Surface layers (S-layers) are paracrystalline protein monolayers that envelop archaea and some bacteria, including Bacillus anthracis. S-layer subunits in B. anthracis are tethered to the underlying cell wall through glycopolymers that are covalently attached to the peptidoglycan (PG) meshwork. Cell growth in this rod-shaped organism occurs by dispersed PG synthesis throughout the cell cylinder. How the crystalline lattice expands in lockstep with the cell wall has remained unclear. Here, using fluorescently labelled S-layer subunits and high-resolution imaging, we show that S-layer expansion during B. anthracis growth is mediated by pervasive hoop-like cracks in the lattice. Pulse-chase experiments reveal two modes of S-layer assembly at these cracks: dispersed and focused. Our data suggest that local pulling forces on the S-layer array generated by dispersed cell wall synthesis and expansion of the underlying PG cause crack formation, with ensuing dispersed and focused synthesis enabling S-layer expansion with bacterial growth. Hoop-like cracking of the S-layer, filled either completely or partially, respectively leading to dispersed or focused modes of S-layer synthesis, enables S-layer expansion during Bacillus anthracis growth.
Viral latency reversal was observed in simian immunodeficiency virus (SIV)-infected rhesus macaques receiving antiretroviral therapy (ART), CD8α lymphocyte depletion and N-803 immunotherapy. However, this therapeutic approach did not reduce the viral reservoir size and treatment interruption resulted in rapid virus rebound. Here, to address this shortfall, we used four anti-SIV Env-specific rhesus IgG1 monoclonal antibodies (RhmAbs) that recognize unique targets on the SIV envelope. SIV mac239 -infected macaques were treated with ART only (group 1); ART + RhmAbs (group 2); or ART + RhmAbs + CD8α-depletion + N-803 (group 3). Robust latency reversal was only achieved in group 3. Viraemia rebounded in all macaques with similar kinetics after treatment interruption. However, compared with pre-ART viral loads, a greater fold reduction in rebound viraemia was seen in groups 2 and 3 and post-treatment control (PTC) required SIV RhmAbs. CD4 + T cells from macaques with PTC maintained low levels of intact SIV proviruses off ART and expressed increased interferon and decreased TGF-β signalling genes. This antiviral gene expression profile was also observed in CD4 + T cells with lower human immunodeficiency virus (HIV)-DNA content from ART-treated people with HIV. These results suggest that reduced virus production may contribute to PTC following ART interruption and provide a target for immune-based strategies to achieve durable viral control.
Martha Nelson revisits the emergence of the 2009 swine flu pandemic and considers what it can teach us about animal movements, viral evolution and prevention of future pandemics.
We propose that dual-use research of concern policies should reflect emerging risks from recent technological innovations, including artificial intelligence, to ensure continued global biosafety, while acknowledging the wider societal benefits of genetic modification of viruses.
We argue that shifts in the abundance and composition of marine particles impacted horizontal gene transfer, consequently shaping the evolutionary landscape of the oceans throughout Earth’s history. We focus on two pivotal transitions — the emergence of cyanobacteria and the rise of eukaryotic algae.
