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MicroRNAs inside dental fluids (spittle and gingival crevicular water) while biomarkers in orthodontics: methodical evaluation and incorporated bioinformatic examination.
Our study uncovers an immune gene signature that associates with HBV cccDNA transcription and increases our understanding of viral persistence.The COVID-19 pandemic has frequently produced more highly transmissible SARS-CoV-2 variants, such as Omicron, which has produced sublineages. It is a challenge to tell apart high-risk Omicron sublineages and other lineages of SARS-CoV-2 variants. We aimed to build a fine-grained deep learning (DL) model to assess SARS-CoV-2 transmissibility, updating our former coarse-grained model, with the training/validating data of early-stage SARS-CoV-2 variants and based on sequential Spike samples. Sequential amino acid (AA) frequency was decomposed into serially and slidingly windowed fragments in Spike. Unsupervised machine learning approaches were performed to observe the distribution in sequential AA frequency and then a supervised Convolutional Neural Network (CNN) was built with three adaptation labels to predict the human adaptation of Omicron variants in sublineages. Results indicated clear inter-lineage separation and intra-lineage clustering for SARS-CoV-2 variants in the decomposed sequential AAs. Accurate classification by the predictor was validated for the variants with different adaptations. Higher adaptation for the BA.2 sublineage and middle-level adaptation for the BA.1/BA.1.1 sublineages were predicted for Omicron variants. Summarily, the Omicron BA.2 sublineage is more adaptive than BA.1/BA.1.1 and has spread more rapidly, particularly in Europe. The fine-grained adaptation DL model works well for the timely assessment of the transmissibility of SARS-CoV-2 variants, facilitating the control of emerging SARS-CoV-2 variants.Many countries have implemented public health and social measures (PHSMs) to control the spread of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Although the PHSMs are targeted at SARS-CoV-2 transmission control, they directly or indirectly impact the epidemiology of different respiratory viral diseases. The purpose of this study was to investigate the collateral impact of PHSMs used during the coronavirus disease 2019 (COVID-19) pandemic on the epidemiology of other respiratory viruses, including influenza, parainfluenza, respiratory syncytial virus, rhinovirus, and adenovirus infections. We conducted a systematic review of the published literature on changes in the incidence of respiratory viral diseases and detection rates of the respiratory viruses during COVID-19 pandemic, lasting from 2020-2021, published between December 2019 and March 2022 in PubMed, Embase, and Cochrane Library databases. We identified an overall decrease of 23-94% in the incidence of respiratory viral diseases and a decrease of 0-98% in the detection of the viruses. Our study suggests that the PHSMs implemented during COVID-19 pandemic reduced the incidence of respiratory viral diseases and transmission of respiratory viruses. At the time of this study, and as governments relax PHSMs, public health authorities should prepare for a probable increase in the burden of respiratory viral diseases.Despite the existence of an effective live-attenuated vaccine, measles can appear in vaccinated individuals. We investigated breakthrough measles cases identified during our surveillance activities within the measles/rubella surveillance network (MoRoNet) in Milan and surrounding areas (Northern Italy). Between 2017 and 2021, we confirmed measles virus (genotypes B3 or D8) infections in 653 patients and 51 of these (7.8%) were vaccinees. Among vaccinated individuals whose serum was available, a secondary failure was evidenced in 69.4% (25/36) of cases while 11 patients (30.6%) were non-responders. Non-responders were more frequently hospitalized and had significantly lower Ct values in both respiratory and urine samples. Median age and time since the last immunization were similar in the two groups. Importantly, we identified onward transmissions from vaccine failure cases. Vaccinees were involved in 20 outbreaks, in 10 of them they were able to transmit the virus, and in 8 of them, they were the index case. Comparing viral hemagglutinin sequences from vaccinated and non-vaccinated subjects did not show a specific mutation pattern. These results suggest that vaccination failure was likely due to the poor immune response of single individuals and highlights the importance of identifying breakthrough cases and characterizing their clinical and virologic profiles.Pseudorabies virus (PRV) is the causative agent of pseudorabies (PR). It can infect a wide range of mammals. PRV infection can cause severe acute neuropathy (the so-called "mad itch") in nonnatural hosts. PRV can infect the peripheral nervous system (PNS), where it can establish a quiescent, latent infection. The dorsal root ganglion (DRG) contains the cell bodies of the spinal sensory neurons, which can transmit peripheral sensory signals, including itch and somatic pain. Little attention has been paid to the underlying mechanism of the itch caused by PRV in nonnatural hosts. In this study, a mouse model of the itch caused by PRV was elaborated. BALB/c mice were infected intramuscularly with 105 TCID50 of PRV TJ. The frequency of the bite bouts and the durations of itch were recorded and quantified. The results showed that the PRV-infected mice developed spontaneous itch at 32 h postinfection (hpi). The frequency of the bite bouts and the durations of itch were increased over time. The mRNA expression levelsV strains. Taken together, the histamine synthesized by the HDC in the DRG neurons was responsible for the PRV-induced itch in the mice.A hallmark of severe acute respiratory syndrome virus (SARS-CoV-2) replication is the discontinuous transcription of open reading frames (ORFs) encoding structural virus proteins. Real-time reverse transcription PCR (RT-qPCR) assays in previous publications used either single or multiplex assays for SARS-CoV-2 genomic RNA detection and a singleplex approach for subgenomic RNA detection. Although multiplex approaches often target multiple genomic RNA segments, an assay that concurrently detects genomic and subgenomic targets has been lacking. To bridge this gap, we developed two duplex one-step RT-qPCR assays that detect SARS-CoV-2 genomic ORF1a and either subgenomic spike or subgenomic ORF3a RNAs. All primers and probes for our assays were designed to bind to variants of SARS-CoV-2. In this study, our assays successfully detected SARS-CoV-2 Washington strain and delta variant isolates at various time points during the course of live virus infection in vitro. The ability to quantify subgenomic SARS-CoV-2 RNA is important, as it may indicate the presence of active replication, particularly in samples collected longitudinally. Furthermore, specific detection of genomic and subgenomic RNAs simultaneously in a single reaction increases assay efficiency, potentially leading to expedited lucidity about viral replication and pathogenesis of any variant of SARS-CoV-2.To evaluate the diagnostic performance of the Liaison® Murex anti-HEV IgM and IgG assays running on the Liaison® instrument and compare the results with those obtained with Wantai HEV assays. We tested samples collected in immunocompetent and immunocompromised patients during the acute (HEV RNA positive, anti-HEV IgM positive) and the post-viremic phase (HEV RNA negative, anti-HEV IgM positive) of infections. The specificity was assessed by testing HEV RNA negative/anti-HEV IgG-IgM negative samples. The clinical sensitivity of the Liaison® IgM assay was 100% for acute-phase samples (56/56) and 57.4% (27/47) for post-viremic samples from immunocompetent patients. It was 93.8% (30/32) for acute-phase (viremic) samples and 71%% (22/31) for post-viremic samples from immunocompromised patients. The clinical sensitivity of the Liaison® IgG assay was 100% for viremic samples (56/56) and 94.6% (43/47) for post-viremic samples from immunocompetent patients. It was 84.3% (27/32) for viremic samples and 93.5% (29/31) for post-viremic samples from immunocompromised patients. Specificity was very high (>99%) in both populations. We checked the limit of detection stated for the Liaison® IgG assay (0.3 U/mL). The clinical performance of the Liaison® ANTI-HEV assays was good. These rapid, automated assays for detecting anti-HEV antibodies will greatly enhance the arsenal for diagnosing HEV infections.A severe course of acute respiratory disease caused by influenza A virus (IAV) infection is often linked with subsequent bacterial superinfection, which is difficult to cure. Thus, synergistic influenza-bacterial co-infection represents a serious medical problem. The pathogenic changes in the infected host are accelerated as a consequence of IAV infection, reflecting its impact on the host immune response. IAV infection triggers a complex process linked with the blocking of innate and adaptive immune mechanisms required for effective antiviral defense. Such disbalance of the immune system allows for easier initiation of bacterial superinfection. Therefore, many new studies have emerged that aim to explain why viral-bacterial co-infection can lead to severe respiratory disease with possible fatal outcomes. In this review, we discuss the key role of several IAV proteins-namely, PB1-F2, hemagglutinin (HA), neuraminidase (NA), and NS1-known to play a role in modulating the immune defense of the host, which consequently escalates the development of secondary bacterial infection, most often caused by Streptococcus pneumoniae. Understanding the mechanisms leading to pathological disorders caused by bacterial superinfection after the previous viral infection is important for the development of more effective means of prevention; for example, by vaccination or through therapy using antiviral drugs targeted at critical viral proteins.Influenza virus types A and B are responsible for acute viral infections that affect annually 1 billion people, with 290,000 to 650,000 deaths worldwide. In this study, we investigated the circulation of influenza B viruses over a 10-year period (2010-2019). Specimens from patients suspected of influenza infection were collected. Influenza detection was performed following RNA extraction and real-time RT-PCR. Genes coding for hemagglutinin (HA) and neuraminidase (NA) of influenza B viruses were partially sequenced, and phylogenetic analyses were carried out subsequently. During the study period, we received and tested a total of 15,156 specimens. Influenza B virus was detected in 1322 (8.7%) specimens. The mean age of influenza B positive patients was 10.9 years. When compared to reference viruses, HA genes from Senegalese circulating viruses showed deletions in the HA1 region. Direct Yellow 7 Phylogenetic analysis highlighted the co-circulation of B/Victoria and B/Yamagata lineage viruses with reassortant viruses. We also noted a clear seasonal pattern of circulation of influenza B viruses in Senegal.Despite occurring at the microscopic scale, the armed race between phages and their bacterial hosts involves multiple mechanisms, some of which are just starting to be understood. On the one hand, bacteria have evolved strategies that can stop the viral infection at different stages (adsorption, DNA injection and replication, biosynthesis and assembly of the viral progeny and/or release of the newly formed virions); on the other, phages have gradually evolved counterattack strategies that allow them to continue infecting their prey. This co-evolutionary process has played a major role in the development of microbial populations in both natural and man-made environments. Notably, understanding the parameters of this microscopic war will be paramount to fully benefit from the application of phage therapy against dangerous, antibiotic-resistant human pathogens. This review gathers the current knowledge regarding the mechanisms of phage resistance in the Staphylococcus genus, which includes Staphylococcus aureus, one of the most concerning microorganisms in terms of antibiotic resistance acquisition.
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