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Microbiology > Viral treatment > Flashcards

Viral treatment Flashcards

1
Q

What is prophylaxis?

A

preventing the disease by either vaccination or by giving drug before infection

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2
Q

Give examples of successful virus vaccines

A

polio

smallpox

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3
Q

What are the main types of viral vaccines?

A
  • live attenuated
  • inactivated
  • purified subunit
  • cloning
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4
Q

Live attenuated vaccines - give examples

A

A natural virus which has had its virulence reduced so it only produces a mild infection.
e.g. smallpox, influenza, measles, pumps, polio, varicella, rotavirus

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5
Q

How are viruses attenuated?

A

• Isolate pathogenic virus from patient
• Grow in human cells
• Take cultured virus and infect monkey cells
Gradually the genome of the virus will adapt to the monkey cells and it will become a monkey virus
• The virus will no longer grow well in human cells

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6
Q

What are the pros and cons of attenuated vaccines?

A

pros:

  • rapid, long lived, broad immunity
  • dose sparing
  • cellular immunity

cons:

  • requires attenutation
  • may revert
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7
Q

What is an inactivated virus vaccine? Give examples

A
  • You take the parental virus and treat it with chemicals and heat to destroy the genome so it is no longer infectious
  • However, if injected into a person, the viral proteins will still be recognised and an immune response will be triggered
  • Getting an immune response from this vaccine is more difficult so you may need to add adjuvants

E.G. polio, rabies, hepatitis A

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8
Q

What are the pros and cons of inactivated vaccines?

A

pros:

  • safe
  • can be made from wild type virus

cons:

  • frequent boosting needed
  • high doses needed
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9
Q

What is a purified subunit vaccine? Give examples

A
  • Original parental genome has been taken and treated with proteases to chop it into little pieces
  • Subunits of the virus which contains antigens that can trigger an immune response
    E.g. influenza
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10
Q

What is a cloned subunit vaccine? Give examples

A
  • Parts of the original viral genome are cloned inside bacteria
  • You can put the DNA into virus-like particles
  • You may just inject viral DNA into people
  • You may make a new virus which doesn’t make people ill but has a segment of virulent material from the original virus
    E.g. hepatitis B, HPV
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11
Q

Which viruses have both live and inactivated vaccines?

A

Polio - inactivated has only spike proteins (HA)

Influenza

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12
Q

Poliovirus - two types of vaccines

A

SALK inactivated vaccine

  • Preparation of virus which has been treated so it can no longer replicate
  • Isn’t a particularly good vaccine - need a large dose

SABINE live attenuated vaccine

  • This is better
  • 1 in 7 million vaccinations result in poliomyelitis
  • If this vaccine was given to people who are immunosuppressed they get a PERSISTING INFECTION - they are reservoirs of live polio virus
  • We must stop using Sabine and switch to Salk for the end game
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13
Q

How can you produce a virus which is immunogenic but not virulent?

A

Pathogenic virus genome typically consists of receptor-binding gene, virulence gene and capsid protein genes

You can either mutate the virulence gene or delete the virulence gene

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14
Q

Rotavirus vaccine

A
  • Rotarix is a live attenuated rotavirus reassortant vaccine
  • Can massively reduce deaths due to rotavirus infection that leads to diarrhoea and vomiting
  • It can cause intussusception (bowel blockage) in older babies (>3 months).
  • So the vaccine is only given to babies <15 weeks
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15
Q

Shingles vaccine

A
  • Painful rash resulting from reactivation of varicella zoster virus infection
  • More common and serious in elderly
  • Even after rash has gone, pain could remain as Post Herpetic Neuralgia (PHN)
  • The live attenuated vaccine is similar but distinct from the chicken pox vaccine
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16
Q

Why was it possible to eradicate smallpox?

A
  • No animal reservoir
  • No latent or persistent infection
  • Smallpox was an easily recognised disease
  • The vaccine was effective against all strains of virus
17
Q

Why is it difficult to target drugs against viruses?

A
  • Viruses don’t have as many distinctive features as bacteria which we can target
  • There isn’t very much that is unique to a virus
18
Q

What is neuraminidase?

A
  • Produced by influenza virus
  • Virus enters the cell by binding to sialic acid
  • During infection and replication, the host cell gradually dies
  • New viruses leave the cell and want to move onto new healthier cells
  • So, virus produces neuraminidase which moves to the cell surface and destroys sialic acid so the original cell is less likely to get infected by the daughter viruses
  • If neuraminidase is inhibited, the enzymes will latch back down to the old cell and will not spread so the infection will be contained within the patient
  • The structure of neuraminidase is well known allowing the design of a substrate analogue
19
Q

Give examples of neuraminidase inhibitors

A
  • Zanamivir

- Oseltamivir

20
Q

HIV treatments and their targets

A

• Nucleoside Reverse Transcriptase Inhibitor

  • Zidovudine
  • Stavudine

• Non-Nucleoside Reverse Transcriptase Inhibitor
Binds enzymes but not at the active site
- Efavirenz
- Viramune

• Integrase Inhibitor (enables genetic material to be integrated into the DNA of the infected cell)
- Raltegravir

•Entry Inhibitors

- Maraviroc which blocks gp120 and CXCR4 interaction 
- Enfuvirtide - binds gp41 which prevents membrane fusion

• Protease Inhibitors
- Atazanavir

21
Q

Hepatitis C

A
  • hepatotropic flavivirus
  • spread widely in the 1970s in blood products before screening was put in place
  • for more than 20 years therapy relied on interferon treatment with ribavirin
22
Q

New antiviral targets for HCV

A
  • NS5B is the viral polymerase that replicates the RNA genome
  • NS5A is the phosphoprotein required by the virus for replication (Daclastivir)
  • Structures of these have been solved using crystallography allowing rational based drug design for Directly Acting Antivirals (DAA)
23
Q

First generation protease inhibitors for HCV

A
  • NS3-4A is the virally encoded protease that processes the polyprotein.
  • The first generation protease inhibitors were telaprivir and boceprivir.
  • Monotherapy results in rapid selection of resistant mutants.
  • They have been used successfully in combination with IFN and RBVN.
24
Q

What is sustained virological response (HCV)?

A

Not only are the patients feeling better, their viral load is going down

25
Q

What is Zmapp?

A

A cocktail of 3 monoclonal antibodies raised against G protein of a previous strain of Ebola virus given as passive immunotherapy. Produced in plants

(Serum therapy: blood from survivors is another forms of passive therapy for ebola)

26
Q

Influenza - treatment

A

Inhibition of M2 channel:

  • Low pH inside the endosome activates the M2 channel
  • Activation and opening of M2 channel on virus capsid allows protons to move into the virus and undo the bonds holding the capsid together
  • This allows uncoating of the virus and the release of its contents into the host cell cytoplasm
  • If M2 is blocked, the virus will remain locked in its own shell and wont gain access to the host cell’s genetic machinery

ADAMANTANES - Amantadine, Rimantadine

  • It is the right shape to fit in the M2 channel and get wedged in there so it stops protons from flowing through the M2 channel
  • However, a single point mutation in the virus genome will mean that amantadine and rimantadine no longer fit in the M2 channel
  • Now, all strains of human influenza are amantadine resistant
27
Q

How are vaccines developed?

A
  • draw replication cycle

- look for anything that can be targetted that isn’t in human cells

28
Q

How are vaccines developed?

A
  • draw replication cycle

- look for anything that can be targeted that isn’t in human cells

29
Q

What is Zidovudine AZT?

A

A nucleoside analogue - first

anti HIV drug but resistance quickly emerged

30
Q

What is HAART?

A

Current HIV therapy - uses three or four different drugs in combination known HAART (highly active antiretroviral therapy). This prevents the virus
from being able to generate resistance mutants but does lead to difficult drug regimens and is associated with significant side effects.

Microbiology (8 decks)

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