Background: TcpB is a TIR domain-containing protein form Brucella. Results: TcpB interacts with the host Toll-like receptor and adaptors, and its structure reveals a dimer essential for activity. Conclusion: TcpB forms a nonfunctional complex with host molecules, thus suppressing signaling. Significance: The work explains the structural and functional basis of immune suppression by the protein TcpB from a pathogenic bacterium.

Cell phones may be an ideal habitat for colonization by bacterial pathogens, especially in hot climates, and may be a reservoir or vehicle in transmitting nosocomial infections. We investigated bacterial contamination on cell phones of healthcare workers in three hospitals in Saudi Arabia and determined antibacterial resistance of selected bacteria. A questionnaire was submitted to 285 healthcare workers in three hospitals, and information was collected on cell phone usage at the work area and in the toilet, cell phone cleaning and sharing, and awareness of cell phones being a source of infection. Screening on the Vitek 2 Compact system (bioMérieux Inc., USA) was done to characterize bacterial isolates. Of the 60 samples collected from three hospitals, 38 (63.3%) were positive with 38 bacterial isolates (4 Gram-negative and 34 Gram-positive bacteria). We found 38.3% of cell phones were contaminated with coagulase-negative staphylococci, particularly Staphylococcus epidermidis (10 isolates). Other bacterial agents identified were S. aureus, S. hominis, Alloiococcus otitis, Vibrio fluvialis, and Pseudomonas stutzeri. Antimicrobial susceptibility testing showed that most coagulase-negative staphylococci were resistant to benzylpenicillin, erythromycin, and rifampicin. Eight isolates were resistant to oxacillin, specifically S. epidermidis (3), S. hominis (2), and S. warneri (2). A. otitis, a cause of acute otitis media showed multidrug resistance. One isolate, a confirmed hetero-vancomycin intermediate-resistant S. aureus, was resistant to antibiotics, commonly used to treat skin infection. There was a significant correlation between the level of contamination and usage of cell phone at toilet and sharing. Our findings emphasize the importance of hygiene practices in cell phone usage among healthcare workers in preventing the transmission of multidrug-resistant microbes.

There are regular reports of extrapulmonary infections and manifestations related to the ongoing COVID-19 pandemic. Coronaviruses are potentially neurotropic, which renders neuronal tissue vulnerable to infection, especially in elderly individuals or in those with neuro-comorbid conditions. Complaints of ageusia, anosmia, myalgia, and headache; reports of diseases such as stroke, encephalopathy, seizure, and encephalitis; and loss of consciousness in patients with COVID-19 confirm the neuropathophysiological aspect of this disease. The brain is linked to pulmonary organs, physiologically through blood circulation, and functionally through the nervous system. The interdependence of these vital organs may further aggravate the pathophysiological aspects of COVID-19. The induction of a cytokine storm in systemic circulation can trigger a neuroinflammatory cascade, which can subsequently compromise the blood-brain barrier and activate microglia- and astrocyte-borne Toll-like receptors, thereby leading to neuronal tissue damage. Hence, a holistic approach should be adopted by healthcare professionals while treating COVID-19 patients with a history of neurodegenerative disorders, neuropsychological complications, or any other neuro-compromised conditions. Imperatively, vaccines are being developed at top priority to contain the spread of the severe acute respiratory syndrome coronavirus 2, and different vaccines are at different stages of development globally. This review discusses the concerns regarding the neuronal complications of COVID-19 and the possible mechanisms of amelioration.

This study evaluates the impact of two separate incubation periods (4 and 6 weeks) on the morphology of sol–gel-fabricated ZnO nanospikes (ZNs), that is, ZN1 and ZN2, respectively. We further analyzed the inhibitory effects of ZN1 and ZN2 on quorum sensing (QS) and biofilm formation in Pseudomonas aeruginosa (PAO1) and Chromobacterium violaceum (strains 12472 and CVO26). The size of the synthesized ZNs was in the range of 40–130 nm, and finer nanoparticles were synthesized after an incubation period of 6 weeks. Treatment with ZNs decreased the production of violacein in the pathogen without affecting the bacterial growth, which indicated that ZNs inhibited the QS signaling regulated by N -acyl homoserine lactone. ZN2 had a higher inhibitory action on the virulence factor productivity than ZN1. Furthermore, ZN2-treated cells displayed a substantial decrease in azocasein-degrading protease activity (80%), elastase activity (83%), and pyocyanin production (85%) relative to untreated P. aeruginosa PAO1 cells. Treatment with ZN2 decreased swarming motility and exopolysaccharide production by 89 and 85%, respectively. ZN2 was effective against both the las & pqs systems of P. aeruginosa and exhibited broad-spectrum activity. Additionally, ZN2 was more efficient in inhibiting the biofilm formation at the attachment stage than ZN1. These findings revealed that in P. aeruginosa , ZN2 demonstrated inhibitory effects on QS as well as on the development of biofilms. Thus, ZN2 can be potentially used to treat drug-resistant P. aeruginosa infections.

Leishmania is an intracellular protozoan parasite which causes Leishmaniasis, a global health problem affecting millions of people throughout 89 different countries in the world. The current treatment which includes use of amphotericin B, antimonials, and others has major drawbacks due to toxicity, resistance, and extraordinary high cost. So there is an urgent need of development of new drug targets to fight against leishmaniasis. In this regard we have selected Leishmania donovani Ca2+ ion channel (Ld-CC) as potential drug target. Ld-CC regulates concentration of Ca2+ ions which is involved in several functions like flagellar motion, mitochondrial oxidative metabolism and entry inside the macrophages. Since Ld-CC has not been characterised yet, we performed homology modelling of Leishmania donovani Ca2+ ion channel (Ld-CC) and docking studies of ligand library against this channel. 542 compound library of National Cancer Institute (NCI) diversity 3 dataset selected for screening studies. The ligands ZINC17287336 and ZINC29590262 were selected as best energy conformers because they show highest binding affinity towards its target (Ld-CC). They interact with the active site residues in the pocket of Ld-CC which suggests that the docked conformations are good and acceptable. Moreover, these two selected compounds also have relatively high binding affinity than nifedipine and verapamil, known human calcium channel blockers which had been reported to have mild anti-leishmanial activity. Among these two top screened inhibitors the ligand ZINC29590262 shows poor binding affinity towards the Human voltagedependent L-type calcium channel subunit alpha-1C in comparison to the Ld-CC. Therefore, we proposed this ligand as the best inhibitor which shows 40% more binding affinity with Ld-CC than the human-VDCC. These results suggest that our screened ligand ZINC29590262 could act as novel drug and may show much better antileishmanial activity.