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Title: Influenza
Description: Useful short questions and answers I wrote based on UCL biomedical sciences third year Influenza lecture.
Description: Useful short questions and answers I wrote based on UCL biomedical sciences third year Influenza lecture.
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Influenza
Questions
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What are the types and subtypes? Which infect humans?
What is it primarily a virus of?
What two reasons can facilitate the accidental infection of other species?
What two protein spikes are on its envelop? What else is on the surface?
What genome does this virus have?
What is the structure of the HA protein? (discuss precursor and metastable states)
How is entry facilitated?
How is fusion facilitated?
What two things can be targeted during this entry/ fusion process?
Upon entry to the nucleus what immediately occurs?
The incoming negative sense genome is in what form?
What are the components of the viral RNA polymerase? This RNA pol lacks activity until
what occurs?
Describe this initial process and elongation
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How does viral exit, i
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budding, occur?
How can budding be inhibited?
Why the need for 8 segments?
What is very noticeable about the distribution of flu?
How many variations of H and N are there? How many infect humans?
What is antigenic drift and shift?
How can shift occur?
Why can pigs be infected with both avian and human flu but humans cant normally be
infected with avian and vica versa?
What were the three serious flu pandemics in the 20 th century? When did they occur?
During the first pandemic, what was the strain? What about the other two?
What made the 2009 swine flu outbreak?
What causes the difference in transmissibility of some flu?
What flu vaccines are there?
Efficacy in inactivated one?
Answers
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Gastric, central, muscular, joints and nasopharyngeal
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Type A and B infect humans, and A subtype H1N1, H2N2, H3N2, H5N1
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Haemagglutinin and neuraminidase
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This cleaves to form the metastable state – homotrimer, with each subunit
composed of HA1 and HA2
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HA1 binds to host cell sialic acid, which allows entry via clathrin-mediated endocytosis
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When the pH = 6 this facilitates pH driven
fusion and the HA changes from a metastable state into its stable state
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The alpha helix of the HA2 then jackknifes bringing the two membranes
together causing complete fusion of membranes
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Inhibitors of HA and inhibitors of the M2 ion channel, as without acidification no capsid
degradation and no infection - amanivir
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RNP (ribonuclearprotein)
PB1, PB2 (endonuclease), PA
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PB1 binds both 3’ and 5’ end of viral gene segment and PB2 provides the cap
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These have the cellular 5’ cap and are
polyadenulated
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vRNP (+ve)
independent
non-resident RNA dependent RNA polymerases I and II
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Then NRP2 binds to the new exposed 5’ end of the replicate causing the association
of NP
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Neuraminidase has enzymatic activity which cleaves host sialic acid, so HA can no longer
bind to it allowing release
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Typically RNA pols cannot access internal promotors, therefore the 8 segments allow
multiple proteins to be made
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6,2
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Shift – big change, recombination event, e
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whole gene segment
changed
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Recombination with another flu strain
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While humans only have one type
of sialic acid… same with birds
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Spanish flu 1918, Asian flu 1969, 1989
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Human HINI recombined with another avian flu (H2N2)
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A pig was infected by a classical swine flu, an avian flu and a human flu
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The combination of HA and NA (144 diff)
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Live attenuated vaccine (cold passage) which is a yearly
guess on the predominant strains (ideally a tetramer)
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Efficacy varies
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Death 80-90%
Title: Influenza
Description: Useful short questions and answers I wrote based on UCL biomedical sciences third year Influenza lecture.
Description: Useful short questions and answers I wrote based on UCL biomedical sciences third year Influenza lecture.