Freshers Flu

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153 Terms

1
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Which influenza viruses cause the disease spectrum known as flu in humans?

Influenza A and influenza B viruses.

2
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Which three membrane glycoproteins are present in influenza A?

Haemagglutinin (HA), neuraminidase (NA) and Matrix-2 (M2).

3
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Which major variable antigens of influenza are targeted by vaccination?

Haemagglutinin (HA) and neuraminidase (NA).

4
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Which seasonal influenza A subtypes are identified in the reading as circulating in humans?

H1N1 and H3N2.

5
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How does influenza C generally differ clinically from influenza A and B?

Influenza C generally causes mild upper respiratory tract illness resembling the common cold, and lower respiratory complications are rare.

6
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What type of molecule is haemagglutinin?

A membrane glycoprotein of influenza virus.

7
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What two functions does influenza haemagglutinin perform?

Haemagglutinin acts as both an attachment factor and a membrane-fusion protein.

8
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What host-cell structure is recognised by influenza haemagglutinin?

Sialic acid on the surface of target cells.

9
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What is the key role of the HA-sialic acid interaction?

It allows influenza virus to attach to susceptible host cells and supports viral entry.

10
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On which cells or tissues does the reading specifically describe sialic acid as being present?

Erythrocytes, upper-airway cells and lung endothelial cell membranes.

11
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What is haemagglutination?

The formation of a network or lattice of interconnected erythrocytes and influenza particles caused by viral HA binding sialic acid on red blood cells.

12
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Why can influenza virus cause haemagglutination of red blood cells?

Influenza HA can bind sialic acid on erythrocytes, linking viral particles and RBCs into an interconnected lattice.

13
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How many haemagglutinin types are described in the reading?

At least 18 HA types.

14
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Are all known influenza haemagglutinin types able to facilitate entry into human cells?

No. Not all HA types can facilitate entry into human cells.

15
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Which haemagglutinin types are described as typically occurring in human influenza viruses?

H1, H2 and H3.

16
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Which HA subtype is associated with the avian influenza H5N1 example in the reading?

H5.

17
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What does the H5 example illustrate about viral protein mutations?

The reading states that H5 was previously unable to infect humans but that single amino-acid changes allowed it to do so, illustrating that small protein changes can alter host-cell entry properties.

18
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Which additional avian-associated HA type has been observed infecting humans according to the reading?

H7.

19
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What type of molecule is influenza neuraminidase?

A membrane glycoprotein and glycoside hydrolase enzyme.

20
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What does influenza neuraminidase enzymatically cleave?

Sialic-acid side groups from glycoproteins.

21
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Why is neuraminidase-mediated cleavage of sialic acid important?

It allows influenza virions to be released from cells rather than remaining attached through HA-sialic acid interactions.

22
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What would happen if influenza HA functioned normally but neuraminidase could not cleave sialic acid?

Virions would attach and enter through HA, but the index virus or progeny would have difficulty leaving the cell because HA would remain bound to sialic acid.

23
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How many neuraminidase types are described in the reading?

At least 9 NA types.

24
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Can different neuraminidase variants differ in virulence?

Yes. The reading states that some NA variants are more virulent than others.

25
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What is the simplest functional distinction between HA and NA?

HA enables attachment and entry into the target cell, whereas NA cleaves sialic acid to facilitate release and onward infection of other cells.

26
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Why must influenza balance HA-mediated binding with NA-mediated release?

HA attachment is required for infection, but without NA-mediated sialic-acid cleavage the virus would remain bound and would be unable to spread efficiently to additional cells.

27
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Which two mechanisms described in the reading alter influenza genetic material and antigens?

Antigenic drift and antigenic shift.

28
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What is antigenic drift?

Natural mutation over time producing small genetic changes in a known viral strain.

29
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Does antigenic drift occur continuously or as a single abrupt event?

It occurs progressively through natural mutation over time.

30
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What is the initial immunological effect of very small genetic changes caused by antigenic drift?

Small changes may initially leave antigenic properties sufficiently similar that the immune system can still recognise the virus.

31
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What happens as antigenic-drift mutations accumulate over time?

The virus can become antigenically different enough that previously acquired immunity recognises the virus less effectively and people can become susceptible again.

32
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How can antigenic drift produce vaccine mismatch?

Accumulated mutations can alter circulating viral antigens so immunity elicited against an earlier strain matches them less effectively.

33
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Why does antigenic drift contribute to the requirement for updated influenza vaccines?

The antigenic properties of circulating influenza viruses can change progressively, meaning vaccines may need to be updated to reflect circulating strains.

34
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Does antigenic drift occur in all influenza subtypes?

Yes. The reading states that antigenic drift occurs in all influenza subtypes.

35
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What is antigenic shift?

An abrupt major alteration in influenza A genetic material associated with reassortment that generates substantially different antigenic characteristics.

36
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Which influenza type undergoes antigenic shift according to the reading?

Influenza A.

37
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Why can antigenic shift produce a pandemic risk?

The new antigenic material may be so different from previously circulating human influenza that most people have little or no pre-existing protection.

38
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What is reassortment in influenza A?

When different influenza strains infect the same cell, their genetic material can combine so progeny contain new combinations derived from the parent viruses.

39
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What happens when two distinct influenza A strains simultaneously infect the same cell?

Their genetic material can reassort, potentially producing progeny with new HA/NA combinations or other new combinations of genetic material.

40
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Why are pigs important in influenza A antigenic shift?

Pigs can be infected by both human and avian influenza A strains and can therefore provide an opportunity for their genetic material to reassort.

41
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Why is simultaneous susceptibility to human and avian influenza important in pigs?

It provides an opportunity for viruses from the two influenza pools to infect the same host and generate reassorted viral genetic material.

42
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What two properties would make a newly reassorted influenza virus particularly concerning for humans?

It would need to remain capable of infecting humans while possessing antigenic material that is new or substantially different to that previously encountered in humans.

43
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Why can avian influenza provide antigenic material that is unfamiliar to humans?

Birds carry numerous influenza HA types, not all of which are normally able to infect humans.

44
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Why does antigenic shift require more than simply an ordinary point mutation?

Shift involves a major genetic and antigenic change associated with reassortment of genetic material, whereas individual accumulating mutations characterise drift.

45
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What is the key difference between antigenic drift and antigenic shift?

Drift is gradual accumulation of small mutations, whereas shift is an abrupt major antigenic change associated with genetic reassortment.

46
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Which process is more likely to gradually erode recognition by existing immunity: drift or shift?

Antigenic drift.

47
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Which process is associated with the sudden appearance of highly antigenically novel influenza A: drift or shift?

Antigenic shift.

48
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Does antigenic shift require the HA or NA subtype number to change?

No. A virus can undergo antigenic shift if reassortment produces sufficiently different antigenic material even when the HA/NA subtype designation remains the same.

49
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Why is the 2009 H1N1 influenza pandemic a useful example of antigenic shift?

The virus remained designated H1N1 but contained a new combination of genes and was sufficiently antigenically different to spread rapidly in humans.

50
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What misconception about antigenic shift does the 2009 H1N1 example correct?

Antigenic shift does not necessarily mean a visible subtype-number change such as H1 becoming H5; major antigenic novelty can arise while the subtype designation remains H1N1.

51
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What is the high-yield chain explaining antigenic drift?

Repeated small mutations → gradual alteration of viral antigens → reduced recognition by existing immunity → possible reinfection or vaccine mismatch.

52
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What is the high-yield chain explaining antigenic shift?

Co-infection by genetically different influenza A viruses → reassortment → major antigenic change → little population immunity → potential pandemic spread.

53
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What is "Freshers' flu"?

"Freshers' flu" is a colloquial term for respiratory illness occurring when many people from different places come together in close proximity; it is not caused by one specific pathogen and may be caused by a variety of respiratory viruses.

54
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Why are new university students particularly susceptible to respiratory viral infections?

Risk factors include close proximity and crowding, meeting many new people carrying different viruses, lack of sleep, psychological stress, alcohol consumption and poor diet.

55
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Why does meeting people from different geographic regions increase the risk of respiratory infection?

Different populations may have somewhat different circulating respiratory viruses, so individuals may encounter viral variants that their immune systems have not previously recognised.

56
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What are important general risk factors for more serious viral respiratory infection?

Extremes of age, chronic diseases such as diabetes, asthma and heart disease, immune disorders or immunosuppression, pregnancy, living in long-term care facilities and severe obesity.

57
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How does crowding increase the risk of respiratory viral infection?

Close proximity increases opportunities for transmission between people, and shared environments increase exposure to contaminated surfaces and respiratory viruses.

58
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How can lack of sleep increase susceptibility to infection?

Adequate sleep supports immune function; prolonged sleep deprivation is associated with worse immune responses and increased susceptibility to respiratory infection.

59
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How can psychological stress increase susceptibility to infection?

Prolonged stress can increase cortisol; high sustained cortisol concentrations can suppress aspects of immune function and increase susceptibility to infection.

60
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Why does moderate exercise tend to be associated with lower infection risk than physical inactivity?

Moderate exercise supports general physiological function and circulation, which can aid movement of immune cells around the body.

61
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Why can extreme exercise potentially increase infection susceptibility?

Extreme exercise is a substantial physiological stressor, increases demands on bodily resources and can increase stress hormones such as cortisol, potentially impairing immune function.

62
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Why can the relationship between exercise and risk of respiratory infection be described as U-shaped?

Infection risk may be greater with physical inactivity, decrease with moderate exercise, and then increase again with very intense or prolonged exercise.

63
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Why can poor diet increase susceptibility to infection?

Effective immune function depends on adequate nutritional resources, so inadequate nutrition can impair normal immune responses.

64
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Why can heavy alcohol consumption increase susceptibility to respiratory infections?

Alcohol in sufficient quantities can impair normal immune function and therefore contribute to susceptibility to infection.

65
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What is the most common viral cause of the common cold?

Rhinoviruses are the most common cause, although many different viruses can produce common-cold symptoms.

66
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Is the common cold a single viral disease?

No. More than one type of virus can produce the syndrome called the common cold, including many rhinoviruses and some coronaviruses.

67
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What virus causes COVID-19?

SARS-CoV-2, which belongs to the coronavirus family.

68
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Why can some coronaviruses cause a common cold while SARS-CoV-2 causes COVID-19?

Coronavirus is a family containing multiple viruses with differences in viral proteins, host-cell targets, tissue distribution, immune responses and other biological properties; SARS-CoV-2 is the particular coronavirus responsible for COVID-19.

69
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What is the major host-cell receptor used by SARS-CoV-2?

ACE2.

70
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Which viral structure of SARS-CoV-2 interacts with ACE2?

The viral spike protein.

71
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What is the functional importance of the SARS-CoV-2 spike protein binding ACE2?

Binding to ACE2 allows SARS-CoV-2 to attach to host cells and supports viral entry.

72
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What host-cell molecule does influenza virus bind during attachment?

Sialic acid on host-cell surface glycoproteins.

73
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Which influenza viral protein binds sialic acid?

Haemagglutinin (HA).

74
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What is haemagglutinin?

A membrane glycoprotein of influenza virus that functions as an attachment factor and membrane-fusion protein.

75
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What is the essential role of influenza haemagglutinin in infection?

Haemagglutinin binds sialic acid on susceptible host cells, allowing influenza virus to attach and subsequently enter the cell.

76
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Where is sialic acid relevant to influenza attachment found?

Sialic acid is present on cell-surface molecules including those of upper-airway cells, lung endothelial cells and erythrocytes.

77
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Why is influenza haemagglutinin called "haemagglutinin"?

Its binding to sialic acid on erythrocytes can cause haemagglutination, producing a lattice of interconnected red cells and viral particles.

78
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What is neuraminidase (NA)?

An influenza viral membrane glycoprotein that acts as a glycoside hydrolase enzyme.

79
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What is the main function of influenza neuraminidase?

Neuraminidase cleaves terminal sialic-acid groups from host glycoproteins, allowing newly produced influenza virions to escape from the cell surface and infect additional cells.

80
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Why would influenza virions remain trapped without neuraminidase activity?

Haemagglutinin would continue binding sialic acid on the host-cell surface, keeping newly released virus attached.

81
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How do haemagglutinin and neuraminidase have complementary roles in influenza infection?

Haemagglutinin promotes attachment to sialic acid and viral entry, whereas neuraminidase cleaves sialic acid to facilitate release and onward spread of progeny viruses.

82
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What simple memory aid distinguishes influenza HA from NA?

HA helps the virus attach and enter; NA helps newly produced virus get away and spread.

83
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How many haemagglutinin types are described in the accompanying reading?

At least 18 HA types.

84
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Which haemagglutinin types are typically associated with human influenza viruses?

H1, H2 and H3, although other HA types have also been observed infecting humans.

85
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How many neuraminidase types are described in the accompanying reading?

At least 9 NA types.

86
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What important surface proteins are found on influenza A viruses?

Haemagglutinin (HA), neuraminidase (NA) and Matrix-2 (M2).

87
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Which influenza viruses are primarily responsible for the spectrum of disease called seasonal flu in humans?

Influenza A and influenza B.

88
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Which seasonal influenza A subtypes are described as circulating in humans in the lecture reading?

H1N1 and H3N2.

89
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What is distinctive about influenza C compared with influenza A and B?

Influenza C is structurally different and generally causes mild upper respiratory tract illness resembling the common cold, with lower respiratory complications being rare.

90
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Why are HA and NA important immunologically?

They are major variant antigens recognised by the immune system and are important targets of influenza vaccination.

91
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Why can someone become infected with influenza despite having encountered influenza previously?

HA and NA antigens can change, meaning a sufficiently different virus may not be efficiently recognised by pre-existing immunity.

92
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What is antigenic drift?

The gradual accumulation of small genetic mutations over time that can progressively alter viral antigens.

93
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Does antigenic drift happen suddenly or progressively?

Progressively; it results from natural mutation accumulating over time.

94
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Does antigenic drift occur only in influenza A?

No. Antigenic drift occurs in all influenza subtypes and natural mutation occurs across viruses generally.

95
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Why can antigenic drift eventually cause loss of effective immunity?

Accumulated mutations can alter viral antigens sufficiently that antibodies and other pre-existing immune responses recognise the virus less efficiently.

96
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Why does antigenic drift contribute to the need for updated influenza vaccines?

Progressive antigenic changes can produce a mismatch between circulating viral antigens and immunity generated against previous strains.

97
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What is antigenic shift?

An abrupt and major change in influenza A antigenic material resulting from genetic reassortment and capable of generating a virus substantially different from viruses previously circulating in humans.

98
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Which type of influenza undergoes antigenic shift?

Influenza A.

99
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Why is antigenic shift more concerning at a population level than ordinary antigenic drift?

A shifted influenza virus can possess antigenic material to which much of the population has little or no pre-existing immunity, creating pandemic potential.

100
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What is genetic reassortment in influenza?

The mixing of viral genome segments when two or more different influenza strains infect the same cell, potentially generating progeny with a new combination of genetic material.