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FunMed Week 8 > Treatment of Viruses > Flashcards

Treatment of Viruses Flashcards

1
Q

how does virus replicate?

A

Varies with each virus but here are the main steps:

Attachment
Entry
Uncoating
mRNA made
Protein synthesis
Virion assembly
Release

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2
Q

what do the following do with rna ?

Reverse transcriptase

Integrase

Protease

RNA polymerase

A

Reverse transcriptase – turns +ssRNA into DNA

Integrase – integrates viral DNA with host genome

Protease – help create viral building blocks

RNA polymerase – forms mRNA before going to ribosome

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3
Q

how does viral evasion of host defence occur?

A

Latency: Dormancy that reactivates when host is immunocompromised e.g. HIV, Herpes
Phagocyte evasion:Prevention of phagosome and lysosome fusione.g. HIV
Antigenic shift and drift: Genetic shuffling and random mutation makes immune system naïve again
Hiding: Within cells: HSV, VZV, malaria

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4
Q

basic ways can prevent viral infection?

A
  • hand hygeine
  • *- cover cough
  • environmental cleaning:**1:10 bleach solution. EPA registered disinfectant
  • PPE
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5
Q

how do viral vaccines work? (basic)

A

viral vaccines: induced a immune repsonse agaisnt viruses in the vaccinated people - helps immune system tofight off future infections. gives immune memory:

  • *immune memory:**
  • rapid increase in response
  • response is faster
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6
Q

what does % of individuals needing to be immunised to acheive herd immunity depend on?

A
  • effectiveness of vaccine
  • characterisitcs of disease

herd immunity creates barriers that protects susceptible people

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7
Q

what is herd immunity?

A

Indirect protection of susceptible individuals from infectious disease when certain percentage of population (normally 95%) has become immune to the disease

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8
Q

what is herd immunity threshold?

Ro ​= ?
1/ Ro = ?
Ro < 1 ?
Ro > 1 ?

1-1/Ro ?

A

Ro = av. number of new transmissions per case over infectious period in sus or non vaccinated pop
1/ Ro = proportion of the population sus. to virus (aka epidemic threshold)
Ro < 1 infection dies out
Ro > 1 infection will spread
Ro = 1 infection stable

proportion of pop. that needs to be vaccinated to eliminate virus: 1-1/Ro

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9
Q

how do you work out what proportion of population needs to be vaccinated?

A

1 - Goal Ro / Current Ro

(goal Ro is 1)

e.g. measles has Ro of 18. so to work out pop that needs to be vaccinated:

1-1/18

= 1 - 0.06

= 94%

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10
Q

if proportion of susceptible individuals is recuded to below X, the diease can be eradicated. what is X?

A

1/Ro

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11
Q

what are different ways can make viral vaccines?

A
  • live attenuated virus (virus is weakend by chemicals or heat inactivation
  • recombinant sub-unit viral protein: part of o.g. virus presented to immune
  • recombinat bacterial vector (take genes of virus and put in bacteria)
  • virus-like particles (look like viruses but dont have pathogen inside, just immunogenic regions required)
  • DNA (inject viral DNA into muscle)
  • *- recombinant viral vector:** (put spike protein into non infectious viral vector, e.g. cold )
  • **synthetic peptides
  • whole inactivated virus**
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12
Q

how do inactiavted vaccines work?

e.g.?

how long does immunity last?

A
  • destroy infectivity but keep the ability to induce immune response (keeps antigenicity)
  • e.g. poliovirus, influenza
  • immunity is often brief: requires boosting
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13
Q

how do live attenuated vaccines work? e.g.?

who cant we give to?

A

Live vaccines use a weakened (or attenuated) form of the germ that causes a disease.

  • long response
  • replication competent but dont cause disease.
  • e.g. measles, oral polio
  • **cant use in immunodeficient patients
  • risk of reversion**
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14
Q

subunit vaccines / virus like particles?

e.g. ?

A
  • break up virus into fragments (like its protein, sugar, or capsid)
  • resemble structure of the virus
  • **no genetic information: safe
  • **cost-effective
  • e.g. HPV and HBV
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15
Q

dna vaccine?

A

no approved vaccines yet!

  • naked DNA
  • does not replicate in viral host
  • go into muscle or skin
  • long lasting
  • dry powder (dont need to fridge)
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16
Q

how can antivirals target viruses?

A

Targets viral replication process:

• Reverse transcriptase: RNA to DNA

  • Integrase: integration of viral genetic material into host genome
  • Protease: cleave precursor proteins
17
Q

what % of pop. needs to be vaccinated for measles?

A

95%

18
Q

why are there so few antivirals?

A
  • the virus life cycle is tied to host cell: difficult to target virus alone
  • viruses are difficult to grow
  • most virus infections are short lived
  • *- compound must block virus replication compelely otherwise the virus will mutate and become resistant**
19
Q

what is herpesvirus?

how work?

A
  • dsDNA viruses
  • stays latent in body after infection:
  • *- chickepon infection:** virus goes into dorsal root ganglia and stays latent and can reemrge later in life as shingles
20
Q

which antivirals do we use for chickenpox and herpes? whats the mechnaism of action?

A
  • *acyclovir**:
  • reduces symptoms but doesnt cure
  • mimics one of the 4 bases for DNA (but misses OH group): **terminates DNA sythesis
  • **prodrug mechanism:
  • has to be activated by HSV enzyme thymdine kinase to add P
  • cellular kinases add 2nd and 3rd P
  • chain termiantes
  • can get resistance
  • need to treat IC patients
21
Q

how do HIV ARV works?

A

drugs: HAART (highly active ART)

Uses a variety of inhibitors in from different classes of anti-viral drugs to reduce the viral load.

  • Entry inhibitors
  • Reverse transcriptase inhibitors (NRTI, NNRTI)
  • Integrase inhibitors
  • Protease inhibitors
  • Fusion inhibitors
22
Q

hiv lifecyle?

A

The seven stages of the HIV life cycle are: 1) binding, 2) fusion, 3) reverse transcription, 4) integration, 5) replication, 6) assembly, and 7) budding.

Binding and fusion (attachment)

  • HIV attaches to a T-helper cell. It then fuses to it and releases its genetic information into the cell.*
  • The types of drugs that stop this stage of the lifecycle are called fusion or entry inhibitor drugs – because they stop HIV from entering the cell.*

Reverse transcription (conversion) and integration

  • Once inside the T-helper cell, HIV converts its genetic material into HIV DNA, a process called reverse transcription. The new HIV DNA then enters the nucleus of the host cell and takes control of it.*
  • The types of drugs that stop this stage of the lifecycle are called NRTIs (nucleoside reverse transcriptase inhibitors), NNRTIs (non-nucleoside reverse transcriptase inhibitors) and integrase inhibitor drugs.*

Transcription and translation (replication)

The infected T-helper cell then produces HIV proteins that are used to produce more HIV particles inside the cell.

Assembly, budding and maturation

  • The new HIV is put together and then released from the T-helper cell into the bloodstream to infect other cells; and so the process begins again.*
  • The type of drugs that stop this stage of the lifecycle are called protease inhibitor (PI) drugs.*
23
Q

what is HIV mutation like? why important?

A

mutates rapidly! use specific targeting of combination therapy: makes it hard for virus to mutate to all of the stages of viral life cycle

24
Q

what are the different types of viral mutations that occur?

A

Antigenic shift: combination of different viral RNA in the host cell to produce a new variant

Antigenic drift: accumulation of random mutations during viral replication

FunMed Week 8 (8 decks)

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