Questions: Emerging Infectious Diseases

Question 1

Deforestation in a tropical region brings agricultural workers into sustained contact with bat colonies that were previously isolated. Shortly afterward, a novel viral disease begins spreading in nearby communities. Which explanation best accounts for this emergence?

• A. Deforestation weakened the immune systems of local populations, allowing existing human pathogens to become more virulent
• B. Deforestation changed ecological conditions that enabled an existing bat virus to spill over into humans, who had no prior immunity to it
• C. The virus spontaneously mutated in a common human pathogen after humans began clearing the forest
• D. Bats evolved a more transmissible virus in response to human encroachment on their habitat

Answer: (B)

Emerging infectious diseases do not arise spontaneously — they represent existing animal pathogens crossing species barriers when ecological conditions change. Deforestation is a primary driver because it eliminates the physical separation between wildlife reservoirs and human communities, increasing the frequency of contact and therefore the probability of spillover. The virus already existed in bats; what changed was the opportunity for human exposure. This is the same mechanism behind HIV (from chimpanzees), Ebola (from bats), and Nipah (from fruit bats).

Question 2

A novel influenza strain emerges with surface proteins from both an avian and a human influenza virus. What mechanism most likely produced this combination?

• A. Rapid accumulation of point mutations in the viral RNA polymerase, which gradually shifted antigenicity
• B. Horizontal gene transfer between influenza and a bacterial co-infection in the same host
• C. Genomic reassortment — co-infection of a single host cell by two different influenza strains caused viral genome segments to shuffle and combine
• D. CRISPR-mediated editing of the viral genome during replication in an intermediate host

Answer: (C)

Influenza is a segmented RNA virus with 8 genome segments. When two different influenza strains co-infect the same cell, the segments can mix during replication, producing progeny viruses with novel combinations — a process called genomic reassortment. This mechanism generated the 1918, 1957, 1968, and 2009 pandemic strains. It is distinct from point mutation, which generates gradual antigenic drift. Reassortment can produce entirely new surface protein combinations overnight, which is why novel reassortant strains can evade existing immunity in the entire population.

Question 3

Viruses reliably evolve toward reduced virulence over time, because killing the host before transmission is disadvantageous and evolution selects against it.

• T. True
• F. False

Answer: False

This is a common but incorrect generalization. Virulence evolution depends on transmission trade-offs specific to each pathogen-host system. If a pathogen transmits primarily through contact with sick individuals, high virulence is disadvantageous. But if transmission occurs before symptoms appear, or through vectors, or via environmental shedding from corpses, there is no consistent selection pressure toward reduced virulence. Ebola, for example, has not evolved significantly reduced virulence despite decades of outbreaks. The 'inevitable attenuation' idea is a myth — virulence evolution is contingent, not directional.

Question 4

More than half of emerging infectious diseases in humans originate as zoonoses — infections that crossed from animal reservoirs into humans.

• T. True
• F. False

Answer: True

Studies of emerging infectious diseases consistently find that over 60% are zoonotic in origin. HIV, SARS-CoV, SARS-CoV-2, Ebola, Nipah, Hendra, Marburg, and many other significant pathogens all originated in animal reservoirs. This pattern reflects the enormous diversity of viruses circulating in wildlife — particularly bats, rodents, and non-human primates — and the increasing frequency of human-wildlife contact. Understanding this pattern is the basis of the One Health framework and motivates wildlife surveillance as a pandemic preparedness strategy.

Question 5

Why does presymptomatic infectiousness — the ability to transmit a pathogen before showing symptoms — make a respiratory virus dramatically harder to contain than a virus that only transmits after symptoms appear?

Model answer: When a virus only transmits after symptoms appear, containment is possible: identify sick people, isolate them, trace their contacts, and quarantine exposed individuals. The symptomatic individual is a visible signal for intervention. Presymptomatic transmission breaks this logic: an infected person who feels well continues normal social activity — commuting, attending events, traveling — while actively spreading the virus. By the time symptoms appear and alert the person or their contacts, the virus has already propagated through one or more transmission chains. Contact tracing becomes retrospective rather than prospective, exponential growth is already underway, and containment requires restricting the movement of apparently healthy people at enormous social and economic cost.

This is exactly why SARS-CoV-2 was so much harder to contain than SARS-CoV-1. SARS-CoV-1 was most infectious after symptom onset, enabling containment by isolating the symptomatic. SARS-CoV-2's substantial presymptomatic transmission window made the standard response toolkit far less effective.