Chemotaxis is typically modeled in the context of cellular motion towards a static, exogenous source of chemoattractant. Here, we propose a time-dependent mechanism of chemotaxis in which a self-propelled particle ({it e.g.}, a cell) releases a chemi
cal that diffuses to fixed particles (targets) and signals the production of a second chemical by these targets. The particle then moves up concentration gradients of this second chemical, analogous to diffusive echolocation. When one target is present, we describe probe release strategies that optimize travel of the cell to the target. In the presence of multiple targets, the one selected by the cell depends on the strength and, interestingly, on the frequency of probe chemical release. Although involving an additional chemical signaling step, our chemical ``pinging hypothesis allows for greater flexibility in regulating target selection, as seen in a number of physical or biological realizations.
Enveloped viruses enter host cells either through endocytosis, or by direct fusion of the viral membrane envelope and the membrane of the host cell. However, some viruses, such as HIV-1, HSV-1, and Epstein-Barr can enter a cell through either mechani
sm, with the choice of pathway often a function of the ambient physical chemical conditions, such as temperature and pH. We develop a stochastic model that describes the entry process at the level of binding of viral glycoprotein spikes to cell membrane receptors and coreceptors. In our model, receptors attach the cell membrane to the viral membrane, while subsequent binding of coreceptors enables fusion. The model quantifies the competition between fusion and endocytotic entry pathways. Relative probabilities for each pathway are computed numerically, as well as analytically in the high viral spike density limit. We delineate parameter regimes in which fusion or endocytosis is dominant. These parameters are related to measurable and potentially controllable quantities such as membrane bending rigidity and receptor, coreceptor, and viral spike densities. Experimental implications of our mechanistic hypotheses are proposed and discussed.
We investigate the dynamics of a one-dimensional asymmetric exclusion process with Langmuir kinetics and a fluctuating wall. At the left boundary, particles are injected onto the lattice; from there, the particles hop to the right. Along the lattice,
particles can adsorb or desorb, and the right boundary is defined by a wall particle. The confining wall particle has intrinsic forward and backward hopping, a net leftward drift, and cannot desorb. Performing Monte Carlo simulations and using a moving-frame finite segment approach coupled to mean field theory, we find the parameter regimes in which the wall acquires a steady state position. In other regimes, the wall will either drift to the left and fall off the lattice at the injection site, or drift indefinitely to the right. Our results are discussed in the context of non-equilibrium phases of the system, fluctuating boundary layers, and particle densities in the lab frame versus the frame of the fluctuating wall.
