An interferometric SETI observation of Kepler-111 b

DATA AVAILABILITY : Data underlying this article are publicly available in the EVN Data Archive at JIVE at www.jive.eu/select -experiment and can be accessed with project codes RSG12 and RSW02. The e -MERLIN data and reduced EVN data will be shared on reasonable request to the corresponding author.This work has made use of data from the European Space Agency (ESA) mission Gaia (https://www.cosmos.esa.int/gaia), processed by the Gaia Data Processing and Analysis Consortium (DPAC, https://www.cosmos.esa.int/web/gaia/dpac/consortium).The application of very long baseline interferometry (VLBI) to the search for extraterrestrial intelligence (SETI) has been limited to date, despite the technique offering many advantages o v er traditional single-dish SETI observations. In order to further develop interferometry for SETI, we used the European VLBI network (EVN) at 21 cm to observe potential secondary phase calibrators in the Kepler field. Unfortunately, no secondary calibrators were detected. Ho we ver, a VLBA primary calibrator in the field, J1926 + 4441, offset only ∼1.88 arcmin from a nearby exoplanet Kepler-111 b, was correlated with high temporal ( 0 . 25 s ) and spectral ( 16384 ×488 Hz channels ) resolution. During the analysis of the high-resolution data, we identified a spectral feature that was present in both the auto and cross-correlation data with a central frequency of 1420.424 ±0.0002 MHz and a width of 0.25 MHz. We demonstrate that the feature in the cross-correlations is an artefact in the data, associated with a significant increase in each telescope’s noise figure due to the presence of H I in the beam. This would typically go unnoticed in data correlated with standard spectral resolution. We flag (excluded from the subsequent analysis) these channels and phase rotate the data to the location of Kepler-111 b aided by the Gaia catalogue and search for signals with SNR > 7 . At the time of our observations, we detect no transmitters with an equivalent isotropically radiated power 4 ×10 15 W.A Newton Fund project, DARA (Development in Africa with Radio Astronomy), the European Commission Horizon 2020, Research and Innovation Programme.https://academic.oup.com/mnrasam2024PhysicsNon

Delayed mucosal antiviral responses despite robust peripheral inflammation in fatal COVID-19

Background While inflammatory and immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in peripheral blood are extensively described, responses at the upper respiratory mucosal site of initial infection are relatively poorly defined. We sought to identify mucosal cytokine/chemokine signatures that distinguished coronavirus disease 2019 (COVID-19) severity categories, and relate these to disease progression and peripheral inflammation. Methods We measured 35 cytokines and chemokines in nasal samples from 274 patients hospitalized with COVID-19. Analysis considered the timing of sampling during disease, as either the early (0–5 days after symptom onset) or late (6–20 days after symptom onset) phase. Results Patients that survived severe COVID-19 showed interferon (IFN)-dominated mucosal immune responses (IFN-γ, CXCL10, and CXCL13) early in infection. These early mucosal responses were absent in patients who would progress to fatal disease despite equivalent SARS-CoV-2 viral load. Mucosal inflammation in later disease was dominated by interleukin 2 (IL-2), IL-10, IFN-γ, and IL-12p70, which scaled with severity but did not differentiate patients who would survive or succumb to disease. Cytokines and chemokines in the mucosa showed distinctions from responses evident in the peripheral blood, particularly during fatal disease. Conclusions Defective early mucosal antiviral responses anticipate fatal COVID-19 but are not associated with viral load. Early mucosal immune responses may define the trajectory of severe COVID-19

SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination

BACKGROUND: Most studies of immunity to SARS-CoV-2 focus on circulating antibody, giving limited insights into mucosal defences that prevent viral replication and onward transmission. We studied nasal and plasma antibody responses one year after hospitalisation for COVID-19, including a period when SARS-CoV-2 vaccination was introduced. METHODS: In this follow up study, plasma and nasosorption samples were prospectively collected from 446 adults hospitalised for COVID-19 between February 2020 and March 2021 via the ISARIC4C and PHOSP-COVID consortia. IgA and IgG responses to NP and S of ancestral SARS-CoV-2, Delta and Omicron (BA.1) variants were measured by electrochemiluminescence and compared with plasma neutralisation data. FINDINGS: Strong and consistent nasal anti-NP and anti-S IgA responses were demonstrated, which remained elevated for nine months (p < 0.0001). Nasal and plasma anti-S IgG remained elevated for at least 12 months (p < 0.0001) with plasma neutralising titres that were raised against all variants compared to controls (p < 0.0001). Of 323 with complete data, 307 were vaccinated between 6 and 12 months; coinciding with rises in nasal and plasma IgA and IgG anti-S titres for all SARS-CoV-2 variants, although the change in nasal IgA was minimal (1.46-fold change after 10 months, p = 0.011) and the median remained below the positive threshold determined by pre-pandemic controls. Samples 12 months after admission showed no association between nasal IgA and plasma IgG anti-S responses (R = 0.05, p = 0.18), indicating that nasal IgA responses are distinct from those in plasma and minimally boosted by vaccination. INTERPRETATION: The decline in nasal IgA responses 9 months after infection and minimal impact of subsequent vaccination may explain the lack of long-lasting nasal defence against reinfection and the limited effects of vaccination on transmission. These findings highlight the need to develop vaccines that enhance nasal immunity. FUNDING: This study has been supported by ISARIC4C and PHOSP-COVID consortia. ISARIC4C is supported by grants from the National Institute for Health and Care Research and the Medical Research Council. Liverpool Experimental Cancer Medicine Centre provided infrastructure support for this research. The PHOSP-COVD study is jointly funded by UK Research and Innovation and National Institute of Health and Care Research. The funders were not involved in the study design, interpretation of data or the writing of this manuscript