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MIMM 324 > 25. Flavivirus > Flashcards

25. Flavivirus Flashcards

1
Q

what is a well-known flavivirus?

A

yellow fever

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2
Q

describe the clinical features of yellow fever

A

PERIOD OF INFECTION:
- minor symptoms: headache, nausea, dizziness

Some can resolve infection but some progress to
PERIOD OF INTOXICATION:
- severe infection: jaundice, haemorrhage, malaise
- 50% recover, 50% die

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3
Q

what was the Yellow Fever Commission? what were the results?

A

to prove that yellow fever was transmitted by mosquitos

volunteers were bitten by mosquitos that had fed on yellow fever patients –> got mild disease but quickly recovered –> still insufficient evidence

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4
Q

what were the Mosquito Brigades?

A

fumigate mosquitos to eradicate disease in Panama –> it worked!

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5
Q

why did yellow fever remain in areas where they eliminated the mosquitos?

A

mosquitos were only a vector –> non-human primates are the stable and persistent reservoir

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6
Q

development of YFV vaccine (4 stages)

A
  1. isolated virus from yellow fever survivor
  2. grew virus in mice
  3. passaged in monkeys
  4. > 100 passages in chicken eggs to form 17D vaccine strain
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7
Q

describe the 17D vaccine strain of yellow fever

A

attenuated virus that can grow and replicate without pathogenesis –> but still had some neurotropism and viscerotropism

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8
Q

baltimore class of flavivirus?

A

class 4 (+RNA)

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9
Q

is flavivirus enveloped or naked?

A

enveloped

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10
Q

shape of flavivirus capsid?

A

icosahedral

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11
Q

size of flavivirus capsid?

A

40-60nm diameter

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12
Q

3 characteristics of flavivirus

A
  1. monopartite
  2. linear
  3. 9.6 - 12.3 kb
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13
Q

6 main viruses in flaviviridae family

A
  1. mosquito-borne flavivirus
  2. insect-specific flavivirus
  3. tick-borne flavivirus
  4. NKV flavivirus
  5. hepacivirus
  6. pestivirus
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14
Q

what does NKV mean?

A

no known vector flavivirus

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15
Q

biggest group of flavivirus?

A

mosquito-borne flavivirus

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16
Q

who does Japanese encephalitis affect?

A

Children and immunocompromised adults

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17
Q

who does West Nile encephalitis?

A

Elderly, immunocompromised, and chronically ill patients

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18
Q

what transmits the Japanese Encephalitis Virus?

A

mosquitos –> JEV = arbovirus

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19
Q

2 primary hosts of JEV

A
  1. birds
  2. pigs
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20
Q

1 incidental/dead-end host of JEV

A

Humans

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21
Q

number of JEV cases in humans each year? mortality?

A

30,000 - 50,000 cases in humans each year –> 25-30% mortality

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22
Q

4 symptoms of JEV

A
  1. fever
  2. headache
  3. vomiting
  4. neurologic symptoms
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23
Q

JEV treatment?

A

no treatment –> just supportive care

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24
Q

JEV vaccine?

A

either formalin inactivated or live attenuated

recommended for travel >1 month

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25
Q

describe encephalitis viruses

A

most are asymptomatic or cause non-specific febrile illness

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26
Q

who do encephalitis viruses affect?

A

children or young adults

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27
Q

4 symptoms of severe encephalitis viruses

A
  1. meningoencephalitis
  2. aseptic meningitis
  3. polio-like acute flaccid paralysis
  4. parkinsonian syndrome
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28
Q

age-specific incidence of JEV vs WNV

A

JEV more common in younger age and most people are sero-positive

WNV more common in older age and sero-positive is rare

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29
Q

what type of mosquito transmits JEV and WNV?

A

Culex mosquito

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30
Q

primary host of WNV?

A

birds

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31
Q

incidental/dead-end host of WNV?

A

humans + other mammals

32
Q

who does WNV infect?

A

elderly/immunocompromised ppl

33
Q

6 symptoms of WNV

A
  1. fever
  2. headache
  3. vomiting
  4. muscle weakness
  5. lower back pain
  6. neurologic symptoms
34
Q

proportion of asymptomatic vs symptomatic cases

A

80% of cases are asymptomatic

20% of cases are symptomatic and develop into neuroinvasive disease

35
Q

treatment of WNV?

A

no treatment, not even vaccine

36
Q

how is the spread of WNV measured

A

regular monitoring of bird sera

37
Q

what type of mosquitos is Dengue Virus transmitted by?

A

Aedes mosquitos

38
Q

primary host of DENV?

A

humans

39
Q

8 symptoms of DENV

A
  1. fever
  2. headache
  3. vomiting
  4. abdominal pain
  5. low BP
  6. tachycardia
  7. seizures
  8. encephalitis
40
Q

treatment of DENV?

A

no treatment, not even vaccine

41
Q

5 stages in DENV clinical progression

A
  1. mosquito bite
  2. viraemia
  3. fever
  4. shock hemorrhage
  5. antibodies increasingly produced
42
Q

what kills people when they get DENV? % lethality?

A

Dengue Hemorrhagic Fever/Dengue Shock Syndrome –> 50% lethality

43
Q

how has the distribution of DENV subtypes throughout the world changed over time?

A

certain subtypes were only in certain areas, but now all 4 genotypes are everywhere

44
Q

what type of mosquitos transmit Zika Virus?

A

Aedes mosquitos

45
Q

6 symptoms of ZIKV

A
  1. fever
  2. maculopapular rash
  3. headache
  4. joint and muscle pain
  5. edema
  6. vomiting
46
Q

tropism of ZIKV

A

nerve cells –> affects myelin

47
Q

recent ZIKV outbreaks lead to: (2)

A
  1. Guillain-Barre syndrome
  2. Fetal microcephaly
48
Q

treatment of ZIKV?

A

No treatment, but working on antibodies and vaccine

49
Q

2 challenges in studying ZIKV in lab

A
  1. no pathogenicity in mice
  2. can only grow in vitro if antiviral defenses are removed, but this doesn’t give full picture of virus
50
Q

challenge in diagnosing ZIKV

A

diagnosed thru PCR –> hard in 3rd world country where rapid diagnostics are better

51
Q

describe flavivirus genome organization

A

5’ UTR and cap, structural proteins, non-structural proteins, 3’ UTR

52
Q

how many ORF in flavivirus genome?

A

1 ORF with structural and non-structural regions

53
Q

3 structural proteins

A
  1. C (core)
  2. prM/M (membrane)
  3. E (envelope glycoprotein)
54
Q

6 non-structural proteins and functions

A
  1. NS1, NS2A, NS4A (RNA replication complex proteins)
  2. NS3 (protease/helicase/NTPase)
  3. NS4B (membranous web)
  4. NS5 (RdRP, guanyltransferase, methyltransferase)
55
Q

what are the only 2 enzymes of flavivirus?

A

NS3 and NS5

56
Q

relationship btwn NS2A and NS3

A

NS2A associates with NS3 as cofactor to help cleavage activity

57
Q

why is NS5 a guanyltransferase?

A

allows G nucleotide to be added at 5’ end

58
Q

why is NS5 a methyltransferase?

A

allows methylation once G is added at 5’ end

59
Q

describe an immature flavivirus

A

upon assembly, has 60 copies of trimer envelope protein

60
Q

describe production of mature flavivirus from immature flavivirus (4 steps)

A
  1. Immature virus is formed in vesicle in transgolgi
  2. pH in vesicle changes
  3. 60 copies of trimer of envelope protein becomes 90 copies of dimer of envelope protein
  4. membrane protein precursor is cleaved by furin, causing structural change into mature
61
Q

describe flavivirus life cycle (6 steps)

A
  1. enters by endocytosis
  2. in low pH endosome, fusion proteins exposed to allow virus protein to fuse with endosome envelope
  3. +RNA translated into polyprotein
  4. polyprotein cleaved by NS3
  5. making mature enzymes that make -RNA for replication
  6. virus assembles, matures, and is released
62
Q

what residue is crucial on fusion peptides?

A

Histidine

63
Q

describe how pH changes histidine

A

histidine has ring where <pH 6 it is protonated and charged –> changing conformation of protein

64
Q

how does histidine affect viral entry?

A

In acidic endosome, His287 and His438 are protonated allowing for fusion protein to change conformation to allow fusion

65
Q

how does histidine affect virus maturation?

A

In acidic vesicle in trans-golgi, His323 and His146 are protonated to allow change from trimer to dimer for maturation

66
Q

what is the role of furin?

A

allows maturation of membrane protein

67
Q

what facilitates flavivirus replication?

A

genome circularization

68
Q

how does genome circularization occur?

A

5’ and 3’ ends are brought together by base-pairing (H bonds)

69
Q

how does replication begin?

A

stem loop A allows RdRP to bind and begin replication, with methylated cap acting as primer

70
Q

flavivirus replication induces ____ and ____

A

flavivirus replication induces vesicle packets and convoluted membranes

71
Q

where do vesicle packets and convoluted membranes derive from?

A

from rough-ER

72
Q

what are vesicle packets and convoluted membrane?

A

sites of replication

73
Q

why do vesicle packets have pores?

A

exit site for newly synthesized viral RNA

74
Q

describe the assembly of flavivirus

A

occurs next to pores of vesicle packets –> virions stack within lumen of VP-containing ER network then leave via golgi

75
Q

what is DENV antibody-dependent enhancement?

A

people who are reinfected get increased severity of infection

76
Q

why does antibody-dependent enhancement occur? 3 results

A

antibodies from first infection recognize different DENV and allow internalization

  1. leukocytes and BBB cells infected
  2. inflammation and cytokine storm
  3. compromises CNS function

MIMM 324 (37 decks)

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