Viral Epidemiology — Questions

Prevalence = 150,000 / 1,000,000 = 15%, the proportion of the population infected at this point in time.

Predictive value depends on prevalence, not only on a test’s sensitivity and specificity. As prevalence rises, the positive predictive value (PPV, the chance that a positive result is a true positive) rises, and the negative predictive value (NPV, the chance that a negative result is a true negative) falls.

At low prevalence a larger share of positive results are false positives, even with a highly specific test, because the few true positives are outnumbered by false positives drawn from a large uninfected majority.

A screening test is therefore most trustworthy for confirming disease when applied in a higher-prevalence setting, such as during an outbreak or in a high-risk group. A positive result in a very-low-prevalence setting should be confirmed before acting.

Because neutralising antibody often persists for years or life, seroprevalence measures a population’s cumulative experience of a virus rather than current activity. Reading it by age group shows how efficiently and how recently the virus has circulated.

It does not by itself indicate active infection, ongoing shedding, or guaranteed protection against reinfection.

A case-control study is retrospective, starting from cases and matched controls and comparing their prior exposures. It is efficient for uncommon or slow diseases but is vulnerable to recall and selection bias.

A cohort works forward from exposure to outcome; a cross-sectional study is a single-time-point snapshot; and a trial assigns the exposure deliberately.

An animal reservoir sustains the virus independently of human immunity, so a zoonosis cannot be eradicated by controlling human infection alone. The absence of a reservoir was one of the decisive factors that made smallpox eradicable.

Such infections can still be diagnosed, vaccinated against, and kept under surveillance.

An epidemic is a rise in incidence that exceeds the expected endemic baseline for a population, implying unusually wide and rapid spread.

Multi-continent spread is a pandemic; the steady background level is endemic; and scattered unrelated cases are sporadic.

Varicella-zoster virus establishes latency and reactivates decades later as zoster, reseeding chickenpox in a new generation and bridging the gap between epidemics without needing a large susceptible pool. Measles, an acute infection with lifelong immunity and no reservoir, fades out below its critical community size.

Measles is in fact the more transmissible of the two, neither has an animal reservoir, and chickenpox does not spread by the water-borne route.

The herd-immunity threshold is 1 minus 1/R₀, so at an R₀ of 5 about 80% of the population must be immune for each case to produce fewer than one further case.

The more transmissible the virus, the higher the threshold, which is why measles, with an R₀ around 12 to 18, needs roughly 92 to 95%.

R₀ is the average number of secondary infections produced by one infected individual in a wholly susceptible population, and its threshold value of 1 separates fade-out from epidemic spread.

The other options describe the immune fraction, the contact rate, the clinical ratio, and the generation time.

Prevalence is a snapshot: the cases present in a population at one moment divided by the population size. It suits chronic or insidious infection, where onset is hard to date.

Incidence and attack rate count new cases over time; the seroconversion rate tracks new antibody responses; and the case-fatality rate is the proportion of cases who die.

Prevalence is a function of both incidence and duration, so with steady new-case rates a rising prevalence reflects longer duration, whether from improved survival or greater chronicity.

Faster transmission or waning immunity would raise incidence; higher case-fatality would shorten duration and lower prevalence; and subclinical infection does not add to the count of recognised cases.

The secondary attack rate is the proportion of susceptible contacts of an index case who become infected within one incubation period. It is a useful measure of infectiousness in closed groups such as households.

The whole-population figure is ordinary incidence; deaths among contacts is a mortality measure; point-source totals describe an outbreak’s size; and the antibody-positive fraction is seroprevalence.

A cross-sectional study takes a snapshot at one time point and measures prevalence, quickly and cheaply, but it captures cause and effect together and cannot show which came first.

Case-control and cohort designs track exposure and disease over time; a trial tests an intervention rather than measuring baseline prevalence.

When a virus reaches a population with no prior experience of it, the attack rate approaches 100% and adults suffer disproportionate mortality, largely because so much of the community is ill at once that care and social life collapse, rather than because of any special genetic susceptibility.

The attack rate is high rather than low, and illness is not confined to children.

Genome sequencing, the tool of molecular epidemiology, distinguishes vaccine from wild poliovirus and can track reversion toward virulence. It also assigns outbreak strains to a geographic origin.

Serology, culture, antigen detection and microscopy can identify or quantify the virus but do not resolve strain origin at the sequence level.

Incidence counts new cases over a defined period and is the natural measure for acute infections, where each case is a discrete, short episode.

Prevalence and seroprevalence suit chronic or persistent infection; the case-fatality rate measures severity rather than frequency; and duration is a component of prevalence, not a frequency measure in its own right.

A prospective cohort follows an exposed population forward and gives the strongest observational evidence of cause and effect, which is why it is essential for defining vaccine safety and efficacy. Its cost is time and expense.

The other designs cannot establish the same forward link between exposure and outcome.

A large share of infections are subclinical, so counting only clinical disease undercounts total infection. The gap can be extreme: under 1% of those infected with poliovirus or an encephalitis-causing arbovirus develop paralysis or encephalitis.

The other options describe reporting delays or immunity effects, not the systematic gap between infection and apparent disease.