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Chung, W.-J.

Publications and source records attributed to Chung, W.-J..

3 recordsLinked to original sources

Electrode pooling preserves movement decoding by retaining neural population dynamics

New implantable-electrode fabrication strategies make dense, ultrafine electrode arrays with lower tissue burden increasingly feasible, shifting a key bottleneck for scalable brain-computer interfaces from electrode placement to readout capacity. Electrode pooling, in which multiple electrodes share a readout channel, could relax this bottleneck by combining extracellular signals before acquisition, but it has remained unclear whether such compression preserves the neural population structure needed for behavioral decoding. Here we evaluate this question using software-emulated electrode pooling in mouse sensorimotor cortex during a cue-guided reach-and-grasp task using a high-density microwire array coupled to a CMOS microelectrode-array platform. Pooled recordings retain forelimb kinematic information more effectively than a channel-matched control that discards electrodes. Pooling reduces the separability of electrode-specific spikes and sorted units, indicating a loss of some neuronal detail, but the mixed signals still preserve task-aligned low-dimensional latent dynamics that support decoding. When readout capacity is fixed, this trade-off allows broader electrode coverage to contribute to behaviorally informative population sampling. Together, these results define electrode pooling as a design trade-off for scalable readout, in which some electrode-specific neuronal information is lost but the population dynamics needed for movement decoding remain accessible.

neuroscience↗

Compartmental structure in the secondary lymphoid tissue can slow down in vivo HIV-1 evolution in the presence of strong CTL responses

Human immunodeficiency virus (HIV-1) replicates in the secondary lymphoid tissues, which are characterized by complex compartmental structures. While Cytotoxic T lymphocytes (CTL) readily access infected cells in the extrafollicular compartments, they do not home to follicular compartments, which thus represent an immune-privileged site. Using mathematical models, we have previously shown that this compartmental tissue structure can delay the emergence of CTL escape mutants. Here, we show computationally that the compartmental structure can have an impact on the evolution of advantageous mutants that are not related to CTL recognition: (i) Compartmental structure can influence the fixation probability of an advantageous mutant, with weakened selection occurring if CTL responses are of intermediate strength. (ii) Compartmental structure is predicted to reduce the rate mutant generation, which becomes more pronounced for stronger CTL responses. (iii) Compartmental structure is predicted to slow down the overall rate of mutant invasion, with the effect becoming more pronounced for stronger CTL responses. Altogether, this work shows that in vivo virus evolution proceeds slower in models with compartmental structure compared to models that assume equivalent virus load in the absence of compartmental structure, especially for strong CTL-mediated virus control. This has implications for understanding the rate of disease progression.

evolutionary biology↗

Human immunodeficiency virus (HIV) dynamics in secondary lymphoid tissues and the evolution of cytotoxic T lymphocyte (CTL) escape mutants

In the secondary lymphoid tissues, human immunodeficiency virus (HIV) can replicate both in the follicular and the extrafollicular compartments. Yet, virus is concentrated in the follicular compartment in the absence of antiretroviral therapy, in part due to the lack of cytotoxic T lymphocyte (CTL)-mediated activity there. CTL home to the extrafollicular compartment, where they can suppress virus load to relatively low levels. We use mathematical models to show that this compartmentalization can explain seemingly counterintuitive observations. First, it can explain the observed constancy of the viral decline slope during antiviral therapy irrespective of the presence of CTL in SIV-infected macaques, under the assumption that CTL-mediated lysis significantly contributes to virus suppression. Second, it can account for the relatively long times it takes for CTL escape mutants to emerge during chronic infection even if CTL-mediated lysis is responsible for virus suppression. The reason is the heterogeneity in CTL activity, and the consequent heterogeneity in selection pressure between the follicular and extrafollicular compartments. Hence, to understand HIV dynamics more thoroughly, this analysis highlights the importance of measuring virus populations separately in the extrafollicular and follicular compartments rather than using virus load in peripheral blood as an observable; this hides the heterogeneity between compartments that might be responsible for the particular patters seen in the dynamics and evolution of the HIV in vivo.

evolutionary biology↗