2013-02-08 VIR Arboviruses, Rubella and Parvovirus B-19 Flashcards
What is phenotypic mixing?
What types of viruses does this process occur in?
two viruses infect same cell
some progeny are made that have the genome of one with (at least part of) the coat of the other
thus, you end up with phenotype that doesn’t make genotype
will go away within one generation as long as further co-infections are avoided
TYPES: “some arboviruses, polioviruses, -myxoviruses and some other viruses”
What are arboviruses?
Which taxonomic groups have arboviruses?
not formal clade, just epidemiological classificaiton term for disease that are arthropod-borne virus
togaviridae, flaviviridae (the two we will consider) and also bunyaviridae (hantavirus! ahh!)
While most togaviruses and flaviviruses are arboviruses, give an example of each family that are not.
rubella (togavirus)
Hep C (flavivirus)
Describe the similarities between togaviruses and flaviviruses in terms of structure/nucleic acide, etc.
Both togaviruses and flavivirues are basically picornaviruses with an envelope (i.e. small, with single piece of (+)ssRNA for genome, with icosahedral symmetry)
Describe the incubation processes for typical arboviruses.
Arboviruses undergo two incubations:
EXTRINSIC INCUBATION - in the vector (usually mosquito) for ~2 weeks leading to lifelong asymptomatic viremia in the arthropod
INTRINSIC INCUBATION - in the human host for ~1 week
What is the serious disease caused by arboviruses?
Which strains cause it in the US?
Encephalitis
In US, caused by EEE, WEE, SLE, WNV California group of E’s ( and Venzuelan E virus sometimes seen in TX)
Which of the two flaviviridae arboviruses would you rather have?
I’d rather have WNV than SLE
Which of the two togaviridae arboviruses would you rather have?
I’d rather have WEE than EEE.
What is the most common cause of encephalitis in the world?
Japanese encephalitis for which there is a vaccine
Horizontal vs. vertical transmission
Vertical = mother to neonate
horizontal = everything else
What are the two types of viral infection patterns in the neonate? What are their general characteristics?
Give examples of each
Perinatal—less big deal; generally like horizontal transmission in other peds pts (e.g. HIV, HBV, HSV2)
Transplacental—congenital anomalies not seen in horizontal trans of same virus; (e.g. parvovirus B-19, rubella, CMV, lymphocytic choriomeningitis)
What defenses do fetuses have against viruses that manage to make it across the placenta?
1) maternal IgG
2) their own IgM after 4 mos
3) their own INF after 4 mos
4) maybe cell-mediated imm., too
EEE
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
Family = togaviridae (classified also as an arbovirus)
Epidem = only in summer/when mosquitoes are alive; mostly children affected; swampy areas and wetlands are worst hit; also kills local horses; mostly kids
Trans = mosquito—>bird*—>mosquit—>horse/human (DEAD END HOSTS)
*the bird is usually unaffected
Incubation = 1 week intrinsic incubation in host (2 week extrinsic incubation in vector)
Pathogen w/ s/sx = direct viremia (delivered from mosquito’s saliva to bloodstream); sudden onset severe headach, n/v, fever—>mental status ∆s—>seizures and nuchal rigidity—>TWO OPTIONS:
1) if you survive: high %—>severe neuro sequelae
2) if a severe case: paralysis—>coma—>death
—EEE usually causes the worst dz w/ ~50% fatality rate
Dx = isolate virus or incr titer
Prevention = kill mosquitoes; wear repellent; monitor mosquito traps via PCRing ground up dead ones; killed vaccine for horses is available
Tx = none
Compare WEE to EEE
Western Equine Encephalitis
Family = togavirus
similar to EEE w/ higher incidence rate and lower death and permanent neuro sequelae rates; usually infants and adults >50 y/o
SLE
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
St. Louis Encephalitis
Family = flaviridae
Epidem = indigenous to North America more common in urban areas; adults >50y/o are most affected
Trans = maintained by bird—>mosq—>bird cycles w/ humans as DEAD END hosts
Incubation = again two: 1 week in humans two weeks in vector
Pathogen w/ s/sx = most infections inapparent but does cause moderately severe encephalitis w/ 10% fatality; sequalae uncommon
Dx = serologically
Prevention = no vaccine
Tx = no antiviral
WNV
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
Family = flaviviridae
Epidem = urban and rural; causes the most cases of viral encephalitis per year in US now; usually in folks over 60
Trans = birdmosquito—> human DEAD END host (also 10% via blood transfusion)
Incubation = same 2wks in vector 1wk in host
Pathogen w/ s/sx =
Dx = isolate virus from: brain tissue, blood, CSF or detect Abs in CSF or blood; PCR also available
Prevention = no vaccine; screen at bloodbanks
Tx = no antiviral
Dengue
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
Family = flavivirus
Epidem = subtropics and tropics S.E. Asia and Caribbean
Trans = Aedes aegypti—>humans—>A. aegypti (i.e. humans are NOT dead ends!)
Incubation = 1 week in host
Pathogen w/ s/sx = fever, severe retro-orbital headache, myalgia and arthralgia (“break-bone” fever”) and rash
—Dengue Hemmorrhagic fever in those native to endemic areas (likely b/c there are 4 cross-reacting antigenic types); severe/fatal: 2nd infection immune complexes form and then either a) activates complement cascade—>incr vasc perm + thrombocytopenia OR b) virus penetrates monocytes and macrophages—>release hella cytokines
—point: hemorrhage—>hematemesis—>shock—death
Dx = isolate—>cell culture or IgM or 4X IgG at convalesecent vs. acute phase
Prevention = no vaccine; insecticides, drain stagnant water, personal protection
Tx = no antiviral
La fièvre jaune
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
Family = flavivirus (w/in arbovirus grouping, too)
Epidem = endemic to rural tropical Africa and South America; can cause import epidemics in U.S., etc.
Trans = Aedes aegypti—>humans—>A. aegypti (i.e. humans are NOT dead end host)
Incubation = 1 week in host, 2 weeks in vector
Pathogen w/ s/sx = instant viremia due to direct injection by mosquito—>multiplies in vasc endothelium—>worsen viremia—>liver, kidney, spleen—>fever, jaundice, n/v w/ hematemesis
—high mortality, occasional subclinical cases
Dx = PCR of plasma specimen
Prevention = 17-D vaccine is live-attenuated and gives great protection
Tx = ?
Parvovirus B-19
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
Family = parvoviridae
Epidem = super common; 50% adults are seropoz
Trans = can go transplacentally
Incubation =
Pathogen w/ s/sx = RBC precursor tropism—>inhibits RBC synth for ~1 week
—usually just leads to ERYTHEMA INFECTIOSUM w/ sometimes a TRANSIENT ARTHRITIS
—can lead to TRANSIENT APLASTIC CRISIS in pts with pre-existing erythrocytopenia (e.g. sickle); fatal w/o transfusion tx
—HYDROPS FETALIS occurs when transplacental route occurs in 1st or 2nd trimester; still can cause fetal demise (just w/o the hydrops fetalis) in 3rd trimester; massive increase in CO b/c anemia leads to edema, etc.
Dx = IgM (would not be present in immunocompromised pts so PCR from blood); fetal infection use PCR of amniotic fluid
Prevention = none
Tx = pool Ig for chronic/immunocomp. pts
Rubella
Family = ?
Epidem = ?
Trans = ?
Incubation = ?
Pathogen w/ s/sx = ?
Dx = ?
Prevention = ?
Tx = ?
Rubella (a.k.a. “German Measles”)
Family = togavirus (though NOT arbovirus)
Epidem = less contagious than measles; near-universal vaccination in U.S.—>last case 2005
Trans = resp drops (spread one week before and after rash!)
Incubation = 18 days
Pathogen w/ s/sx = resp epithel—>viremia; 3 days of rash w/ fever and lymphadenopathy; even subclinical cases—>lifelong immunity
—TRANSPLACENTAL: cataracts, PDA, deafness, MR; less and less a risk as you move along in pregnancy
Dx = ?
Prevention = live-attenuated vaccine (in MMR); major purpose is to prevent congenital rubella
Tx = ?
togavirus
Nucleic acid set-up?
Virion structure?
How does it multiply?
Examples?
NA = single (+)ssRNA
virion = icosahedral enveloped
REPLICATION:
1) uncoats in cytosol, 2) (+)ssRNA genome is translated into several structural and non-structural proteins (i.e. not just one large polypeptide like poliovirus), 3) makes RDRP to make (-)ssRNA template of its genome, 4) buds out through plasmalemma
EXAMPLES: rubella, arboviral encephalitises (WNV, EEE, WEE, etc.)
parvovirus
Nucleic acid set-up?
Virion structure?
Replicaiton ?
Examples?
NA = single, linear ssDNA
virion = smallest human virus; icosahedral naked
Replication: adsorption—>moves to nuc for replication—>ssDNA has “hairpin loops” that ~=dsDNA where cell’s DNA pol’s synth progeny genomes—>mRNA from dsDNA intermediate by cell’s RNA pols—>assembled in nucleus
EXAMPLES: B-19 (slapped cheeks)
Flaviviruses
Nucleic acid set-up?
Virion structure?
How does it multiply?
Examples?
NA = (+)ssRNA
virion = enveloped
REPLICATION:
1) rep in cyto
2) translate RNA genome into large polyprots
3) cleaved by virion-encoded proteases
Examples: HCV, plus several arboviruses including- Yellow Fever, Dengue, West Nile, St. Louis and Japanese encephalitis
