Table 1.

Impact and empirical evidence of physiological variation in phage infection processes.

Infection process	Physiological mechanism	Effect on coexistence	Empirical data available	Empirical data missing
Adsorption	Phage subpopulation with lower adsorption efficacy	Likely minor as this subpopulation only plays a role once the efficient phages have adsorbed	Proportion of different phage populations failing to adsorb for different media conditions (Storms et al. 2010, Storms et al. 2012); intrinsic variation in (average) adsorption between different phages (Marianne and Taddei 2006)	Dynamics of low-adsorbing phage subpopulations over time and ‘heritability’ of the subpopulation size
Adsorption	Phenotypic resistance due to population heterogeneity (noise) in the number of receptor molecules on the bacterial cell surface	Increases the probability of coexistence between phages and bacteria of low- and high-susceptibility	Phage Lambda receptor number heterogeneity within an E. coli population for different media conditions (Chapman-McQuiston and Wu 2008a)	Transition rates between subpopulations with different receptor numbers
	Phenotypic resistance due to other mechanisms of switching between subpopulations	Increases the probability of coexistence between phages and bacteria of low- and high-susceptibility (Bull et al. 2014) in dependence of the susceptibility-switching rate and the cost of phenotypic resistance	Population dynamics for phase variation- (Kim and Ryu 2012; Turkington et al. 2019) and quorum sensing- (Høyland-Kroghsbo et al. 2013; Tan, Svenningsen, and Middelboe 2015) induced reduction in receptor number; percentage of non-adsorbed phages for receptor masking by phage T7 (Decker et al. 1994); plaque assays on cells with glycosylated (Harvey et al. 2018) or alanylated (Tzipilevich et al. 2022) receptors	Susceptibility-switching rates in the presence of phages; classification of differences in dynamics and subpopulation size for different mechanisms
Adsorption	Bacterial density-dependence of phage adsorption	Likely minor by itself as phage infection needs to be delayed until bacteria can escape by metabolic shutdown in the stationary phase but increases the likelihood of bacterial survival and coexistence in combination with phage density-dependence	Phage adsorption dependence on host growth rate at the population level through fitting to infection dynamics (Krysiak-Baltyn, Martin, and Gras 2018; Santos et al. 2014; Schrag and Mittler 1996); direct empirical measurements of growth rate dependence using different media (Golec et al. 2014; Hadas et al. 1997; Nabergoj, Modic, and Podgornik 2018)	Changes in adsorption heterogeneity within a population across growth phases; comparison between the effects of growth rate due to changes in media and due to changes in the growth phase
Adsorption	Saturation of infection efficiency at high phage densities	Increases the probability of coexistence in the absence of genetic resistance and in combination with bacterial density-dependence or fast phage decay also in the presence of genetic resistance	Population dynamics and molecular mechanisms of lysis inhibition, i.e. a prolonged time to lysis in coinfections of the same cell (Abedon 2019); Correlation between effective burst size and effective MOI (Gadagkar and Gopinathan 1980); Effect of MOI on burst size and latent period (Ellis and Delbrück 1939); Inference of infection saturation from bacterial killing in an in vivo mouse model (Roach et al. 2017)	The functional form of saturation of phage infection efficacy with MOI; intracellular effects of clonal phage coinfection other than lysis inhibition
Burst size	Bacterial density-dependence of the number of phage progeny produced	Likely minor under nutrient-limited conditions if phage infection is not delayed long enough for bacteria to enter the stationary phase	Burst size dependence on the host growth rate at the population level through fitting to infection dynamics (Choua and Bonachela 2019; Krysiak-Baltyn, Martin, and Gras 2018; Schrag and Mittler 1996); direct empirical measurements of growth rate dependence using different media (Birch, Ruggero, and Covert 2012; Golec et al. 2014; Hadas et al. 1997; Nabergoj, Modic, and Podgornik 2018; You, Suthers, and Yin 2002)	Changes in burst size heterogeneity within a population across growth phases
Latent period	Bacterial density-dependence of lysis timing	Likely minor (see burst size)	Latent period dependence on host growth rate at the population level through fitting to infection dynamics (Choua and Bonachela 2019; Krysiak-Baltyn, Martin, and Gras 2018); direct empirical measurements of growth rate dependence using different media (Birch, Ruggero, and Covert 2012; Golec et al. 2014; Hadas et al. 1997; Nabergoj, Modic, and Podgornik 2018; You, Suthers, and Yin 2002)	Changes in latent period heterogeneity within a population across growth phases
Latent period	Latent period distribution	Low variance of latent period distributions destabilizes coexistence	Latent period distributions through fitting to empirical data (Santos et al. 2014; Schrag and Mittler 1996); determination of stochasticity in lysis timing within a population in different growth conditions (Dennehy and Wang 2011)	Impact of phage density on latent period distribution and its correlation with burst size (other than lysis inhibition)
Decay	Intrinsic phage properties or environmental conditions	Faster decay increases the likelihood of bacterial survival and phage extinction	Intrinsic variation of average decay rates between different phages (Marianne and Taddei 2006); influence of environmental stressors on phage decay (Blazanin et al. 2022; Wommack et al. 1996)	Heterogeneity of decay within a phage population; Decay rate ranges in natural environments