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Medical virology > Influenza > Flashcards

Influenza Flashcards

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USMLE® Step 1 flashcards
1
Q

What kind of virus is influenza?

A
  • negative sense ssRNA
  • A, B + C -
    A = public health issue
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2
Q

What is the current status of influenza vaccination?

A
  • available and provides good protection
  • new variants and strains can appear regularly due to antigenic shift
  • vaccines must be regulated constantly
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3
Q

What are the symptoms of the flu?

A
  • headache, fever, cough etc
  • routinely life-threatening in vulnerable patients
  • usually recover in 7-14 days
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4
Q

Describe the epidemiology of influenza

A
  • peaks a troughs as the weather changes throughout the year especially in temperate climates
  • in an edpidemic year 20-30,000 people might die in the UK
  • elderly and young often die as a result of secondary bacterial infecitons
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5
Q

What is the structure of influenza A?

A
  • 8 segments encoding 10 proteins and acessories
  • HA - Haemagglutinin
  • N - neuraminidase
  • MI = matrix
  • M2 = ion channel
  • RNA polymerase
  • Nuclear export protein
  • NP - nucleoprotein
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6
Q

What is the role of the hemagglutinin (HA) segment of the influenza genome?

A
  • major determinant of host range
  • virus attachment factor
  • binds sialic acid on the host cell surface which is different in different animals
  • major antigenic target for antibodies and vaccines
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7
Q

What is the role of the neuraminidase (NA) of influenza virus?

A
  • appears on the infected cell surface and cleaves sialic acids
  • prevents new virus from infected already infected cells to make disease more efficient
  • also allows virus release from the cell surface during budding
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8
Q

What are the roles of the M1 and M2 proteins in influenxa?

A
  • Matrix of the viral capsid that contains everything
  • acid-dependent ion channel on the viral envelope that allows ions into the virion as a decrease in pH is required for release
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9
Q

What is the role of the nuceloprotein (NP) of influenza virus?

A
  • associated with viral RNA
  • one NP monomer per 24 nucleotides
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10
Q

What is the role of the PA, PB1 and PB2 (RNA polymerase)?

What is the role of the nuclear export protein?

A

production and export of viral ribonuclear proteins

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11
Q

How does influenza virus enter the cell and then the nucleus?

A
  • HA attaches and is taken into an endosome
  • endosome is acidified
  • HA is folded and inserts itself into the endosome membrane to allow fusion
  • M2 ion channel allows H+ ions into the virus particle leading to dissociation of the genome from the matrix - leaves the particle and enters the nucleus
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12
Q

What are the basic steps of influenza replication?

A
  • mRNA made from the genome and translated into viral proteins
  • polymerase makes antigenomes that act as a template for viral replication
  • progeny genomes make more mRNA or are packaged and exit at the cell membrane
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13
Q

How does influenza virus use host mRNA to transcribe its own mRNA?

A
  • cap snatching
  • polymerase binds to host mRNA and cuts near the 5’ cap
  • uses the host mRNA as a primer
  • can sometimes result in the production of viral-host fusion proteins that contribute to virulence
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14
Q

Describe influenza serology?

A
  • 16 H serotypes
  • 9 N serotypes
  • many sequence variations within them
  • H1N1 e.g.
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15
Q

What is antigenic drift?

A
  • polymerase can make mistakes that result in new genomes
  • if changes are in major surface proteins such as H/N it can reduce protective immunity in a population
  • accumulation of minor changes can render a vaccine useless in around 4 years
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16
Q

What results from influenza’s ability to infect a variety of animals?

A
  • human trachea epithelium express one type of sialic acid
  • birds express another
  • bigs both
  • pigs can act as mixing pots for different chimeras of the flue
  • human flu doesnt replicate well in birds and vice vera
17
Q

Why can genome assortment in mixing pots occur in influenza?

A
  • genome is segmented with H and N on diffferent segments
  • can give rise to flu that can infect humans + birds or that are different to other flus previously encountered
18
Q

What ist eh structure of the influenza HA protein?

A
  • made as HA0 and cleaved into HA1 and HA2 linked by a disulphide bond
  • cleavage is required for infection
  • when and how cleavage occurs depends on strain and host
19
Q

What other ways can influenza genome reassortment leading to antigenic shift occur other than in pig mixing pots?

A
  • avian infects human and adapts (spanish flu)
  • avian and human infect a human at the same time and reassortment occurs within the human
20
Q

What was the Spsnish flu pandemic:

A
  • worst known flu pandemic
  • mostly healthy 18-30 year olds
  • flu death rate was 25 times higher then usual
  • origin unkown
  • first mild wave followed by a second lethal one
21
Q

Describe the conformational change that occurs in influenza HA in the endosome in more detail

A
  • cleaved protein changes to expose a fusogenic region on HA2
  • enabled fusion of the endox=some and viral membranes
22
Q

What are the 2 possible pathogenic determinants in NA of influenza?

A
  • influenza mutants with no NA aggregate with each other
  • NA affects pathogenicity through HA cleavage
  • mutant NA binds plasminogen on the cell surface and converts it into plasmin which cleaves H0 with no arginine rich region increasing pathogencity
23
Q

What is a likely pathogenic determinant of HA proteins in influenza? on the cell surface

A
  • HA cleavage site changes between strains
  • HA proteins with additional arginines at the cleavage site can be recongnise by intracellular proteins
  • HA proteins can be primed for action as soon as they reach teh cell surface
24
Q

What is a likely pathogenic determinant of HA proteins in influenza? intracellular/extracellular

A
  • HA proteins that aren’t cleaves intracellularly must be matured extracellularly and are less pathogenic
  • in birds, viruses that cleave H0 intracellularly can infect a wide range of organs. those that do it extracellularly can only infect the respiratory tract as the enzymes required for maturation are only available extracellularly in this location
25
Q

How is the genetics of the 1918 Spanish influenza strain analysed? What was seen

A
  • can create recombinant viruses with the genes seen in the strain using reverse genetics
  • HA + NA support lethal infections even without mutations
  • acted synergistically but HA the major determinant
  • NA allows the strain to grow without extracellular trypsin
26
Q

Describe the reverse genetics used to make spanish flu recombinantly

A
  • 8 plasmids each encode 1 segment of the genome and a promoter
  • each produce a segment of RNA like in virus
  • 4 more plasmids contain polymerase and NP with promoters that generate mRNA for these proteins
  • NP is wrapped around the genome and polymerase and creates particles as seen in the nucleus of infected cells
27
Q

What is the role of the 1918 spanish Influenza strain polymerase in its high pathogenecity?

A
  • produces large amounts of mini viral RNAs that bind RIG-1 and trigger expression of IFN-B
  • provides a strong innate immune reponse, cytokine storm and high lethality
28
Q

What was different about the 1997 Hong Kong flu?

A
  • direct transfer from avian to human does not normally occur
  • luckily virus did not apart or reassort in humans so was limited
  • 33% mortality rate
  • has an ariginine rich cleavage site on HA - high pathogenicty
29
Q

What gene doesn’t allow avian flu to replicate in humans?

A
  • ANP32
  • a larger protein in birds than in humans
  • means the polymerase can’t interact with it
  • a point mutation in avian polymerase along with HA sialic acid binding can allow avian flu to jump to humans
30
Q

Are there antivirals against influenza?

A
  • some block M2 function
  • some block NA function
  • side effects
  • only reduce severity + duration
  • must be given witht=in 2 days
  • RNA viruses build resistance very quickly
31
Q

How do Amantadine and Flumadine block M2 function?

A
  • block the M2 ion channel
  • virion is not acidified in the endosome
  • prevents M1 and viral RNA/N protein complexes ffrom dissociating and interferes with uncoating
32
Q

How is a recombinant HSN1 vaccine against influenza produced?

A
  • influenza’s with high growth in chickn embyros have HA and NA genes replaced with H5N1 genes
  • work well in the lab but not as well in practice as you have to guess the strain
33
Q

What vaccine IS routinely used?

A
  • live attenuated vaccine
  • cold-adapted viruses with mutations in polymerase and/or NP
  • given to young children
  • similar to the traditional split vaccine that is made of virus killed by detergents
34
Q

Why is M2 a future target for influenza vaccine?

A
  • M2e extracellular domain is highly conserved among humans strains and overlaos the M1 gene
  • has very little scope for mutational escape
  • reduces mortality and morbidiy but not always disease
35
Q

What are defective interfering particles?

A
  • virus particles with deletions in their largest RNA segments
  • have a replicative advantage due to having a shorter genome but slow or block infection
  • cannot propagate and need normal influenza to infect the same cell to survive
  • can be created by radiation which affects larger segments first
  • works on any strain and may induce an immune response
  • still has HA and N
36
Q

What is Tamiflu and Relenza?

A
  • NA blocking antivirals
  • cause aggregation
37
Q
A

Medical virology (15 decks)

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