Infectious Disease Epidemiology and Virulence Concepts

Vocabulary flashcards covering core terms, epidemiological models, virulence factor classifications, and disease evolution principles based on quiz review notes.

Basic reproduction number ($R_0$)

The average number of secondary infections due to the first infected individual introduced into a completely susceptible population.

Infectious disease

A disease caused by a transmissible biological agent such as a virus, bacterium, fungus, parasite, or prion.

Emerging infectious disease

An infectious disease that has newly appeared in a population or is rapidly increasing in incidence or geographic range.

Pathology

The study of disease, particularly the structural and functional changes caused by disease.

Pathobiology

The study of the biological mechanisms underlying disease development and progression.

Virulence

Harm that a parasite does to its host, measured in terms of the reduction in host fitness (measured as number of offspring or population growth rate).

Adhesins

Bacterial virulence factors that allow bacteria to bind preferentially to particular host cells or locations.

Impedins

Bacterial virulence factors that help bacteria evade or resist host defenses, protecting them from the host immune response.

Aggressins

Bacterial virulence factors that damage host tissues, often through toxins or tissue-damaging enzymes.

Invasins

Bacterial virulence factors that allow bacteria to invade and spread through host cells or tissues.

Plasmids

Small, usually circular, extrachromosomal DNA molecules that replicate independently of the bacterial chromosome and can carry traits such as antibiotic resistance or virulence genes.

Susceptible ($S$)

In the SIR model, the compartment representing individuals capable of becoming infected.

Infectious ($I$)

In the SIR model, the compartment representing individuals who are infected and capable of transmitting disease.

Recovered/Removed ($R$)

In the SIR model, the compartment representing individuals who are no longer infectious and assumed immune.

Theobald Smith hypothesis

A hypothesis suggesting that emerging pathogens should be more virulent than pathogens that have a long evolutionary history with their hosts.

Trade-off hypothesis

A hypothesis assuming a positive relationship between transmission and parasite-induced mortality, predicting that $R_0$ is maximized at an optimal intermediate level of virulence.

Endotoxins

Molecules (primarily LPS/Lipid A) associated with the outer membrane of Gram-negative bacteria that provoke generalized inflammatory responses and are not actively secreted in the same way as classical exotoxins.

Exotoxins

Proteins produced and usually secreted or released by bacteria that act on specific host targets and can be extremely potent.

Highly pathogenic avian influenza (HPAI H5N1)

An influenza strain that tends to cause severe disease because its cell receptors are preferentially expressed in the lower respiratory tract.

Wild reservoir of influenza viruses

Waterfowl.

Public health component of $R\_0$ targeted by safe burial practices

Transmission/contact rate between infectious individuals and susceptible hosts.

Public health component of $R\_0$ targeted by vaccination

The proportion/number of susceptible individuals ($S$) in the population.

Public health component of $R\_0$ targeted by case isolation and rapid diagnosis

The duration of effective infectiousness by separating infected hosts from susceptible individuals.

Selective forces acting on initial Myxoma virus virulence in rabbits

Very high virulence was selected against because it killed hosts too quickly to allow vector transmission, while very low virulence achieved insufficient replication/transmission, favoring intermediate virulence.

Influenza viral components required for mammalian airborne transmission

Viral polymerase and hemagglutinin.

Fraser et al. findings on HIV set-point viral load correlations

Set-point viral load is positively correlated with transmission probability to partners and negatively correlated with time to AIDS symptom onset.

Genetic timeline estimate for the emergence of HIV in humans

Approximately $100\, \text{years}$ before HIV was first detected in the United States.

Evolutionary advantage of a segmented genome in influenza viruses

Allows rapid antigenic change via gene segment reassortment to evade host immune defenses.

Non-evolutionary causes for decreased SARS-CoV-2 case fatality rates

Increased population immunity from vaccination/prior infection, improved medical treatments, and changing age demographics of infected individuals.

Difference in virulence definitions between theoretical and experimental biologists

Theoretical biologists typically define virulence as parasite-induced host mortality, whereas experimental biologists often measure non-lethal host effects or symptoms.

Condition on virulence increase for a finite optimal level under the trade-off model

Parasite-induced mortality rate must increase faster than transmission rate as parasite load increases.

Denominator components of $R\_0$ in the trade-off model

Non-parasite induced host mortality rate, parasite-induced host mortality rate (virulence), and recovery rate.

Impact of co-infection or multiple strain competition on pathogen virulence

Selection favors higher virulence than predicted by single-strain trade-off models because strains compete for host resources.

Measure of virulence used in the de Roode et al. Plasmodium chabaudi malaria study

Anaemia in infected mice.

Mechanism by which 1990s Myxoma virus lineages evolved increased virulence in rabbits

Suppression of the host's innate immune response.

Findings of Froissart et al. regarding plant virus transmission and viral load

Transmission of plant viruses is positively correlated with viral load.

Primary metric used to quantify virulence in plant virus studies according to Froissart et al.

Severity of physical symptoms rather than host mortality.

Timing of viral load measurement in the Fraser et al. HIV virulence study

During the asymptomatic period of HIV infection.

Primary driver of $R\_0$ optimization in the trade-off hypothesis

Balancing transmission rate against host mortality to maximize total secondary infections before host death or recovery.

Expected immunopathology traits in short-lived organisms with high reproduction

Low immunopathology and high pathogen transmission.

Hypothesized evolutionary factors maintaining immunopathology according to Graham et al.

Multicellularity, coevolution with symbionts, and trade-offs in life history strategies.

Key features of the 2020 influenza panzootic

Global distribution in wild birds, widespread spillover into diverse mammal species, and detection in cattle.

Socio-environmental drivers of early HIV emergence and spread

Viral mutations enhancing transmission, accompanied by increased human mobility driven by economic forces and armed conflicts.

Receptor location contributing to the severe pathogenicity of HPAI H5N1

Sialic acid cell receptors preferentially located in the lower respiratory tract of humans.

Role of viral polymerase mutations in influenza adaptation

Enhances replication efficiency and airborne transmission capability within mammalian hosts.

Mechanism of action of bacterial adhesins

Surface proteins or structures that bind specifically to host cell receptors, facilitating bacterial attachment and colonization.

Primary distinction between endotoxins and exotoxins regarding secretion

Exotoxins are actively secreted proteins, whereas endotoxins are structural lipopolysaccharides released mainly upon cell lysis.

Primary host cell target for hemagglutinin in influenza viruses

Sialic acid residues on host epithelial cells.

Relationship between host lifespan and duration of infectiousness in vector-borne pathogen evolution

Pathogens must keep the host alive long enough to allow vectors (such as mosquitoes or fleas) to feed and transmit the pathogen.

Mathematical condition for an infectious disease to spread in a population

The basic reproduction number must satisfy $R\_0 > 1$.

Relationship between total population size $N$ and SIR compartments

The population sum satisfies $S + I + R = N$.

Role of bacterial aggressins in disease pathogenesis

Production of toxins or tissue-damaging enzymes that directly injure host tissues.

Function of bacterial invasins in infection

Virulence factors that enable bacteria to breach host tissue barriers and spread into adjacent cells or tissues.

Function of bacterial impedins in host defense evasion

Virulence factors that inhibit or evade host immune defenses without directly damaging host tissue.

Reason why very low virulence was selected against in initial Myxoma virus outbreaks

Low-virulence strains produced lower viral loads, leading to reduced transmission rates by insect vectors.

Role of plasmids in bacterial virulence evolution

Facilitate horizontal gene transfer of virulence factors, exotoxin genes, and antibiotic resistance traits between bacterial strains.

Primary target compartment of $R\_0$ altered by quarantine measures

Duration of infectiousness ($I$) by isolating infected hosts from the susceptible population.

Primary wild reservoir species for influenza A viruses

Wild waterfowl.

Cytokine implicated in suppressing virus-specific CD8+ T cell proliferation during chronic infection

$IL\text{-}10$.

Evolutionary prediction of the Theobald Smith avirulence hypothesis

Pathogens and hosts co-evolve over time toward benign coexistence, making newly emerged pathogens more virulent than ancient ones.