.
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.
Coronaviruses
