Two mechanisms for the elimination of pinch singularities in out of equilibrium thermal field theories

We analyze ill-defined pinch singularities characteristic of out of equilibrium thermal field theories. We identify two mechanisms that eliminate pinching even at the single self-energy insertion approximation to the propagator: the first is based on the vanishing of phase space at the singular point (threshold effect). It is effective in QED with a massive electron and a massless photon. In massless QCD, this mechanism fails, but the pinches cancel owing to the second mechanism, i.e., owing to the spinor/tensor structure of the single self-energy insertion contribution to the propagator. The constraints imposed on distribution functions are very reasonable.Comment: 24 pages, Latex, no figures, revised version, many minor changes and correction

Real-time propagators at finite temperature and chemical potential

We derive a form of spectral representations for all bosonic and fermionic propagators in the real-time formulation of field theory at finite temperature and chemical potential. Besides being simple and symmetrical between the bosonic and the fermionic types, these representations depend explicitly on analytic functions only. This last property allows a simple evaluation of loop integrals in the energy variables over propagators in this form, even in presence of chemical potentials, which is not possible over their conventional form

On the thermal sunset diagram for scalar field theories

We study the so-called `` sunset diagram'', which is one of two-loop self-energy diagrams, for scalar field theories at finite temperature. For this purpose, we first find the complete expression of the bubble diagram, the one-loop subdiagram of the sunset diagram, for arbitrary momentum. We calculate the temperature independent part and dependent part of the sunset diagram separately. For the former, we obtain the discontinuous part first and the finite continuous part next using a twice-subtracted dispersion relation. For the latter, we express it as a one-dimensional integral in terms of the bubble diagram. We also study the structure of the discontinuous part of the sunset diagram. Physical processes, which are responsible for it, are identified. Processes due to the scattering with particles in the heat bath exist only at finite temperature and generate discontinuity for arbitrary momentum, which is a remarkable feature of the two-loop diagrams at finite temperature. As an application of our result, we study the effect of the diagram on the spectral function of the sigma meson at finite temperature in the linear sigma model, which was obtained at one-loop order previously. At high temperature where the decay $\sigma\to\pi\pi$ is forbidden, sigma acquires a finite width of the order of $10 {\rm MeV}$ while within the one-loop calculation its width vanishes. At low temperature, the spectrum does not deviate much from that at one-loop order. Possible consequences with including other two-loop diagrams are discussed.Comment: 30 page

Analytic structure of rho meson propagator at finite temperature

We analyse the structure of one-loop self-energy graphs for the rho meson in real time formulation of finite temperature field theory. We find the discontinuities of these graphs across the unitary and the Landau cuts. These contributions are identified with different sources of medium modification discussed in the literature. We also calculate numerically the imaginary and the real parts of the self-energies and construct the spectral function of the rho meson, which are compared with an earlier determination. A significant contribution arises from the unitary cut of the pi-omega loop, that was ignored so far in the literature

QCD sum rule for nucleon in nuclear matter

We consider the two-point function of nucleon current in nuclear matter and write a QCD sum rule to analyse the residue of the nucleon pole as a function of nuclear density. The nucleon self-energy needed for the sum rule is taken as input from calculations using phenomenological NN potential. Our result shows a decrease in the residue with increasing nuclear density, as is known to be the case with similar quantities

Evaluating the Effects of SARS-CoV-2 Spike Mutation D614G on Transmissibility and Pathogenicity

Global dispersal and increasing frequency of the SARS-CoV-2 spike protein variant D614G are suggestive of a selective advantage but may also be due to a random founder effect. We investigate the hypothesis for positive selection of spike D614G in the United Kingdom using more than 25,000 whole genome SARS-CoV-2 sequences. Despite the availability of a large dataset, well represented by both spike 614 variants, not all approaches showed a conclusive signal of positive selection. Population genetic analysis indicates that 614G increases in frequency relative to 614D in a manner consistent with a selective advantage. We do not find any indication that patients infected with the spike 614G variant have higher COVID-19 mortality or clinical severity, but 614G is associated with higher viral load and younger age of patients. Significant differences in growth and size of 614G phylogenetic clusters indicate a need for continued study of this variant

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease