SignificanceThe composition of the biosphere is a fundamental question in biology, yet a global quantitative account of the biomass of each taxon is still lacking. We assemble a census of the biomass of all kingdoms of life. This analysis provides a holistic view of the composition of the biosphere and allows us to observe broad patterns over taxonomic categories, geographic locations, and trophic modes.
The current SARS-CoV-2 pandemic is a harsh reminder of the fact that, whether in a single human host or a wave of infection across continents, viral dynamics is often a story about the numbers. In this snapshot, our aim is to provide a one-stop, curated graphical source for the key numbers that help us understand the virus driving our current global crisis. The discussion is framed around two broad themes: 1) the biology of the virus itself and 2) the characteristics of the infection of a single human host. Our one-page summary provides the key numbers pertaining to SARS-CoV-2, based mostly on peer-reviewed literature. The numbers reported in summary format are substantiated by the annotated references below. Readers are urged to remember that much uncertainty remains and knowledge of this pandemic and the virus driving it is rapidly evolving. In the paragraphs below we provide "back of the envelope" calculations that exemplify the insights that can be gained from knowing some key numbers and using quantitative logic. These calculations serve to improve our intuition through sanity checks, but do not replace detailed epidemiological analysis.
Quantitatively describing the time course of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection within an infected individual is important for understanding the current global pandemic and possible ways to combat it. Here we integrate the best current knowledge about the typical viral load of SARS-CoV-2 in bodily fluids and host tissues to estimate the total number and mass of SARS-CoV-2 virions in an infected person. We estimate that each infected person carries 109 to 1011 virions during peak infection, with a total mass in the range of 1 μg to 100 μg, which curiously implies that all SARS-CoV-2 virions currently circulating within human hosts have a collective mass of only 0.1 kg to 10 kg. We combine our estimates with the available literature on host immune response and viral mutation rates to demonstrate how antibodies markedly outnumber the spike proteins, and the genetic diversity of virions in an infected host covers all possible single nucleotide substitutions.
Quantitatively describing the time course of the SARS-CoV-2 infection within an infected individual is important for understanding the current global pandemic and possible ways to combat it. Here we integrate the best current knowledge about the abundance of potential SARS-CoV-2 host cells and typical concentrations of virions in bodily fluids to estimate the total number and mass of SARS-CoV-2 virions in an infected person. We estimate that each infected person carries 109-1011 virions during peak infection, with a total mass of about 1 μg-0.1 mg, which curiously implies that all SARS-CoV-2 virions currently in the world have a mass of only 0.1-1 kg. Knowledge of the absolute number of virions in an infected individual can put into perspective parameters of the immune system response, minimal infectious doses and limits of detection in testing.
Unlike their model membrane counterparts, biological membranes are richly decorated with a heterogeneous assembly of membrane proteins. These proteins are so tightly packed that their excluded area interactions can alter the free energy landscape controlling the conformational transitions suffered by such proteins. For membrane channels, this effect can alter the critical membrane tension at which they undergo a transition from a closed to an open state, and therefore influence protein function \emph{in vivo}. Despite their obvious importance, crowding phenomena in membranes are much less well studied than in the cytoplasm. Using statistical mechanics results for hard disk liquids, we show that crowding induces an entropic tension in the membrane, which influences transitions that alter the projected area and circumference of a membrane protein. As a specific case study in this effect, we consider the impact of crowding on the gating properties of bacterial mechanosensitive membrane channels, which are thought to confer osmoprotection when these cells are subjected to osmotic shock. We find that crowding can alter the gating energies by more than $2\;k_BT$ in physiological conditions, a substantial fraction of the total gating energies in some cases. Given the ubiquity of membrane crowding, the nonspecific nature of excluded volume interactions, and the fact that the function of many membrane proteins involve significant conformational changes, this specific case study highlights a general aspect in the function of membrane proteins.Comment: 20 pages (inclduing supporting information), 4 figures, to appear in PLoS Comp. Bio
Fluid infusion is one of the most common critical care interventions, yet approximately 50 % of all fluid interventions are unnecessary and potentially harmful. An improved approach to identification of fluid responsiveness is of clinical importance. Currently fluid responsiveness is most frequently identified by blood pressure (BP) measurements or a surrogate. However fluid responsiveness is simply the increase in stroke volume (SV) associated with volume expansion, and may not be reflected in BP or BP surrogates. Guyton demonstrated that BP = CO x SVR, and it is know that baroreceptor mediated autonomic nervous system regulation of SV and SVR to preserve BP may mask significant and critical changes in haemodynamics. Dr Pinsky in his recent J Clin Monit Comput Editorial evaluated the relative merits of pulse pressure variability (PPV) methods, a variant on BP measurement, for assessment of fluid responsiveness and promoted the use of physiologic challenges to augment the applicability of PPV. However this guidance is only half right. This letter reminds clinicians of the physiologic limitations of PPV as a measure of fluid responsiveness, even when combined with physiologic challenges, and recommends the replacement of BP with SV measurements. The combination of accurate Doppler measurement of SV and physiologic challenges, as Dr Pinsky recommends, is a physiologically rational and effective approach to identification of fluid responsiveness with established evidence. The direct monitoring of SV and SV changes has the potential to improve a long standing critical care and anaesthetic conundrum; when to give fluid and when to stop.
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