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Photoplethysmography (PPG) is a low-cost, noninvasive optical technique that uses change in light transmission with changes in blood volume within tissue to provide information for cardiovascular health and fitness. As remote health and wearable medical devices become more prevalent, PPG devices are being developed as part of wearable systems to monitor parameters such as heart rate (HR) that do not require complex analysis of the PPG waveform. However, complex analyses of the PPG waveform yield valuable clinical information, such as: blood pressure, respiratory information, sympathetic nervous system activity, and heart rate variability. Systems aiming to derive such complex parameters do not always account for realistic sources of noise, as testing is performed within controlled parameter spaces. A wearable monitoring tool to be used beyond fitness and heart rate must account for noise sources originating from individual patient variations (e.g., skin tone, obesity, age, and gender), physiology (e.g., respiration, venous pulsation, body site of measurement, and body temperature), and external perturbations of the device itself (e.g., motion artifact, ambient light, and applied pressure to the skin). Here, we present a comprehensive review of the literature that aims to summarize these noise sources for future PPG device development for use in health monitoring. [ABSTRACT FROM AUTHOR]

The demand for advanced water treatment solutions necessitates the development of multifunctional, photodynamically active membranes. Phthalocyanines (Pcs), a class of organic photosensitizers, offer significant potential for enhancing treatment efficacy through photodynamic activity. This study reports the development of Pc-modified polymeric microfiltration membranes as visible-light-responsive, multifunctional membrane reactors with enhanced photodynamic and filtration properties. Cobalt phthalocyanine (CoPc), zinc phthalocyanine (ZnPc), tetra-amino zinc phthalocyanine (TAZnPc), and tetra-sulfonated aluminum phthalocyanine (TSAlPc) were integrated into the membranes, imparting notable changes in morphology, surface wettability, and chemical functionality. Characterization revealed improvements in optical responsiveness and surface properties that contributed to robust photodynamic and filtration performance. Static photodynamic evaluations demonstrated high efficacy, with ZnPc mixed matrix membrane (MMM) achieving superior dye degradation and TSAlPc grafted membrane (GM) yielding significant bacterial inactivation. Filtration trials confirmed ZnPc MMM's biofouling resistance and permeance stability, reaching 99.97 % rejection of bio-fouled microplastics (MPs) and a 45 % permeance enhancement under irradiation. Virus filtration results demonstrated TSAlPc MMM's viral retention efficacy, achieving a 2.05-log reduction against Influenza A virus. These findings underscore the potential of Pc-functionalized membranes as promising candidates for advanced water treatment applications, offering robust contaminant rejection, biofouling control, and broad-spectrum antimicrobial efficacy in a single, multifunctional platform., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2025 Elsevier Ltd. All rights reserved.)

Mosquitoes are important vectors for transmission of many viruses of public and veterinary health concern. These viruses most commonly have an RNA genome and infect mosquitoes for life. The principal mosquito antiviral response is the RNAi system which destroys virus RNA. Here, we confirm an earlier study that Aedes aegypti mosquitoes infected with positive-stranded RNA arboviruses can transmit specific immunity to their offspring. We show that this trans -generational immunity requires replication of virus RNA and reverse transcription of vRNA to vDNA in the infected parents and intergenerational transfer of vDNA. This vDNA is both genome-integrated and episomal. The episomal vDNA sequences are flanked by retrotransposon long-terminal repeats, predominantly Copia -like. Integrated vDNA sequences are propagated along several generations but specific immunity is effective only for a few generations and correlates with the presence of vRNA and episomal vDNA. This understanding raises new possibilities for the control of important mosquito-borne virus diseases., Competing Interests: The authors declare no competing interests., (© 2023 The Authors.)

Although waterborne virus removal may be achieved using separation membrane technologies, such technologies remain largely inefficient at generating virus-free effluents due to the lack of anti-viral reactivity of conventional membrane materials required to deactivating viruses. Here, a stepwise approach towards simultaneous filtration and disinfection of Human Coronavirus 229E (HCoV-229E) in water effluents, is proposed by engineering dry-spun ultrafiltration carbon nanotube (CNT) membranes, coated with anti-viral SnO 2 thin films via atomic layer deposition. The thickness and pore size of the engineered CNT membranes were fine-tuned by varying spinnable CNT sheets and their relative orientations on carbon nanofibre (CNF) porous supports to reach thicknesses less than 1 µm and pore size around 28 nm. The nanoscale SnO 2 coatings were found to further reduce the pore size down to ∼21 nm and provide more functional groups on the membrane surface to capture the viruses via size exclusion and electrostatic attractions. The synthesized CNT and SnO 2 coated CNT membranes were shown to attain a viral removal efficiency above 6.7 log 10 against HCoV-229E virus with fast water permeance up to ∼4 × 10 3 and 3.5 × 10 3 L.m -2 .h -1 .bar -1 , respectively. Such high performance was achieved by increasing the dry-spun CNT sheets up to 60 layers, orienting successive 30 CNT layers at 45°, and coating 40 nm SnO 2 on the synthesized membranes. The current study provides an efficient scalable fabrication scheme to engineer flexible ultrafiltration CNT-based membranes for cost-effective filtration and inactivation of waterborne viruses to outperform the state-of-the-art ultrafiltration membranes., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 Elsevier Ltd. All rights reserved.)

Mosquito-borne diseases remain a major cause of morbidity and mortality. Population replacement strategies involving the wMel strain of Wolbachia are being used widely to control mosquito-borne diseases. However, these strategies may be influenced by temperature because wMel is vulnerable to heat. wMel infections in Drosophila melanogaster are genetically diverse, but few transinfections of wMel variants have been generated in Aedes aegypti. Here, we successfully transferred a wMel variant (termed wMelM) originating from a field-collected D. melanogaster into Ae. aegypti. The new wMelM variant (clade I) is genetically distinct from the original wMel transinfection (clade III), and there are no genomic differences between wMelM in its original and transinfected host. We compared wMelM with wMel in its effects on host fitness, temperature tolerance, Wolbachia density, vector competence, cytoplasmic incompatibility and maternal transmission under heat stress in a controlled background. wMelM showed a higher heat tolerance than wMel, likely due to higher overall densities within the mosquito. Both wMel variants had minimal host fitness costs, complete cytoplasmic incompatibility and maternal transmission, and dengue virus blocking under laboratory conditions. Our results highlight phenotypic differences between Wolbachia variants and wMelM shows potential as an alternative strain in areas with strong seasonal temperature fluctuations., (© 2022 The Authors. Environmental Microbiology published by Society for Applied Microbiology and John Wiley & Sons Ltd.)

The continuing emergence of arbovirus disease outbreaks around the world, despite the use of vector control strategies, warrants the development of new strategies to reduce arbovirus transmission. Superinfection exclusion, a phenomenon whereby a primary virus infection prevents the replication of a second closely related virus, has potential to control arbovirus disease emergence and outbreaks. This phenomenon has been observed for many years in plants, insects and mammalian cells. In this review, we discuss the significance of identifying novel vector control strategies, summarize studies exploring arbovirus superinfection exclusion and consider the potential for this phenomenon to be the basis for novel arbovirus control strategies.

Flaviviruses are emerging and re-emerging arthropod-borne pathogens responsible for significant mortality and morbidity worldwide. The genus comprises more than seventy small, positive-sense, single-stranded RNA viruses, which are responsible for a spectrum of human and animal diseases ranging in symptoms from mild, influenza-like infection to fatal encephalitis and haemorrhagic fever. Despite genomic and structural similarities across the genus, infections by different flaviviruses result in disparate clinical presentations. This review focusses on two haemorrhagic flaviviruses, dengue virus and yellow fever virus, and two neurotropic flaviviruses, Japanese encephalitis virus and Zika virus. We review current knowledge on host-pathogen interactions, virus entry strategies and tropism.

Although mosquitoes serve as vectors of many pathogens of public health importance, their response to viral infection is poorly understood. It also remains to be investigated whether viruses deploy some mechanism to be able to overcome this immune response. Here, we have used an RNA-Seq approach to identify differentially regulated genes in Culex quinquefasciatus cells following West Nile virus (WNV) infection, identifying 265 transcripts from various cellular pathways that were either upregulated or downregulated. Ubiquitin-proteasomal pathway genes, comprising 12% of total differentially regulated genes, were selected for further validation by real time RT-qPCR and functional analysis. It was found that treatment of infected cells with proteasomal inhibitor, MG-132, decreased WNV titers, indicating importance of this pathway during infection process. In infection models, the Culex ortholog of mammalian Cul4A/B (cullin RING ubiquitin ligase) was found to be upregulated in vitro as well as in vivo, especially in midguts of mosquitoes. Gene knockdown using dsRNA and overexpression studies indicated that Culex Cul4 acts as a pro-viral protein by degradation of CxSTAT via ubiquitin-proteasomal pathway. We also show that gene knockdown of Culex Cul4 leads to activation of the Jak-STAT pathway in mosquitoes leading to decrease viral replication in the body as well as saliva. Our results suggest a novel mechanism adopted by WNV to overcome mosquito immune response and increase viral replication.

Unlabelled: Wongabel virus (WONV) is an arthropod-borne rhabdovirus that infects birds. It is one of the growing array of rhabdoviruses with complex genomes that encode multiple accessory proteins of unknown function. In addition to the five canonical rhabdovirus structural protein genes (N, P, M, G, and L), the 13.2-kb negative-sense single-stranded RNA (ssRNA) WONV genome contains five uncharacterized accessory genes, one overlapping the N gene (Nx or U4), three located between the P and M genes (U1 to U3), and a fifth one overlapping the G gene (Gx or U5). Here we show that WONV U3 is expressed during infection in insect and mammalian cells and is required for efficient viral replication. A yeast two-hybrid screen against a mosquito cell cDNA library identified that WONV U3 interacts with the 83-amino-acid (aa) C-terminal domain of SNF5, a component of the SWI/SNF chromatin remodeling complex. The interaction was confirmed by affinity chromatography, and nuclear colocalization was established by confocal microscopy. Gene expression studies showed that SNF5 transcripts are upregulated during infection of mosquito cells with WONV, as well as West Nile virus (Flaviviridae) and bovine ephemeral fever virus (Rhabdoviridae), and that SNF5 knockdown results in increased WONV replication. WONV U3 also inhibits SNF5-regulated expression of the cytokine gene CSF1. The data suggest that WONV U3 targets the SWI/SNF complex to block the host response to infection., Importance: The rhabdoviruses comprise a large family of RNA viruses infecting plants, vertebrates, and invertebrates. In addition to the major structural proteins (N, P, M, G, and L), many rhabdoviruses encode a diverse array of accessory proteins of largely unknown function. Understanding the role of these proteins may reveal much about host-pathogen interactions in infected cells. Here we examine accessory protein U3 of Wongabel virus, an arthropod-borne rhabdovirus that infects birds. We show that U3 enters the nucleus and interacts with SNF5, a component of the chromatin remodeling complex that is upregulated in response to infection and restricts viral replication. We also show that U3 inhibits SNF5-regulated expression of the cytokine colony-stimulating factor 1 (CSF1), suggesting that it targets the chromatin remodeling complex to block the host response to infection. This study appears to provide the first evidence of a virus targeting SNF5 to inhibit host gene expression., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

As well as being vectors of many viral, bacterial, and protozoan pathogens of medical and veterinary importance, ticks harbour a variety of microorganisms which are not known to be pathogenic for vertebrate hosts. Continuous cell lines established from ixodid and argasid ticks could be infected with such endosymbiotic bacteria and endogenous viruses, but to date very few cell lines have been examined for their presence. DNA and RNA extracted from over 50 tick cell lines deposited in the Roslin Wellcome Trust Tick Cell Biobank (http://tickcells.roslin.ac.uk) were screened for presence of bacteria and RNA viruses, respectively. Sequencing of PCR products amplified using pan-16S rRNA primers revealed the presence of DNA sequences from bacterial endosymbionts in several cell lines derived from Amblyomma and Dermacentor spp. ticks. Identification to species level was attempted using Rickettsia- and Francisella-specific primers. Pan-Nairovirus primers amplified PCR products of uncertain specificity in cell lines derived from Rhipicephalus, Hyalomma, Ixodes, Carios, and Ornithodoros spp. ticks. Further characterisation attempted with primers specific for Crimean-Congo haemorrhagic fever virus segments confirmed the absence of this arbovirus in the cells. A set of pan-Flavivirus primers did not detect endogenous viruses in any of the cell lines. Transmission electron microscopy revealed the presence of endogenous reovirus-like viruses in many of the cell lines; only 4 of these lines gave positive results with primers specific for the tick Orbivirus St Croix River virus, indicating that there may be additional, as yet undescribed 'tick-only' viruses inhabiting tick cell lines., (Copyright © 2012 Elsevier GmbH. All rights reserved.)

Several components of the mosquito immune system including the RNA interference (RNAi), JAK/STAT, Toll and IMD pathways have previously been implicated in controlling arbovirus infections. In contrast, the role of the phenoloxidase (PO) cascade in mosquito antiviral immunity is unknown. Here we show that conditioned medium from the Aedes albopictus-derived U4.4 cell line contains a functional PO cascade, which is activated by the bacterium Escherichia coli and the arbovirus Semliki Forest virus (SFV) (Togaviridae; Alphavirus). Production of recombinant SFV expressing the PO cascade inhibitor Egf1.0 blocked PO activity in U4.4 cell- conditioned medium, which resulted in enhanced spread of SFV. Infection of adult female Aedes aegypti by feeding mosquitoes a bloodmeal containing Egf1.0-expressing SFV increased virus replication and mosquito mortality. Collectively, these results suggest the PO cascade of mosquitoes plays an important role in immune defence against arboviruses.

RNA interference (RNAi) is an important mosquito defense mechanism against arbovirus infection. In this paper we study the processes underlying antiviral RNAi in Aedes albopictus-derived U4.4 mosquito cells infected with Semliki Forest virus (SFV) (Togaviridae; Alphavirus). The production of virus-derived small interfering RNAs (viRNAs) from viral double-stranded RNA (dsRNA) is a key event in this host response. dsRNA could be formed by RNA replication intermediates, by secondary structures in RNA genomes or antigenomes, or by both. Which of these dsRNAs is the substrate for the generation of viRNAs is a fundamental question. Here we used deep sequencing of viRNAs and bioinformatic analysis of RNA secondary structures to gain insights into the characteristics and origins of viRNAs. An asymmetric distribution of SFV-derived viRNAs with notable areas of high-level viRNA production (hot spots) and no or a low frequency of viRNA production (cold spots) along the length of the viral genome with a slight bias toward the production of genome-derived viRNAs over antigenome-derived viRNAs was observed. Bioinformatic analysis suggests that hot spots of viRNA production are rarely but not generally associated with putative secondary structures in the SFV genome, suggesting that most viRNAs are derived from replicative dsRNA. A pattern of viRNAs almost identical to those of A. albopictus cells was observed for Aedes aegypti-derived Aag2 cells, suggesting common mechanisms that lead to viRNA production. Hot-spot viRNAs were found to be significantly less efficient at mediating antiviral RNAi than cold-spot viRNAs, pointing toward a nucleic acid-based viral decoy mechanism to evade the RNAi response.

In their vertebrate hosts, arboviruses such as Semliki Forest virus (SFV) (Togaviridae) generally counteract innate defenses and trigger cell death. In contrast, in mosquito cells, following an early phase of efficient virus production, a persistent infection with low levels of virus production is established. Whether arboviruses counteract RNA interference (RNAi), which provides an important antiviral defense system in mosquitoes, is an important question. Here we show that in Aedes albopictus-derived mosquito cells, SFV cannot prevent the establishment of an antiviral RNAi response or prevent the spread of protective antiviral double-stranded RNA/small interfering RNA (siRNA) from cell to cell, which can inhibit the replication of incoming virus. The expression of tombusvirus siRNA-binding protein p19 by SFV strongly enhanced virus spread between cultured cells rather than virus replication in initially infected cells. Our results indicate that the spread of the RNAi signal contributes to limiting virus dissemination.

The double-stranded RNA-activated protein kinase (PKR) is a key regulator of protein translation, interferon (IFN) expression and cell survival. Upon infection of vertebrate cells in continuous culture, the alphavirus Semliki Forest virus (SFV) initiates apoptosis and IFN synthesis. To determine the effect of PKR on SFV infection, we studied the course of infection in wild-type (wt) mice, mice with a genetic deletion of PKR (PKR-/-) and mouse embryo fibroblasts (MEFs) derived from these mice. In MEFs, PKR delayed virus protein synthesis, production of infectious virus and caspase-3-activated cell death and reduced the yield of infectious virus by 90%. Small interfering RNA suppression of PKR levels in NIH-3T3 cells also reduced virus production and apoptosis. In MEFs, PKR was not required for initiation of IFN-beta gene transcription, but contributed strongly to the magnitude of this response. Levels of IFN-beta transcripts in PKR-/- MEFs at 8 h were 80% lower than those in wt MEFs and levels of functional IFN at 24 h were 95% lower. Following infection of wt and PKR-/- mice, SFV4 and SFV A7(74) were avirulent. PKR increased levels of serum IFN and the rate of clearance of infectious virus from the brain. In summary, in response to SFV, PKR exerts an early antiviral effect that delays virus protein production and release of infectious virus and, whilst PKR is not required for induction of apoptosis or activation of the type I IFN response, it strongly augments the type I IFN response and contributes to clearance of infectious virus from the mouse brain.