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IMIN 324 > Viral infection strategies > Flashcards

Viral infection strategies Flashcards

1
Q

How did the first virus evolve likely?

A

first parasite existed in the form of endogenous transposing virus

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2
Q

When did herpesvirus arise?

A

500mya to paratize the neural nets of cnidarians (jellyfish)

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3
Q

What are Koch’s postulates?

A
  1. the microorganism must be found in abundance in all organisms suffering from the disease but shouldn’t be found in healthy organisms
  2. the microorganism must be isolated from a diseased organism and grown in pure culture
  3. the cultured micoorganism should cause disease when introduced into a healthy model organism
  4. the microorganism must be reisolated from the inoculated, diseased experimental host and indentified as being identical to the original specific causative agent
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4
Q

What are the four courses of virus infections, describe each one and name a virus for each course of infection

A
  1. aboritive infection - virus infects a cell but cannot complete the entire rep cycle
  2. acute infection - virus is completely eliminated by the immune system and immune memory is developed (e.g. rhinovirus)
  3. chronic infection - not cleared by the host; virus is present and replicating within the host for its entire lifetime (e.g. HIV)
  4. latent infection - a period following an acute infection in which the viral genome is present in cells but viral genes are not expressed and no replication occurs (e.g HSV-1)
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5
Q

What are the three basic requirements for successful infection within a host?

A
  1. sufficient virus to initiate infection
    - this is a substantial barrier to infection
    - one virion may be sufficient for infection in tissue culture but not in the host
  2. cells at the initial site of infection must be susceptible
  3. host antiviral defense must be absent or ineffective initially
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6
Q

What are the three entry routes into the body and describe each route?

A
  1. skin is a highly effective barrier
    - requires skin abrasions for infection
  2. alimentary canal (mouth/gut)
    - viruses that infect via this route have to survive/remain viable in a hostile environ
    - there is constant opportunity for infection
  3. respiratory tract
    - most frequent site of infection
    - these viruses are transmitted to and form the respiratory tract on saliva droplets and in aerosols
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7
Q

How is ebola transmitted, where is it’s spread amplified?

A

transmitted via blood and sputum contacting the mucus membranes, especially the conjunctiva of the eye

in a resource poor, setting hospitals are amplification nodes

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8
Q

How can the natural environment be a barrier to infection?

A

UV, pH, temperature, and humidy/drying

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9
Q

What is vertical transmission, name a virus that uses vertical transmission?

A
  • transmisson from one generation of hosts to the next
  • can occur by infection, before, during, or shortly after birth
  • can also involve direct transmisson of the virus via the germline itself
  • e.g. rubella, HSV, HIV
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10
Q

What is horizontal transmission, name a virus that uses this?

A
  • direct host to host transmission
  • requires a large rate of infection to be maintained in a population
  • most usual reservoirs are humans and animals
  • e.g. varicella-zoster virus
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11
Q

Could ebola mutate to become airborne and transmitted as easily as seasonal influenza?

A

Highly unlikely - viruses already replicate as fast as they can (they are optimized), so it would require a lot of pressure to mutate to become airborne

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12
Q

What are Schlieren optics?

A

tool to visualize the dispersion of expelled air during coughing

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13
Q

How can respiratory viruses enter via the eye (conjunctiva)?

A
  • the conjunctiva is a highly vascularized area with ready access to the blood stream and many different types of cells
  • likely seeded by digital transmission
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14
Q

What is the typical course of an infection?

A
  1. symptoms occur after incubation period
  2. immune response is initiated (plays a significant role in disease)
  3. specific organs and tissues are infected
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15
Q

What is the incubation period? What occurs during this time? Why is there an incubation period even?

A
  • time between initial infection and observed clinical features of the disease
  • this period ranges in the time depending on the virus
  • only a limited amount virus is introduced (takes time of replication)
  • must overcome the host immune response
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16
Q

What is the incubation period for ebola Why?

A

7-21 days
- depends on the amount of inoculum exposed to
- takes time to amplify in early target organs like the liver, spleen and lymph nodes

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17
Q

What is virus tropism, what kind of tropism does Hepatitis viruses and HIV have?

A

tropism = the propensity of a virus to infect and replicate in a particular cell type or tissue

Hepatitis -> hepatotrophic
HIV -> T-trophic or M-trophic

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18
Q

What are the three main modes of virus spread in the host? Briefly describe each mode. Which is the most fequent?

A
  1. direct cell-cell contact
    - major factor for virus spread and is determined by the presence of virus specific cellular receptors
  2. viremia
    - spread via the blood stream
    - most frequent mode of spread
  3. nervous system viruses (neurotrophic)
    - can directly infect neurons or they can 1st spread via viremia
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19
Q

What are the three ways that viruses can travel in the blood?

A
  1. spread by free virus
  2. spread by infected lymphocyte
  3. spread by virus attached to the surface of cells (e.g. HIV)
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20
Q

What virus infects B cells?

A

Epstein-Barr

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21
Q

What viruses infect T cells?

A
  • HIV
    -HTLV
  • Human herpes 6
  • human herpes 7
  • VZV
22
Q

What viruses infect monocytes/macrophages?

A
  • HIV
  • rubella
23
Q

VZV:
- how does it transmit
- where does it infect first
- how long is the incubation period
- what kind of virus is it
- what distinguishes the acute vs recurrent form
- what is the big symptom
- what is the infection course (acute, chronic, latent, etc)
- how does the virus spread in the body

A
  • transmits via the airborne route (via respiratory droplets of shedding from pox)
  • begins replication in upper respiratory tract
  • incubation = 20 days
  • herpesvirus
  • varicella = chicken pox (acute), zoster = shingles (recurrent, delayed)
  • symptom = rash that develops into pustules
  • latent virus infection
  • spreads to lymph nodes and infects monocytes, primary viremia, virus spreads to epithelial cells, pox on skin
24
Q

How does shingles occur, what is the mechanism? Can it transmit?

A
  • virus is sequested in neurons
  • reactivation likely caused by stress and waning immunity
  • reactivation -> travels down neurons -> skin rash
  • shingles cannot spread from person to person, but causes chickenpox in unvaccinated individuals
25
Q

Describe the VZV vaccine

A
  • live attenuated vaccine
  • vaccine is generated via serial passage
  • virus as several mutations
  • virus replicates efficiently in human cells, but doesn’t pass human to human
26
Q

What kind of protection does the VZV vaccine offer? Why do we vaccinate against an acute/nonlethal virus? Describe the Zostavax vaccine

A
  • shingles is often very painful and can lead to serious health complications
  • vax -> leads severe shingles

Zostavax:
- higher concentration version of the normal chicken pox vaccine
- effectively stimulates immune response and prevents shingles

27
Q

What is the tropism of rabies rhabdovirus?

A

Neurotrophic
- perfers to replicate in neuons
- can replicated in epithelial cells

28
Q

Describe how rabies transmits/life cycle

A

bite -> limited replication at wound site (tingling sensation at bite site) -> spreads to nerve at site of infection -> replicates to high levels -> infect neurons of the CNS -> virus replication -> behavioural changes and moves to salivary glands -> bite

29
Q

How is rabies diagnosed?

A
  • preliminary diagnosis is based upon obvious neurological symptoms
  • brain biopsy performed post-mortem using anti-rabies virus Ab.s
30
Q

How is rabies prevented?

A

prevention and control of infected animal populations: vaccination, quarantine, culling

don’t handle bats

31
Q

What is the treatment for rabies? Why does this treatment work?

A

Vax those at high risk with a heat killed vaccine
- post exposure vaccination is effective due to the long incubation period
- body creates lots of anti-rabies Ab.s

32
Q

Describe the infection course of HSV-1 (where does it begin replicating and where does it end up, etc)

A
  1. replicates in mucosal epithelial cells
  2. results in early/IE and late gene expression
  3. acute infection that’s cleared by the host immune response
  4. virus infects nearby neurons
  5. virus travels down the neuron to the cell body where it becomes latent
    - viral DNA is episomal and associated with histones
33
Q

How does HSV-1 maintain latency in neurons?

A

Latency associated transcripts (LAT) are present during latency:
- no protein encoded
- the LAT is the only region that is transcriptionally active during latency
- LAT regulates histones and promotes the localization of the virus episome into heterochromatin
- necessary for reactivation from latency

34
Q

Why is it important for RNA to be used to maintain latency is HSV-1?

A

Can’t be presented on MHC -> no immune response

35
Q

What viruses belong to the family flaviviridae?

A
  • yellow fever
  • West Nile virus (WNV)
  • HepC
  • Zika
36
Q

What are the three genera in the family flaviviridae, name a representative of each genus?

A
  1. pestivirus
    - e.g. bovine viral diarrhea
  2. hepacivirus
    - e.g. HepC
  3. flavivirus
    - e.g. WNV and zika
37
Q

Describe the genome of flaviviridae (what is the nucleic acid, and what proteins does it encode?)

A
  • (+)ssRNA
  • a single polyprotein is translated from the RNA genome and is proteolytically cleaved into individual proteins

Structural Proteins:
- C = capsid protein
- M = structural protein of lipid envelope
- E = envelope protein, assembly, binding, fusion, elicits most Ab.s

Non-structural proteins:
- Ns5 = RdRp

38
Q

What is the morphology of flaviviridae (capsid, env?, appearance)

A
  • capsid = icosahedral
  • contains a lipid env (contains two proteins = E +pM)
  • appears as rough spheres under EM
39
Q

How is zika virus spread?

A

Mosquito-borne virus

40
Q

What is zika’s transmisson cycle?

A

sylvatic cycle (jungle) -> urban cycle via mosquito transmission

41
Q

How severe are the zika symptoms?

A

mild:
- symptoms last 2-7 days
- only 1/4 people show any symptoms at all

42
Q

What are the potential complications of zika?

A
  • microcephaly
  • gullian barre syndrome
43
Q

Could ebola be transmitted by mosquitoes (viremia)?

A

No, ebola has not evolved with mosquitoes (can’t infect mosquito cells) - there are barriers to infection; probably degrades in the gut of mosquitoes

44
Q

Describe flavivirus replication in mosquitoes, also note what factors affect replication, and what kind of transmission occurs mosquito-mosquito?

A
  1. virus multiplies in midgut epithelia
  2. body cavity
  3. salivary glans

depends on:
- amount of virus
- time
-temperature

vertical transmission and over wintering do occur

45
Q

Describe the general scheme of flavivirus infection

A
  1. subcutaneous injection
  2. regional lymph nodes
  3. plasma (viremia)
  4. epithelium
  5. neurons
46
Q

What is the tropism of flaviviruses?

A

neurotrophic

47
Q

Why are sentenial chickens used to surveillance WNV?

A
  • highly susceptible
  • produce a lot of Ab.s -> take sera -> look for anti-WNV Ab.s -> if positive put out public health notice
  • resistant to mortality
  • non-infectious to each other, handlers and mosquitos
48
Q

Describe the structure of lamda phage

A
  1. isometric head
  2. dsDNA
  3. non-contractile tail
49
Q

Describe the two lifecycles of lamda phages

A

Lytic infection:
1. phage DNA enters bacterium
2. genes ts in set order
3. phage genetic material is replicated
4. phage is released when the bacterium lyses

Lysogenic infection:
1. phage DNA enters bacterium
2. phage DNA is integrated into bacterial genome
3. phage DNA is excised from bacterial genome upon stimulus/stress on bacterium
4. lytic pathway occurs

50
Q

How does the lytic infection of lamda phage occur? Lysogenic infection?

A

Lytic:
Cro protein inhibits cI transcription -> inhibits expression of integrase gene -> favors lysis

Lysogenic:
cI protein inhibits cro transcription -> inhibits expression of genes for replication and structural proteins -> favors lysogeny

51
Q

How are the levels of Cro and cI altered in lamda phage?

A

Metabolic conditions alter relative transcription of cI and Cro:
- lysogency favoured in healthy cells
- lysis favoured in unhealthy cells

IMIN 324 (14 decks)

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