Baochen She

In this Letter, we present the experimental observation of squeezed phonon generation in semiconductor germanium (Ge) induced by x-ray excitation. Prior x-ray pump, x-ray probe studies reported coherent longitudinal acoustic phonon generation in insulating oxides like strontium titanate and potassium tantalate. In contrast, such signals were not observed in semiconductors likely due to limited signal-to-noise ratio. Now, with an improved experimental setup, we observe a phonon response in single-crystal germanium. Utilizing x-ray split-delay optics with enhanced stability, we extract the phonon dispersion relation, which shows strong agreement with the calculated transverse acoustic phonon mode. Our results reveal that responses to x-ray excitations in semiconductors are of a similar nature to optical excitations. This suggests that the initial response to x-ray core–hole excitations rapidly diffuses to a non-local excitation, similar to what is observed with optical laser valence excitation on a femtosecond timescale.

The formation of a membrane-enveloped virus starts with the assembly of a curved layer of capsid proteins lining the interior of the plasma membrane (PM) of the host cell. This layer develops into a spherical shell (capsid) enveloped by a lipid-rich membrane. In many cases, the budding process stalls prior to the release of the virus. Recently, Brownian dynamics simulations of a coarse-grained model system reproduced protracted pausing and stalling, which suggests that the origin of pausing/stalling is to be found in the physics of the budding process. Here, we propose that the pausing/stalling observed in the simulations can be understood as a purely kinetic phenomenon associated with the neck geometry. A geometrical potential energy barrier develops during the budding that must be overcome by capsid proteins diffusing along the membrane prior to incorporation into the capsid. The barrier is generated by a conflict between the positive Gauss curvature of the assembling capsid and the negative Gauss curvature of the neck region. A continuum theory description is proposed and is compared with the Brownian simulations of the budding of enveloped viruses. Despite intense study, the life-cycle of the HIV-1 virus continues to pose mysteries. One of these is the fact that the assembly of an HIV-1 virus along the plasma membrane (PM) of the host cell—the budding process—stalls prior to release of the virus. Many other important viral pathogens with a surrounding lipid membrane envelope display similar stalling. Combining numerical and analytical methods, we demonstrate that the neck-like shape of the membrane that forms prior to release of the virus creates a barrier that blocks the proteins required for the assembly process from reaching the budding virus. An improved understanding of the physics of the blocking process could enable new strategies to combat enveloped viruses.

The formation of a membrane-enveloped virus such as HIV-1 starts with the assembly of a curved layer of capsid proteins lining the interior of the plasma membrane (PM) of the host cell. This layer grows into a spherical shell enveloped by a lipid membrane that is connected to the PM via a curved neck (“budding”). For many enveloped viruses the scission of this neck is not spontaneous. Instead, the elaborate “ESCRT” cell machinery needs to be recruited to carry out that task. It is not clear why this is necessary since scission is spontaneous for much simpler systems, such as vesiculation driven by phase-separation inside lipid bilayers. Recently, Brownian dynamics simulations of enveloped virus budding reproduced protracted pausing and stalling after formation of the neck [1], which suggest that the origin of pausing/stalling is to be found in the physics of the budding process. Here, we show that the pausing/stalling observed in the simulations can be understood as a purely kinetic phenomenon associated with a “geometrical” energy barrier that must be overcome by capsid proteins diffusing along the membrane prior to incorporation into the viral capsid. This geometrical energy barrier is generated by the conflict between the positive Gauss curvature of the capsid and the large negative Gauss curvature of the neck region. The theory is compared with the Brownian simulations of the budding of enveloped viruses. Author summary: Despite intense study, the life-cycle of the HIV-1 virus continues to pose mysteries. One of these concerns the assembly of the HIV-1 virus inside infected host cells: it is interrupted at the very last moment. During the subsequent pause, HIV-1 recruits a complex cell machinery, the so-called “ESCRT pathway”. The ESCRT proteins pinch-off the “viral bud” from the host cell. In this paper, we propose that the reason for the stalling emerges from the fundamental physics of the lipid membrane that surrounds the virus. The membrane mostly follows the spherical geometry of the virus, but in the pinch-off region the geometry is radically different: it resembles a neck. By combining numerical and analytical methods, we demonstrate that a neck geometry creates a barrier to protein entry, thus blocking proteins required to complete viral assembly. This “geometrical barrier” mechanism is general: such a barrier should form during assembly of all membrane-enveloped viruses – including the Ebola and Herpes viruses. Indeed many families of enveloped viruses also recruit the ESCRT machinery for pinch-off. A fundamental understanding of the budding process could enable a new strategy to combat enveloped viruses, based on selective stabilization of membrane neck geometries.