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MIMM 324 > Flaviviruses > Flashcards

Flaviviruses Flashcards

1
Q

Where was yellow fever most prevalent

A

when the panama canal was getting constructed

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2
Q

How was yellow fever transmitetd

A

by mosquities
aedes egypti

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3
Q

how did people discover how yellow fever was getting transmitted

A

they recruited volunteers and paid them

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4
Q

what is the type of virus of yellow fever

A

flaviviruses

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5
Q

What put an end to human experiments

A

clara maass a nurse that got paid for be bitted by yellow fever mosquitoes and she got killed

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6
Q

Mosquito brigades

A
  • Colonel Gorgas arrived in Panama as the Chief Medical Officer (1904)
  • Discoveries linking mosquitos with malaria
  • Decides to act on possibility that insects could be transmitting yellow fever
  • In 1905: “mosquito brigades”
    -campaign to fumigate and eradicate the disease
  • By Aug 1906, there were just 7 cases of yellow fever along the Panama canal
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7
Q

Control of yellow fever

A

In 1915, the Rockefeller Foundation funded a project to eliminate breeding places for Aedes aegypti in areas where yellow fever was prevalent

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8
Q

why was yellow fever nor eradicated?

A

-transmission cycle is complicated
-humans get the disease from mosquitoes
-there is a third reservoir: monkeys

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9
Q

facts about the flaviviridae family

A
  • Flavus (Latin = yellow)
  • type virus: YFV
  • Enveloped viruses
  • Icosahedral capsid
  • 40-60 nm in diameter
  • Genome: (+) ssRNA
  • monopartite, linear
  • 9.6 -12.3 kb in length
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10
Q

JEV is part of which virus fam

A

flaviviridae

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11
Q

true or false: JEV is transmitted by mosquitoes

A

true

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12
Q

Hosts of JEV

A
  • Primary hosts: birds, pigs
  • Incidental/dead-end hosts: humans
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13
Q

Symptoms of JEV

A
  • Symptoms: fever, headache, vomiting,
    neurologic symptoms (mental status,
    movement disorders, etc)
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14
Q

true or false: there is a vaccine for JEV

A

true

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15
Q

Encephalitis Viruses facts

A
  • Majority are asymptomatic or cause
    nonspecific febrile illness
  • Primarily affects children or young adults
    (0-15 yrs old) but west nile is older people
  • More severe cases:
  • Meningoencephalitis
  • Aseptic meningitis
  • Polio-like acute flaccid paralysis
  • “Parkinsonian” syndromes (tremor,
    cogwheel rigidity, masklike facies)
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16
Q

how can you get west nile

A

culex mosquitos

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17
Q

host of west nile

A
  • Primary hosts: birds
  • Incidental/dead-end hosts: humans, other
    mammals
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18
Q

who gets west nile virus

A

Primarily elderly/immunocompromised

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19
Q

symptoms of west nile virus

A

Symptoms: fever, headache, vomiting, muscle
weakness, lower back pain, neurologic symptoms (loss
of motor function, encephalitis, meningitis)

20
Q

true or false: the is no vaccine for west Nile virus

A

true

21
Q

true or false: most of the cases of west nile are symptomatic

A

false they are mostly asymptomatic

22
Q

How can you get dengue

A

Arbovirus, transmitted by
Aedes mosquitos (Aedes
aegypti and Aedes albopictus)

23
Q

What are the primary host of dengue

A

human

24
Q

symptoms of dengue

A

Fever, headache,
vomiting, abdominal pain, low
blood pressure, tachycardia,
seizures, encephalitis

25
Q

True or false: there are no vaccines for dengue

A

true

26
Q

True or false: mostly kids get dengue

A

false there is no age distingtion

27
Q

How many subtypes of dengue are there and how are they spreaded our

A

there are four and they are all spreaded out over the world

28
Q

where is zika the most prevalent?

A

in south america

29
Q

how is zika spreaded

A

Arbovirus, transmitted by Aedes
mosquitos (primarily Aedes
aegypti)

30
Q

What are the symptoms of zika

A

Symptoms (20%): fever,
maculopapular rash, headache,
joint and muscle plain, edema,
vomiting

31
Q

when was the last outbreak of zika and what happenend

A

Recent outbreaks (2013-
Present): Guillain-Barré
syndrome and fetal
microcephaly

32
Q

True or false: there is no vaccine for zika

A

true

33
Q

what are the necessities to tackle an emerging virus

A

-model systems
-diagnostics
-vector control
-therapeutic strategies

34
Q

true or false: flavivirus encode for a polyproteins

A

true

35
Q

which +ssrna virus had an immature and a mature configuration

A

flavivirus

36
Q

Virus entry: flavivirus

A
  • E protein mediates attachment to receptor
  • in late endosome, low pH —> E protein
    conformational change
  • sticks into endosomal membrane
  • results in fusion
37
Q

What does facilitate flavivirus replications

A

genome circularizatio

38
Q

what is the ration of + and - strand during replication?

A

there is always more + strands that are being made than - strands

39
Q

Flavivirus replication results in sfrnas

A
  • produced by XRN1 stalling on RNA knots in 3’UTR
  • inhibit antiviral responses in both hosts
  • type I IFN response in mammals
  • RNAi pathway in mosquitos
  • modulate cytopathic effects and cell death in mammals
40
Q

what is srn-1

A

host exonuclease that degrades uncapped RNA

41
Q

How did flaviviruses have to adapt to 2 hosts

A
  • ie. conserved deletions in DENV 3’UTR upon mosquito- adaptation
  • disrupts one of the XRN1- resistant structures
  • leads to different primary sfRNA species
  • increased fitness in mosquitos, reduced in humans
  • reversion of deletions when re-adapted to humans
42
Q

Infection involves a diverse population of viruses: flavivirus mutations

A

-the virus mutates a lot
* flavivirus RdRp’s introduce 1 mutation per new strand on average
* each new host/tissue/cell type will create different
selective pressures
* ie. in mosquitos:
* virus must first escape gut
* virus must eventually enter
salivary glands

43
Q

True or false: flavivirus replication induces vps and cms

A
  • DENV induces rough-ER- derived vesicle packets
    (VPs) and convoluted membranes (CMs)
  • Sites of replication
  • Vesicles have pores (presumed exit site for
    newly synthesized viral RNAs)
44
Q

Flavivirus assembly sites

A
  • Budding viruses can be observed next to the
    pores of VPs
  • Virions stack within the lumen of the VP- containing ER network
  • Virions egress through the Golgi
45
Q

how does flavivirus matures

A

the host furin will cleave the PrM into the M protein so that it is able to fuse with the host membrane

46
Q

DENV Antibody-dependent Enhancement

A
  • Increased severity of secondary infections
  • Antibodies from 1º infection recognize different
    serotypes weakly and facilitate DENV binding and internalization
  • Leukocytes and BBB cells (= encephalitis)
  • Inflammation and cytokine secretion (cytokine storm)
  • Compromises CNS function

MIMM 324 (26 decks)

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