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*B33VPI - Biology & Physiology > Influenza and Cold > Flashcards

Influenza and Cold Flashcards

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1
Q

What are the general symptoms of the common cold?

(Diff. w/flu?) 16:49

A
  • Affects the upper respiratory tract
  • Coughing
  • Sore throat
  • Runny nose
  • Nasal congestion
  • Sneezing (TRANSMISSION)
  • Fever
  • Muscle aches
  • Fatigue
    »> Mainly head symptoms
Flu:
• High fever
• Joint pain
• Muscle ache
>>> Whole body symptoms
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2
Q

What are colds caused by?

A

Several viruses:

  • Rhinoviruses (main cause)
  • Influenza
  • Adneoviruses
  • Human coronaviruses (SARS/MERS)
  • Human parainfluenza viruses, human respiratory syncytial virus (RSV), enteroviruses other than rhinovirus, metapneumovirus too
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3
Q

How does transmission of cold/flu virus occur?

A

Respiratory disease thus:

  • Airborne droplets (aerosols; sneezing, coughing)
  • Direct contact with infected nasal secretions
  • Fomites (contaminated objects e.g. tissues)
  • Hand-to-hand contact (handshake etc.; Contagion film)
  • Hand-to-surface-to-hand contacts (e.g. door handles, lift buttons)
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4
Q

What are fomites?

A

Any object that can transmit pathogens/disease.

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5
Q

Explain the public health campaign: ‘Catch it, bin it, kill it’

A

Catch it:

  • Germs spread easily
  • Always carry tissues and use them to catch cough/sneeze

Bin it:

  • Germs can live for several hours on tissues
  • Dispose of tissue soon as possible

Kill it:

  • Hands transfer germs to every surface you touch
  • Clean hands with soap + water ASAP
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6
Q

What do Rhinovirus, Influenza and Adenovirus have in common?

A
  • ONLY their symptoms (overlapping); they are not related to each other
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7
Q

Describe the differences between Rhinovirus, Influenza and Adenovirus; some common causes of the common cold.

A

Rhinovirus:

  • Small (30 nm)
  • Enveloped
  • ss(+)RNA virus (Baltimore IV)
  • Picornavirus

Influenza:

  • Large (80-120 nm)
  • Enveloped
  • ss(-)RNA virus (Baltimore V)

Adenovirus:

  • Large (100 nm)
  • Non-enveloped
  • dsDNA virus (Baltimore I)
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8
Q

What is SARS and MERS respectively?

A

SARS:
- Severe acute respiratory syndrome

MERS:
- Middle East respiratory syndrome

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9
Q

What are the three genera (genus) of influenza viruses?

A 
Influenza A (widest host spectrum), infects:
- Humans, horses, pigs, other (also marine e.g. seals) mammals and birds (birds more difficult to control)

Influenza B:
- Humans, seals (less likely to catch as smaller host spectrum)

Influenza C (not thought to cause epidemics; only mild respiratory symptoms):
- Humans, pigs and dogs
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10
Q

What are the physical features of the influenza virus?

A
  • Enveloped
  • ss(-)RNA; Baltimore Group V
  • 80-120nm

Characteristic spikes:
• Haemagglutinin (HA)
• Neuraminidase (NA)
»> Proteins on surface of envelope like GP120 in HIV (key role in invasion of cell)

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11
Q

Describe the influenza virus structure.

A
  • Haemagglutinin (HA; Trimer)
  • Neuraminidase (NA; Tetramer)
  • Ion channel (M2; good drug target, goes right through to lumen: RNA)
  • Lipid bilayer
  • Matrix protein (M1, shell)
  • Ribonucleoprotein (RNA, inside envelope)
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12
Q

Describe the influenza genome structure.

A
  • Organised into 8 separate (-) ssRNA molecules
  • 8 RNA non-identical strands, all encode different genes
    E.g. one for NA, one for HA
    • PB2
    • PB1
    • PA
    • HA
    • NP
    • NA
    • M1, M2
    • NS1, NS2
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13
Q

What are the subtypes of Influenza A based on?

A

Based on the HA and NA proteins on their surface:

  • 16 antigenically different HA subtypes (H1 to H16, like 16 different viruses; immunity to H1 does not protect against H11 etc.)
  • 9 distinct NA subtypes
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14
Q

How are the subtypes of Influenza A differentiated?

A
  • Subtypes distinguished serologically

|&raquo_space;> Antibodies to one virus subtype do not react with another

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15
Q

How do Influenza Subtypes occur?

A

In all manner of combinations:
• H1-16
• N1-9
E.g. H1NA (Bird flu), H5N1 (swine flu), H2N3 etc.

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16
Q

What are the nomenclature rules for the Influenza virus?

A

By the following rule:

  • Influenza Type (A, B, or C)
  • Species from which isolated (unless human)
  • Place of isolation
  • Strain designation
  • Year isolation
  • (HxNx) Subtype (for Influenza A only)
E.g:
• A/seal/Massachusetts/1/80 (H7N7)
• A/duck/Hong Kong/960/1980 (H6N2)
• B/Yamagata/16/88 (Human)
• C/Mie/199/2012 (Human)
17
Q

What are the common Zoonotic influenza strains?

A
  • Swine flu (H1N1)
  • Avian (bird) flu (H5N1)
    »> Transmitted by animals
18
Q

Does immunity against one influenza subtype confer immunity to another?

A
  • No
  • Immunity acquired against any particular strain by infection or vaccination confers little or no cross-protective immunity against other subtypes
19
Q

How does the influenza virus attach and enter the host cell?

A
  • HA protein mediates attachments to sialic acid on epithelial cell surface
  • Uptake by endosomes follows (vesicle; but with a membrane too, additional to just an envelope)
    »> HIV (envelope virus too) enters host cell via membrane fusion; influenza is an exception
20
Q

Where is sialic acid on the host cell?

A
  • Sialic acid are the terminal parts of transmembrane glycoproteins
  • Act as attachment sites for influenza viruses
21
Q

Explain the selectivity of influenza viruses.

A

Human influenza viruses:
- Preferentially bind in the α-2, 6 configuration with galactose (glycosidic bond)

Avian influenza viruses:
- Preference for α-2, 3 configuration

> > > Hence why avian flu is not very infectious for humans

22
Q

Why are pigs influenza sluts? (selectivity)

A
  • Have either type of glycosidic linkage between galactose and sialic acid; α-2, 6 or α-2, 3(human vs. avian)
  • Thus makes them susceptible to both human and avian flu viruses
    »> Pigs can be infected with different strains at the same time; co-infection means genes get mixed up, results in avian flu being able to infect humans (gaining α-2, 6 activity)
23
Q

How does influenza strain mixing occur?

A
  • Pigs are susceptible to infection from strains with α-2,6 or α-2,3
  • Genetic exchange between influenza viruses from different hosts can occur in pigs as a result, creating new subtypes
  • Genetic exchange involves random packaging of 8 RNA genes from different subtypes infected
  • Copies of the viral genes from different strains get mixed up inside the host cell and are packaged into new viral particles without regard to their original make up
24
Q

Why does avian flu normally not infect humans?

A
  • Human influenza binds preferentially bind in α-2, 6 configuration with galactose (glycosidic bond)
  • Avian influenza preference for α-2, 3 configuration

> > > Haemagglutinin protein (galactose?) on the outside of the virus has trouble hooking up to the receptor (sialic acid)

25
Q

How does influenza virus uptake by the nucleus occur once the virion is already in the cell?

A
  • Endosome (has lipid bilayer) contains protein pumps which gradually decrease endosomal lumen pH from 7 to 5
  • M2 ion channel (from lumen endosome into viral lumen) is also a protein pump which channels the protons from the endosomal lumen into the virion, lowering the pH
  • Results in FUSION of the viral envelope with the endosomal membrane, and subsequent release of the viral genome (8 x RNA) into the cytoplasm
  • Matrix disassembles, RNA released
  • This occurs via HA (haemagglutinin) fusion peptide (trimer); normally hidden at neutral pH, conformational change of HA at low pH exposes peptide at tops of trimer, inserts into endosomal membrane
    »> Influenza uses its envelope to fuse with endosomal envelope, unlike HIV which fuses with the cell surface membrane
26
Q

Amantadine is a drug used for Parkinson’s. How is it also efficacious for influenza?

A
  • Can be used for influenza as it blocks the M2 ion channel; blocking pump blocks virus release from endosome = blocks virus release from endosome
  • Interferes with the influenza life cycle
27
Q

What is the function of HA (haemagglutinin) of influenza?

A
  • Mediates access to host cell (initial adhesion)

- Trimer mediates attachment to sialic acid and fusion with the endosome (fusion peptide at low pH)

28
Q

What is the function of neuraminidase (NA) of influenza?

A
  • Tetramer
  • Enables viral release from host cell by cleaving sialic acid on host cell and from mucin to allow access to new target cells
  • Virus reinfects old cell as sialic acid closer, but cell is now dead thus NA cleaves glycosidic bond between sialic acid and galactose for release
29
Q

How do neuraminidase (NA) inhibitors work? Give examples.

A
  • Sialic acid-mimic drugs
  • Designed to mimic the NA natural ligand, sialic acid
  • Blocks viral escape from infected cells; virus doesn’t get released from old sialic acid on old cells

E.g.
• Oseltamivir (Tamiflu)
• Zanamivir (Relenza)

30
Q

What are the receptors on the host cell for human rhinovirus (HRV)? What occurs as a result?

A
  • Intercellular Adhesion Molecule 1 (ICAM-1)
  • Low-Density Lipoprotein Receptor (LDLR)
  • Forms endosome etc
    »> HRV upregulates ICAM-1 expression, allowing more virus to infect cells (positive feedback loop)
31
Q

What receptors do Adenovirus bind to on the host cell? (RED)

A

Several receptors:
- CAR (Coxsackie Adenovirus Receptor)
- CD46
- Several integrins, recognising RGD loop
»> Virus can attach w/tip (terminal knob) or base of protruding fibres
> Shape of adenovirus akin to ‘Sputnik’ satellite
> Icosahedral capsid

*B33VPI - Biology & Physiology (8 decks)

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