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Virology > Influenza > Flashcards

Influenza Flashcards

1
Q

Influenza genome

A

Neg. Sense ssRNA => 8 segments

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2
Q

Influenza envelope

A

Host-derived envelope with 2 glycoproteins (Hemagglutinin and Neuraminidase)

M2 ion channel embedded in membrane

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3
Q

Nucleoprotein

A

Covers RNA of Influenza viruses => protection?

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4
Q

Viral polymerase complex

A

Holds together ends of viral RNA
consists of 3 proteins
transcribes -ssRNA to mRNA for translation by host machinery & copy RNA as template = replication

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5
Q

Influenza virus life cycle

A

Entry upon bindingbof HA with sialic acid on cell membrane

Endosome, at low pH e.g. 5.5 => conf change in HA enables fusion woth endosomal membrane

Release genome

import RNA into nucleus

transcription and replication in nucleus

assembly at plasma membrane

Neuraminidase (sialidase) => cleaves interactions btw HA and sialic acid => ensures release

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6
Q

Antigenic variability of influenza

A

diff. subtypes
Infection with one does not protect from infection with other

And variation within subtypes
e.g. H1N1 2005 only weak protection against H1N1 2014

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7
Q

Viral pathogenesis

A

• cell death caused by cytolytic viruses (e.g. influenza destroys respiratory cells)
• immune suppression (e.g. measles)
• immune pathology (Hepatitis B/C) => virus doesn’t kill cells, but reaction to virus by immune system does
• oncogenesis (Hepatitis B/C)

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8
Q

What impacts pathogenesis?

A

Viral strategy (acute, persistent)
Viral tropism (where does virus replicate => respiratory, gut etc
Virus strain
Infectious dose
Host fitness
Host genetics

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9
Q

What are viral strategies?

A

Acute
Latent
Persistent (asymptomatic and pathogenic)

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10
Q

What are advantages and disadvantages of mice and ferrets as model organisms?

A

Mice:
+ low cost
+ transgenic mice
+ immunological reagents => track infection
- don’t reflect disease very well: have to use high doses and causes lower airway tract infection

Ferrets:
+ clinical disease manifestation similar to humans
+ suceptible to unadapted human influenza virus isolates
- complex husbandry requirements
- expensive

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11
Q

Polybasic cleavage site in HA

A

Precursor (HA0) needs to be cleaved into H1 and H2 => connected via disulfide bond

=> marker of virulence

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12
Q

Which proteases cleave viral HA

A

Host cell proteases
HAT (cytoplasmamembrane) TMPRSS2 (cytoplasmamembrane, Golgi)
Furin (Golgi)

HAT and TMPRSS2 limited to respiratory epithelium
Furin ubiquitously expressed in host body

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13
Q

HA Cleavage of diff viral strains

A

Monobasic cleavage site => TMPRSS2 & HAT => local infection (only in respiratory epithelium)
Polybasic cleavage site => Furin => (avian viruses) => systemic infection

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14
Q

Transmission of viruses

A

Vertical transmission

Shedding:
Respiratory secretions
Salvia
Feces
Blood
Urine
Semen
Milk
Skin lesions

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15
Q

Animal models for influenza virus transmission

A

Ferrets
+ display flu-like symptoms
+ transmission pattern reflects situation in humans
- expensive, low numbers of animals

Guinea pigs
+ less expensive, more animals
+/- transmission patterns similar for H3N2 viruses
- do not display flu-like symptoms

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16
Q

What types of transmission can be studied?

A

Contact transmission
Respiratory droplet transmission

17
Q

Transmission of influenza viruses depends on

A

Temp.
Low temp. favours virus transmission

Humidity
Low humidity favours transmission

18
Q

Vaccines

A

Biological perpetration that provides immunity against a disease, typically contains a modified form of a pathogen

Goal: faster and less harmful immune response, avoid disease upon encountering a pathogen

19
Q

First vaccine

A

Smallpox
Milkmaids immune => injected a boy with fluid from lesion of a milkmaid

=> infects boy with smallpox and boy survived

Vaccine led to eradication of smallpox in 1980

20
Q

What are conditions for virus eradication programs?

A

Virus must have only one host (human specific)
Vaccine must confer lifelong protection

Current programsto eliminate polio and measles

21
Q

What conditions must be met for enabling virus eradication programs

A

The virus must have only one host (human-specific)
The vaccine must confer lifelong protection

Current programs to eliminate polio and measles

22
Q

Passive immunization

A

Components of immune response (antibodies) from donor

(Post-exposure e.g. rabies or prophylaxis for immuno-compromised)

23
Q

Active immunization

A

Induction of a protective immune response in a patient

24
Q

Attenuated live vaccines

A

Weakened virus
Can replicate and induce potent immune responses but not cause disease in humans and not transmit

=> passage viruses in animals/cell cultures => adaption to other hosts => bring back into humans

25
Q

Rationale design for attenuation

A

Study pathogenesis of virus => genetically modulate viruses

26
Q

Pros and Cons of live attenuated vaccines

A

Pros:
Potent, long-lived immunity

Cons:
Transmission of undiscovered viruses from cell line/medium used
Viruses may gain back virulence

27
Q

Pros and cons of inactivated vaccines

A

+Inactivation with formalin or beta-propiolactone is fast and virologically safe

  • inactivation may lead to alteration in antigenic surface
  • not suitable for all viruses
  • inactivating substances often present in injection solution
28
Q

How many doses of vaccines?

A

Inactivated: multiple boosts
Live attenuated: replication, strong immune response after one dose => & more long lived

29
Q

mRNA vaccine

A

Two doses required
Strong antibody and T cell response
safe
duration of protection not clear yet

Chemically modified (not immunogenic => should get translated in cells => reaction to protein) mRNA of vaccine encodes for spike protein

=> enveloped in lipid nanoparticles

30
Q

Antivirals against

A

HIV & Hepatitis C (no vaccine available)
Herpes
Influenza (limited success)

Less success than vaccines
Not many
Most of the ones we have against HIV

31
Q

HIV treatment

A

Different drug classes inhibit different (all) steps of viral lifecycle

Standard triple therapy (usually 2 reverse transcriptase inhibitors and 1 integrase inhibitor)

Multiple combinations possible => low chance of resistance and even then there is the possibility to switch to other drugs

Control of viral replication, no cure!

32
Q

Hepatitis

A

Inflammation of the liver
HCV can cause chronic infection that increases risk of liver cirrhosis and hepatocellular carcinoma

Transmission through blood/sexual contact/vertical transmission

33
Q

Anti-HCV treatments

A

Previous:
INF + Ribavirin (50% success)
HCV protease inhibitors + INF + Ribavirin (70-80%)

Current:
IFN-free, combination of 2-3 HCV protease, polymerase and NS5A inhibitors
(95-100% success rate, very few side effects)

34
Q

HepC vs HIV treatment

A

HIV infection cannot be cleared, HCV can

35
Q

Influenza antivirals

A

Inhibitors of viral ion channel M2: Amantadine, Rimantadine (also used for parkinson’s disease)
=> block entry: release of genome
=> current strains all resistant to M2 inhibitors!

Inhibitors of viral neuraminidase NA: Oseltamivir, Zanamivir, Peramivir, Laninamivir
=> block release of virus
=> have to be given early!

Inhibitors of viral endonuclease PA:
Baloxavir: inhibits part of viral polymerase
=> block transcription

Virology (2 decks)

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