3.34 Flashcards
Paramyxoviruses (Family = Paramyxoviridae) Chapter 34
Species (4)
measles virus
mumps virus
respiratory syncytial virus (RSV)
parainfluenza viruses
Rhabdoviruses (Family = Rhabdoviridae) Chapter 35
Species: (1)
rabies virus
Orthomyxoviruses (Family = Orthomyxoviridae) Chapter 36
Species: (1)
influenza viruses A, B and C
Paramyxoviruses characteristics (4)
Helical nucleocapsid
Pleomorphic envelope (variable shape)
Hemagglutinin (measles virus) on envelope binds sialic acid on cell surface glycoproteins
measles virus binds CD46 protein present on most cells
minus stranded RNA genome
minus stranded RNA genome
=
one segment of RNA (~16,000 bases in length)
Paramyxovirus replication
Virus brings in RNA polymerase which transcribes minus RNA
into plus RNAs (full length and mRNAs)
Replication is cytoplasmic
Measles virus (~— nt –strand RNA genome)
16000
hemagglutinins -
envelope glycoproteins attachment proteins (bind virus to host cells)
F protein -
causes membranes to fuse together
role in viral entry into cells
expression on infected cells causes cell-cell fusion
Giant cells (syncytia)
All paramyxoviruses can induce — formation
syncytia
Measles (Rubeola)
characteristics (3)
• caused by measles virus
• enters body through
respiratory tract
• extremely contagious
Measles (Rubeola)
— involvement (partly, inflammation due to host response)
humoral and cellular immune responses modulate outcome
skin
Measles (Rubeola)
3 Cs=
cough, coryza,
conjunctivitis
Also morbilliform appearance
(rash = exanthem)
Coryza is a word describing the symptoms of a
head cold. It
describes the inflammation of the mucous membranes lining
the nasal cavity which usually gives rise to the symptoms of
nasal congestion and loss of smell, among other symptoms.
Measles (Rubeola)
complications (3)
– Pneumonia (giant cell pneumonitis) – Bacterial superinfections of middle ear and lung – pneumococci, staphylococci, and meningococci
Measles (Rubeola)
• subacute sclerosing panencephalitis (1)
– rare progressive degeneration of central
nervous system caused by a type of
measles virus
Measles (Rubeola)
• treatment, prevention, and control (2)
– symptomatic/supportive therapy – attenuated measles vaccine • MMR vaccine (measles, mumps, rubella) • Live Measles vaccine - 1993
Mumps
• caused by (3)
mumps virus – Paramyxovirus pleomorphic, enveloped virus – helical nucleocapsid – negative strand RNA (~15,000 nt)
mumps clinical manifestations (3)
– develop 16-18 days after infection
– fever, and swelling and tenderness of salivary glands
– complications include meningitis and orchitis
(inflammation of testis)
mumps
tx
– live, attenuated vaccine (MMR)
Respiratory syncytial virus
characteristics (3)
minus stranded RNA
genome = one segment of RNA
enveloped
Respiratory syncytial virus
G protein binds
host cells
instead of a hemagglutinin
Respiratory syncytial virus
F protein -
causes membrane fusion
syncytia formation
Respiratory syncytial virus
virus enter respiratory epithelial cells, then spreads
downward
along the respiratory mucosa
Respiratory syncytial virus
no clinically significant spread to distant sites (3)
necrosis of epithelial cells
infiltration of lymphocytes
increased mucous production
Respiratory syncytial virus (RSV) (2)
• considered to be most dangerous respiratory infections
in young children
• spread by hand contact and respiratory secretions
RSV clinical manifestations (3)
– acute onset of fever, cough, rhinitis, and nasal
congestion
– often progresses quickly to severe bronchiolitis and
pneumonia
host response may account for most serious
• bronchiolitis -
bronchiole obstruction that can
lead to respiratory failure
RSV
tx
– rapid immunologic tests
Rabies
• caused by — virus (3)
rabies
– negative strand RNA virus
– highly neurotropic
Rabies
transmitted by: (3)
– 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 virus (Lyssavirus) characteristics (3)
minus stranded RNA
genome = one segment of RNA (~12,000 bases in length)
enveloped, bullet shaped virus
replication is entirely cytoplasmic
incubation can be up to – months after
virus enters body
depends on size of: —
location of bite: — bite has shorter incubation
12
inoculum
face
Negri bodies
masses of nucleocapsids in cytoplasm
seen in brain tissue of 70-90% of infected
humans
rabies clinical manifestations (5)
clinical manifestations
– 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
– quickly progresses to paralysis
– death results from destruction of regions of brain that
regulate breathing
Hydrophobia:
contractions of muscles involved in
swallowing (sometimes sight of water elicits this)
rabies
tx (3)
– 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 (Family = Orthomyxoviridae) Chapter 36 (3)
Genus: Influenzavirus - influenza virus A, B and C
minus stranded RNA
enveloped
Orthomyxoviruses
genome=
8 segments of RNA (for influenza viruses A and B)
7 segments of RNA (for influenza virus C)
cap-snatching -
uses 5 end of host mRNA to prime viral mRNA synthesis
Random packaging of the 8 segments (11 segments packaged per virion)
Surface spikes (peplomers) hemagglutinin (HA)
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
neuraminidase (NA)
release of virus from envelope
cleaves sialic acid (NA has enzymatic activity)
Typical flu symptoms (fever, headache, muscle aches, malaise) due to —
interferon induction
rabies tx (2)
–Treat with amantidine,
rimantidine (A strain only);
ribavirin (A and B)
–inactivated virus vaccine
Antigenic shifts in influenza virus are caused by
— of viral genomic fragments during a
mixed infection by two different influenza viruses
reassortment
Reassortment creates an
influenza virus that can infect humans but has a hemagglutinin from the animal influenza virus strain. (H3 vs. H2 in original human infleunza virus strain)
Changes in influenza virus surface proteins
(hemagglutinin and neuraminidase) due to
— that occur during viral
replication is called antigenic drift.
point mutations
Antigenic shifts in influenza virus are caused
by reassortment of viral genomic fragments
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.
Example:
Diagram of the origin of a new human virus
with a shift from H3N2 to H5N1.
Pigs were infected with a duck influenza virus,
and another set of pigs with the human
influenza virus.
At some time, one pig underwent mixed
infection with both viruses.
The resulting virus created by reassortment of
the viral gene segments could be transmitted
to and infect humans. In this example,
genomic segments from the duck virus
contribute the genes for hemagglutinin and
neuraminidase, shifting the original human
virus from H3N2 to H5N1.
1918 flu pandemic: “spanish influenza”
characteristics (2)
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 à tissue damage
H1N1 virus:
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
