Paramyxo-Rabies-Influenza Flashcards
negative strand RNA viruses genuses
paramyxoviruses
rhabdoviruses
orthomyxoviruses
paramyxoviruses spp
measles
mumps
respiratory syncytial
parainfluenza
rhabdovirus spp
rabies
othromyxovirus spp
influenza A, B, and C
Paramyxoviruses structure
Helical nucleocapsid Pleomorphic envelope (variable shape)
surface adhesin of paramyxoviruses
hemagglutin
hemagglutin of paramyxoviruses
measles?
on envelope, will bind sailic acid on cell surface glycoproteins
on measels will bind CD46 protein
paramyxoviruses genome
negative single strand RNA
Paramyxovirus replication
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
measles virus
genus
surface proteins
paramyxovirus
hemagglutins
F protein
hemagglutin for measles
envelope glycoproteins attachment proteins (bind virus to host cells)
F protein of measles
- causes membranes to fuse together: role in viral entry into cells
expression on infected cells causes cell-cell fusion= Giant cells (syncytia)
paramyxoviruses and syncytia
All paramyxoviruses can induce syncytia formation
Measles (Rubeola)
caused by?
enters thru?
contagious?
- caused by measles virus
- enters body through respiratory tract
- extremely contagious
measles spread thru body
skin involvment of measles due to?
skin involvement (partly, inflammation due to host response) humoral and cellular immune responses modulate outcome
symptoms of measles
3 C’s = cough, coryza, conjunctivitis
Also morbilliform appearance (rash = exanthem)
Early sign of Koplik spots in oral cavity
complcaitions asscoiated with measles infection
Pneumonia (giant cell pneumonitis)
Bacterial superinfections of middle ear and lung
subacute sclerosing panencephalitis
bacterial infection associated with measles
spp?
– Bacterial superinfections of middle ear and lung
– pneumococci, staphylococci, and meningococci
subacute sclerosing panencephalitis
rare progressive degeneration of central nervous system caused by a type of measles virus
treatment, prevention, and control of measles
– symptomatic/supportive therapy
– attenuated measles vaccine
• MMR vaccine (measles, mumps, rubella)
• Live Measles vaccine - 1993
Mumps caused by? genus? shape? envelope? geometry? Genome?
caused by mumps virus Paramyxovirus pleomorphic enveloped virus helical nucleocapsid negative strand RNA
mumps spread thru the body
clinical manifestations of mumps
occur when?
complications?
– develop 16-18 days after infection
– fever, and swelling and tenderness of salivary glands
– complications include meningitis and orchitis (inflammation of testis)
mumps prevention
live attenuated vax (MMR)
respiratory syncytial virus (RSV)
genome
envelope
-RNA
enveloped
RSV surface proteins/ functions
G protein binds host cell not hemagglutinin
F protein causes membrane fusion and syncytia formation
RSV F protein
RSV entry/spread in body
enters what cells? spreads down what?
spread to distant sites?
effects in lungs?
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
RSV and kids
considered to be most dangerous respiratory infections
in young children
RSV spreads by?
spread by hand contact and respiratory secretions
RSV clinical manifestations
what may account for more serious symptoms?
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
test for RSV
rapid immunological tests
rabies
caused by?
target?
rabies virus
highly neurotrophic= CNS target
rabies genome
-RNA
rabies transmitted by
– bites of infected animals
– aerosols in caves where bats roost
– contamination of scratches, abrasions, open wounds, or mucous membranes with saliva of infected animals
rabies
envelope?
shape?
enveloped
characteristic bullet shape
where does rabies replication occur in host cell?
RNA poly?
entirely cytoplasmic, brings its own RNA poly
main source of rabies
wild animals, less common in domesticated animals due to vax
incubation period of rabies
depends on?
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
Negri bodies
masses of nucleocapsids of rabies in cytoplasm seen in brain tissue of 70-90% of infected
humans
rabies spread thru body
rabies clinical manifestations begin? symptoms? hydrophobia? death from?
– 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
treatment, prevention, and control of rabies
– 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
Orthomyxoviruses
genome
envelope
-RNA
enveloped
Orthomyxoviruses spp
flu A, B and C
Orthomyxoviruses genome
8 segments of RNA (for influenza viruses A and B)
7 segments of RNA (for influenza virus C)
Orthomyxoviruses replication
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
cap-snatching of Orthomyxoviruses
uses 5 end of host mRNA to prime viral mRNA synthesis
Orthomyxoviruses random packaging
Random packaging of the 8 segments (11 segments packaged per virion)
Orthomyxoviruses surface proteins
Surface spikes (peplomers)
hemagglutinin (HA)
neuraminidase (NA)
Orthomyxoviruses hemagglutinin binds? promotes? what cells does it aggregate? eleicits what response?
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
Orthomyxoviruses neuraminidase (NA
release of virus from envelope
cleaves sialic acid (NA has enzymatic activity)
pathogenesis/ spread of influenza A
flu symptoms usually due to?
interferon induction
treatment, prevention, and control of influenza
–Treat with amantidine, rimantidine (A strain only); ribavirin (A and B)
–inactivated virus vaccine
late complications of the flu
Later, pneumonia may result from bacterial
pathogenesis, viral pathogenesis, or
immunopathogenesis.
Antigenic shift
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
Antigenic drift
Changes in influenza virus surface proteins (hemagglutinin and neuraminidase) due to
point mutations that occur during viral replication is called antigenic drift.
antigenic drift and shift prevent what
life long immunity from the flu
pigs as a “mixing vessel” for the flu
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
1918 flu pandemic: “spanish influenza” # killed usually what demo mechanism of death genome
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
