Inactivation of Campylobacter jejuni by exposure to high-intensity 405-nm visible light

Although considerable research has been carried out on a range of environmental factors that impact on the survival of Campylobacter jejuni, there is limited information on the effects of violet/blue light on this pathogen. This investigation was carried out to determine the effects of high-intensity 405-nm light on C. jejuni and to compare this with the effects on two other important Gram-negative enteric pathogens, Salmonella enteritidis and Escherichia coli O157:H7. High-intensity 405-nm light generated from an array of 405-nm light-emitting diodes was used to inactivate the test bacteria. The results demonstrated that while all three tested species were susceptible to 405-nm light inactivation, C. jejuni was by far the most sensitive organism, requiring a total dose of 18J cm−2 of 405-nm light to achieve a 5-log10 reduction. This study has established that C. jejuni is particularly susceptible to violet/blue light at a wavelength of 405nm. This finding, coupled with the safety-in-use advantages of this visible (non-ultraviolet wavelength) light, suggests that high-intensity 405-nm light may have applications for control of C. jejuni contamination levels in situations where this type of illumination can be effectively applied

Lethal effects of high intensity violet 405-nm light on saccharomyces cerevisiae, candida albicans and on dormant and germinating spores of aspergillus niger

This study assessed the effects of high-intensity violet light on selected yeast and mould fungi. Cell suspensions of Saccharomyces cerevisiae, Candida albicans, and dormant and germinating spores (conidia) of the mould Aspergillus niger were exposed to high-intensity narrow band violet light with peak output at 405 nm generated from a light-emitting diode (LED) array. All three fungal species were inactivated by the 405-nm light without a requirement for addition of exogenous photosensitiser chemicals. Of the fungal species tested, S. cerevisiae was most sensitive and dormant conidia of A. niger were most resistant to 405-nm light exposure. Five-log10 colony forming units per millilitre (CFU ml1) reductions of the tested species required exposure doses of 288 J cm2 for S. cerevisiae, 576 J cm2 for C. albicans, and a much higher value of 2.3 kJ cm2 for dormant conidia of A. niger. During germination, A. niger conidia became more sensitive to 405-nm light exposure and sensitivity increased as germination progressed over an 8 h test period. Light exposure under aerobic and anaerobic conditions, together with results obtained using ascorbic acid as a scavenger of reactive oxygen species, revealed that 405-nm light inactivation in fungi involved an oxygen-dependent mechanism, as previously described in bacteria. The inactivation results achieved with yeast cells and fungal spores together with operational advantages associated with the use of a visible (nonultraviolet (UV)) light source highlight the potential of 405-nm light for fungal decontamination applications

SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human-induced pluripotent stem-cell-derived kidney organoids with SARS-CoV-2. Single-cell RNA sequencing indicated injury and dedifferentiation of infected cells with activation of profibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in long COVID

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

Prevention of photo-repair recovery following pulsed UV-light treatment of straphylococcus aureus : implications for decontamination applications

Pulsed UV-rich (PUV) light is a sterilisation technology which utilises high peak power applied over short time periods, resulting in rapid microbial inactivation. It inactivates microorganisms through the generation of DNA mutations which prevent bacterial replication, rendering cells inactive. Many bacteria, however, possess DNA repair mechanisms, the most notable being photoreactivation, which utilises 300-500 nm wavelength light to repair UVinduced damage. The present study examines the photoinactivation and photoreactivation capability of Staphylococcus aureus, an important bacterial pathogen. A xenon flashlamp was used for inactivation of suspensions of varying population density, with fewer than 10 pulses of UV-rich light required to achieve a 7-log10 reduction in population. Photoreactivation of sub-lethally damaged cells was investigated and exposure to 370 nm light was found to induce up to a 3-log10 increase in viable cell count, with this maximum decreasing upon increasing pulsed UV-rich light damage. The use of PUV-light is effective for inactivation of bacteria, however elucidation of the lethal doses required for complete inactivation is necessary to prevent the possibility of subsequent photoreactivation of sub-lethally damaged cells, which could compromise the use of this technology in medical and commercial decontamination applications