Questions

Viral Virulence and Host Factors — Questions

Study questions for Viral Virulence and Host Factors.

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Sit this set one question at a time. Multiple-choice questions mark themselves; written questions reveal a tickable mark scheme so you can score your own answer. You get a combined score at the end.

5 questions: 3 MCQ, 2 written.

High-priority (past-paper) questions only

The median tissue culture infectious dose (TCID50) is the dilution of a virus preparation that infects half of the inoculated cell cultures, and it gives a quantitative measure of infectious titre. In virulence studies, such as those on highly pathogenic avian influenza H5N1, it allows the replication and infectivity of different strains or conditions to be compared on a common scale, alongside related endpoints such as the median lethal dose (LD50) and median infective dose (ID50) in animals. It measures infectivity rather than disease severity directly, and human virulence cannot be assessed experimentally in this way; it is inferred instead from the severity observed in natural infection.

Emergence is driven by viral, host, and ecological factors acting together.

Viral factors. Error-prone replication generates a quasispecies from which variants with new properties are selected; reassortment (as in influenza A) and recombination can produce sudden, large genetic change. A virus long adapted to its natural host is often of low virulence there, but the same virus on jumping to a new host species, with which it has no evolutionary history, may cause severe disease. Acquisition of a new receptor usage or a virulence determinant, such as a polybasic haemagglutinin cleavage site, can extend host range or pathogenicity.

Host and ecological factors. Most emerging viruses are zoonotic, crossing from an animal reservoir at points of contact widened by deforestation, agricultural intensification, the wildlife trade, and urbanisation. Expanding vector ranges, human population growth, displacement and travel, and growing numbers of immunocompromised hosts all increase spillover and onward spread. Breakdown of control measures, including falling vaccine coverage, allows re-emergence of agents once suppressed.

Examples. SARS-CoV-2 (a coronavirus spillover causing a pandemic), pandemic and highly pathogenic avian influenza (reassortment and host-range change), Zika and Ebola viruses (expansion from limited foci into large outbreaks), and mpox (spread beyond its previous range). Re-emergence is seen where measles or poliovirus return as vaccination coverage falls. The unifying theme is a virus meeting a new or newly susceptible host population.

Haemagglutinin must be cleaved by a host protease to become fusion-active. A monobasic cleavage site is recognised only by trypsin-like proteases confined to the respiratory and gastrointestinal tracts, so infection stays local. A polybasic site is cleaved by furin-like proteases present in tissues throughout the body, allowing systemic spread and severe disease.

Option B describes the monobasic, low-pathogenicity site. The polybasic site enables rather than blocks cleavage and fusion (C). Sialic-acid linkage preference is a separate determinant of tropism and transmissibility, not a function of the cleavage site (D), and the cleavage site is not an antibody-escape mechanism (E).

Age at infection is the strongest determinant of whether hepatitis B becomes chronic: persistence follows over 90% of infections acquired in infancy but only 5 to 10% of those acquired in adulthood, with intermediate rates in between. Immune immaturity at first encounter favours persistence, which is why interrupting neonatal transmission is the prevention priority.

Option B reverses the relationship, and age clearly does influence chronicity (A). Most adults clear the virus rather than progressing to chronic disease (C), and infancy infection usually persists rather than clearing in the first year (E).

Pathogenicity is the qualitative capacity of a virus to cause disease at all: a virus either is pathogenic or it is not. Virulence is the quantitative degree of disease it causes, the property used to compare a virulent strain against an attenuated one. Option A reverses the two.

The terms are not synonymous (C), and neither describes transmissibility or infectivity, which are separate properties (D). Virulence is not fixed: it is relative to the host and is meaningfully compared only between related viruses (E).

High prioritySAQExplain the use of the median tissue culture infectious dose (TCID50) in measuring viral virulence. [4]
Model answer
The median tissue culture infectious dose (TCID50) is the dilution of a virus preparation that infects half of the inoculated cell cultures, and it gives a quantitative measure of infectious titre. In virulence studies, such as those on highly pathogenic avian influenza H5N1, it allows the replication and infectivity of different strains or conditions to be compared on a common scale, alongside related endpoints such as the median lethal dose (LD50) and median infective dose (ID50) in animals. It measures infectivity rather than disease severity directly, and human virulence cannot be assessed experimentally in this way; it is inferred instead from the severity observed in natural infection.
High priorityExam-styleDiscuss the factors influencing the emergence and re-emergence of viral pathogens, with examples. [6]
Model answer
Emergence is driven by viral, host, and ecological factors acting together.

Viral factors. Error-prone replication generates a quasispecies from which variants with new properties are selected; reassortment (as in influenza A) and recombination can produce sudden, large genetic change. A virus long adapted to its natural host is often of low virulence there, but the same virus on jumping to a new host species, with which it has no evolutionary history, may cause severe disease. Acquisition of a new receptor usage or a virulence determinant, such as a polybasic haemagglutinin cleavage site, can extend host range or pathogenicity.

Host and ecological factors. Most emerging viruses are zoonotic, crossing from an animal reservoir at points of contact widened by deforestation, agricultural intensification, the wildlife trade, and urbanisation. Expanding vector ranges, human population growth, displacement and travel, and growing numbers of immunocompromised hosts all increase spillover and onward spread. Breakdown of control measures, including falling vaccine coverage, allows re-emergence of agents once suppressed.

Examples. SARS-CoV-2 (a coronavirus spillover causing a pandemic), pandemic and highly pathogenic avian influenza (reassortment and host-range change), Zika and Ebola viruses (expansion from limited foci into large outbreaks), and mpox (spread beyond its previous range). Re-emergence is seen where measles or poliovirus return as vaccination coverage falls. The unifying theme is a virus meeting a new or newly susceptible host population.
MCQ
Highly pathogenic avian influenza viruses carry a polybasic cleavage site in their haemagglutinin. Why does this increase virulence?
- A. Furin-like proteases in many tissues can cleave it, allowing spread beyond the airway
- B. Only trypsin-like proteases of the respiratory tract can cleave it, confining infection
- C. It blocks cleavage of the haemagglutinin altogether, which would prevent membrane fusion
- D. It switches receptor preference from alpha-2,3 to alpha-2,6 linked sialic acid
- E. It shields the cleavage loop from neutralising antibody, aiding immune escape
Show answer
Correct answer: A
Haemagglutinin must be cleaved by a host protease to become fusion-active. A monobasic cleavage site is recognised only by trypsin-like proteases confined to the respiratory and gastrointestinal tracts, so infection stays local. A polybasic site is cleaved by furin-like proteases present in tissues throughout the body, allowing systemic spread and severe disease.

Option B describes the monobasic, low-pathogenicity site. The polybasic site enables rather than blocks cleavage and fusion (C). Sialic-acid linkage preference is a separate determinant of tropism and transmissibility, not a function of the cleavage site (D), and the cleavage site is not an antibody-escape mechanism (E).
MCQ
How does age at infection influence the outcome of hepatitis B virus infection?
- A. Age at infection has little consistent effect on the likelihood of chronicity
- B. Chronic infection follows over 90% of adult infections but few of those acquired in infancy
- C. Adults acquiring infection usually progress to chronic disease
- D. Chronic infection follows over 90% of infections in infancy but only 5 to 10% in adults
- E. Infection acquired in infancy usually clears within the first year of life
Show answer
Correct answer: D
Age at infection is the strongest determinant of whether hepatitis B becomes chronic: persistence follows over 90% of infections acquired in infancy but only 5 to 10% of those acquired in adulthood, with intermediate rates in between. Immune immaturity at first encounter favours persistence, which is why interrupting neonatal transmission is the prevention priority.

Option B reverses the relationship, and age clearly does influence chronicity (A). Most adults clear the virus rather than progressing to chronic disease (C), and infancy infection usually persists rather than clearing in the first year (E).
MCQ
Which statement best distinguishes pathogenicity from virulence?
- A. Pathogenicity is the quantitative degree of disease; virulence is its qualitative basis
- B. Pathogenicity is the qualitative basis of disease; virulence is its quantitative degree
- C. The two terms are synonymous and may be used interchangeably in practice
- D. Pathogenicity refers to transmissibility, and virulence refers to infectivity
- E. Virulence is a fixed property of a virus, independent of the host involved
Show answer
Correct answer: B
Pathogenicity is the qualitative capacity of a virus to cause disease at all: a virus either is pathogenic or it is not. Virulence is the quantitative degree of disease it causes, the property used to compare a virulent strain against an attenuated one. Option A reverses the two.

The terms are not synonymous (C), and neither describes transmissibility or infectivity, which are separate properties (D). Virulence is not fixed: it is relative to the host and is meaningfully compared only between related viruses (E).