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Virology > Week 11 > Flashcards

Week 11 Flashcards

1
Q

Arboviruses?

A
  • Arthropod-borne
  • Virus replicates in salivary gland tissue of athropod vector
  • Vertebrate hosts - e.g. pigs and Japanese encephalitis
  • Humans usually incidental hosts - yellow fever, dengue
    *
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2
Q

Arbovirus belongs to which families?

A

Toga, reo, flavi & bunya

All are RNA viruses - use own RNA dependant RNA polymerases (error prone)–> genetic diversity

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3
Q

Arbovirus transmission

A

Bird populations susceptible to WNV, transmitted through mosquitos

Mosquitos –> horses and humans

Dead end host: USUALLY once infected, not able to transmit to a naive athropod, doesn’t develop sufficiently high blood viraemia

Exceptions: dengue and yellow fever - infected humans source of infection to biting mosquitoes

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4
Q

Endemic australian arbovirus

A

Ross river

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5
Q

Flavivirus genome

A

Non structural proteins

Structural - mature virion e.g. capsid, prM protein (cleaved by host proteases when virus exits cell), envelope protein (major surface protein and target of humoral immune response)

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6
Q

Flavivirus replication

A
  1. Enters cell through endocytosis
  2. low pH environment of endosome –> release viral RNA into cytoplasm
  3. 1 long protein generated –> post translationally cleaved, occurs on ER membrane
  4. Viral RNA replicated - encodes RDRNP which introduced mutations
  5. Virus assembly
  6. Virion maturation through exocytic Golgi system - host proteases act on prM protein to cleave it –> mature virion extracellularly
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7
Q

Flavivirus polyprotein

A

Some on cytoplasm some on extracellular side

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8
Q

Flavivirus structure

A

180 copies of E proteins & pRM as dimers

Host purinases cleaved pRM protein

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9
Q

Dengue

A
  • Systemic mosquito-born infection (Aedes aegypti)
  • 4 types - not that similar
  • Member of flavivurs
  • Infection with 1 DENV confers life-long immunity to that type, but not the other 3
  • 2nd infection with different DENV type –> enhanced risk for severe disease
  • No animal model of disease, vaccine or antivirals
  • Mainly pediatric
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10
Q

Flavivirus phylogeny based on gene sequence of ____

A

NS5

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11
Q

2 cycles of dengue

A
  • Urban: between humans, transmitted by mosquitoes
  • Sylvatic: transmit dengue between non-human primates, rarely spilling over to human populations
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12
Q

Features of dengue evolution

A

Purifying selection - virus can’t include too many mutations because it has to be fit for replication in both humans and mosquitoes

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13
Q

Dengue life cycle - Urban cycle

A
  1. Human infected
  2. Mosquito feeds

Extrinsic incubation period: Time takes for virus to infect and replicate in mosquito and to appear in saliva of mosquito (7-15 days)

  1. Mosquito refeeds
  2. Inoculates human –> new infection –> viraemia
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14
Q

Dengue vector

A

Aedes aegypti

Lay eggs in artificial containers

Daytime-biting, preference for humans

Multiple feedings within one reproductive cycle

Mosquito infective for life

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15
Q

Outcomes of DENV infection

A

Mostly asymptomatic (50-70%)

Symptoms: fever, headache, myalgia, fatigue, retro-orbital pain, vomiting, anorexia, joint pain

Severe plasma leakage and haemorrhage - with warning signs

Severe organ impairment - without warning

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16
Q

Risk factors for severe dengue

A

Vascular permeability –> dengue shock syndrome

Risk factors for dengue shock syndrome:

  • Secondary infection
  • young age
  • female
  • High BMI
  • Virus strain
  • Host genetics
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17
Q

Antibody dependent enhancement

A
  • Pre-existing antibodies bind to heterologous serotype but fail to neutralise it –> alter cellular tropism, more cells infected and higher virus burden
  • Seen in secondary infection or primary infection of babies from immune mothers
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18
Q

Capillary permeability driven by

A

…host immune response

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19
Q

Challenges for DENV vaccine

A
  • Acute, self-limiting infection
  • Immune enhancement - protection against all 4 serotypes at once
  • Lack of animal disease models
20
Q

Flavivirus structure - making vaccines

A

Envelope glycoprotein: top-tail dimer

  • Major virion surface protein
  • Induces virus-neutralizing antibody
  • Involved in virus attachment
  • Mediates virus-specific membrane fusion
21
Q

Sanofi pasteur vaccine

A
  • Chimeric vaccine between Dengue and Yellow fever 17D (live attenuated) vaccine strains
  • Swap in prM and E genes from each dengue type into yellow fever backbone
  • 56% efficacy - serotype dependant, doesn’t work that well against Dengue 2
  • 3 dose vaccine, 6 months apart

Other vaccines: attenuated whole virus, DNA vaccine, recombinant subunit vaccine (E protein)

22
Q

Dengue virus treatment

A
  • No licensed vaccine and drugs
  • Vector control - doesn’t work wide scale
  • Indivdually: prevent mosquito bites
  • Avoid ibuprofen, aspirin, Naproxen
  • Rest + fluids
23
Q

Wolbachia

A

Insect bacterium introduced artificially from fruitfly to Aedes aegypti mosquitoes

  • When mosquitoes carry Wolbachia, partially resistant to arboviruses
  • Male wolbachia x WT female –> no eggs
  • Female wolbachia –> normal fecundity
24
Q

Yellow Fever

A
  • Original haemorrhagic disease
  • Female mosquito bites (Aedes, haemagogus, sabethes)
  • Involves mosquito and vertebrate hosts, usually sylvatic non-human primates
  • Safe & effective vaccine developed
  • South America and central africa
  • Jungle –> urban populations
  • Re-emerging, sporadic
25
Q

Yellow fever clinical manifestations

A

Early symptoms: muscle pain, fever, headache

Toxic phase: damage liver, kidneys, heart

Severe: jaundice, kidney failure, internal bleeding, coma

Death: 6-7 days post infection

26
Q

Yellow fever 17D vaccine

A

One of the most efficacious vaccines in use

1 dose, immune for life

Used as vaccine vector for Flaviviruses e.g. dengue, JEV

27
Q

Most viral infections in GIT are ____ infections?

A

Acute

  • When you feel ill/mount detectable immune response - infections are complete
  • Virus has spread to next host
28
Q

Viral gastroenteritis

A
  • Responsible for 75% of infective diarrhoeas
  • 2nd most common viral illness after URT infection
  • Major killer of infants in developing countries
29
Q

Entry via Gi may involve…

A
  1. Local infection - rotavirus, adenovirus, coronaviurs
  2. System - hepatitis A (invasion of tissues underlying mucosal layer)
30
Q

Alimentary tract

A
  • Surface coat of glycoproteins and glycolipid with overlying mucous layer able to be penetrated by adenovirus/Norwalk calicivirus
  • Lymphoid follicles point of entry for some - M cells ingest and deliver antigens to underlying lymphoid tissue by transcytosis
31
Q

Gastroenteritis immune response

A
  • Primary defence = innate
  • Adaptive rseponse: essential for final clearance of virus and providing memory defence
32
Q

Norovirus

A
  • Caliciviridae
  • ssRNA, non-enveloped
  • 1 capsid protein - small as a ribosome (25-35nm)
  • Previous name = Norwalk-like viruses
  • 20% of serious gastroenteritis, 60% of viral gastroenteritis
33
Q

Norovirus classification

A
  • Named after where it is discovered e.g. Hawaii virus
  • Can cross species barrier
34
Q

Norovirus clinical features

A
  • Adults and children equally affected
  • IP: <24 hours
  • Duration of illness: <3 days
  • Nausea, fever, headache (innate response)
  • Abdominal cramping
  • Watery diarrhoea, vomiting
35
Q

Norovirus Genotype GII.4

A
  • Most common variant associated with at least 6 pandemics
  • Demonstrates rapid evolution and antigenic variation (RNAP error prone)
  • 11 breakpoints in NoV GII.4 linkage at 3 recombination hot spots
  1. ORF 1/2 overlap
  2. ORf 2/3 overlap
  3. ORF2 - encodes viral capsid
36
Q

Epidemiology of outbreaks

A
  • Cruishe ships, schools, nursing homes
  • Contaminatd food/water e.g. seafood
37
Q

Why is NoV a class b bioterrorism agent?

A
  • Highly contagious
  • Low infectious dose: 10-100
  • Extremely stable: non-enveloped, exists in environment, resistant to chlorine/alchol disinfectants
  • Associated with debilitating illness
38
Q

Viral excretion & aysmptomatic infections

A
  • Asymptomatic infections - still have seroconversion and shedding of virus
  • Viral excretion 4-6 weeks afer symptoms resolve
39
Q

Transmission of norovirus

A

Primary transmission

  • Contamination of foods in raw material - e.g. oysters
  • Application of contaminated water to fruit/veg crops e.g. leafy vegetable

Secondary transmission

  • Processing, stroage, distribution - infected food handlers, contaminated surfaces, field workers
40
Q

Detection of norovirus

A
  • Stool, vomitus, environmental swabs
  • RT-PCR
  • Serology for epidemiologic purposes
  • No tissue culture system for human norovirus - use mouse norovirus
41
Q

Treatment of norovirus

A
  • Usually runs its course in 1-2 days
  • Hydration - water and electrolytes
  • Avoid sugary beverages - worsen diarrhoea
  • IV fluids and electrolyte resuscitation if nausea is too severe
  • Antiperistaltic agents for severe diarrhoea - not for infectious diarrhoea
  • Symptoms: resolve in 24-48 hours
42
Q

Prevention

A
  • No vaccine
  • WASH hands
  • Sanitize with bleach wash
  • Protect water supplies
  • Education
43
Q

Mouse norovirus

A
  • Tropism for dendritic cells and macrophages
  • Remodels membrane architecture
  • Genome: ++SRNA
  • ORF1 - structural genes e.g. NS6 protease, NS7- RdRP
  • VP1 - capsid, from sub-genomic RNA
  • ORF4: VF1 - virulence factors
  • Processing of polyprotein into individual NS proteins performed by NS6
44
Q

_____ and _____ required for control of MNV-1 infection

A

MDA5: cells deficient in MDA5 cannot produce cytokines

and Stat 1

45
Q

MNV replicates in ______

A
  • Peyer’s patches - can cross intestinal epithelial monolayer via M-cells
  • Infection with some strains of MNV contribute to Paneth cell dysfunction, leading to inflammation (Crohn’s)
46
Q
A

Virology (9 decks)

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