Cough is a very common symptom causing medical consult. Several remedies are readily available in the market however these are currently not recommended among the pediatric population due to a few reasons which include the benign nature of acute cough, limited effectivity and lack of support from the United States Food and Drug Administration (USFDA) due to abuse potential.

We report a case of a 2-year-old male, no known co-morbidities with a 2 week history of upper respiratory tract infection. Initial assessment showed viral infection hence patient was given medications for symptomatic treatment. However, l week after, patient still presented with symptomatic persistent coughing that disrupted his activities of daily living, hence antitussive medication was already prescribed. After another 7 days, there was still persistence of symptoms, hence patient was given a trial medication of Pregabalin 0.7 milligram/kg/dose which noted instant cough relief one hour after the initial intake. Patient also reported to be more playful, improved sleep at night and improved appetite. Patient received total of 2 doses of Pregabalin in the span of 48 hours. On the third day, patient was still coughing but reported to be significantly less frequent and more productive, hence medication was then put on hold. Patient continuously improved after 5 more days and was eventually cough free.

This case report demonstrates the adequacy of Pregabalin as a supportive antitussive medication in a patient with an acute cough secondary to a viral infection.

Rabies remains a persistent public health issue in the Philippines, despite the existence of national and local policies and programs aimed at addressing its eradication. The viral disease, which elicits fatality yet is preventable, disproportionately affects rural areas, especially geographically isolated and disadvantaged area due to the junction of socio-cultural and technical challenges. This commentary article explores the myriad of barriers to rabies prevention and control, including poverty, cultural beliefs, limited health literacy, health delivery, and access inequity. However, the implementation of Rabies Act of 2007, which mandates mass vaccination, education, and the establishment of Animal Bite Treatment Centers (ABTCs), has gaps in the implementation that compromises the program’s sustainability and effectiveness. Deep-rooted cultural practices and beliefs delay or, more so replace evidence-informed medical practices, while geographic isolation and underfunded healthcare facilities hinder optimal provision of care. Moreover, interagency coordination and fragmented reporting surveillance systems further complicate effective rabies control. To address the gaps, this paper advocates for a culturally tailored and community-centered One Health approach that addresses both social and technical aspects of rabies prevention. Important recommendations include decentralizing ABTCs, sustaining vaccination programs with local government support and funding, integrating rabies education into schools and community outreach, and intensifying through multisectoral collaboration both government and nongovernment institutions. Achieving a rabies-free country requires not only biomedical interventions but also a holistic approach – equitable access to healthcare, trust building in communities, and long-term political commitment. In this manner, regardless of location and socioeconomic status, it ensures that this viral disease will be controlled and prevented.

Viral infectious diseases, characterized by their intricate nature and wide-ranging diversity, pose substantial challenges in the domain of data management. The vast volume of data generated by these diseases, spanning from the molecular mechanisms within cells to large-scale epidemiological patterns, has surpassed the capabilities of traditional analytical methods. In the era of artificial intelligence (AI) and big data, there is an urgent necessity for the optimization of these analytical methods to more effectively handle and utilize the information. Despite the rapid accumulation of data associated with viral infections, the lack of a comprehensive framework for integrating, selecting, and analyzing these datasets has left numerous researchers uncertain about which data to select, how to access it, and how to utilize it most effectively in their research.This review endeavors to fill these gaps by exploring the multifaceted nature of viral infectious diseases and summarizing relevant data across multiple levels, from the molecular details of pathogens to broad epidemiological trends. The scope extends from the micro-scale to the macro-scale, encompassing pathogens, hosts, and vectors. In addition to data summarization, this review thoroughly investigates various dataset sources. It also traces the historical evolution of data collection in the field of viral infectious diseases, highlighting the progress achieved over time. Simultaneously, it evaluates the current limitations that impede data utilization.Furthermore, we propose strategies to surmount these challenges, focusing on the development and application of advanced computational techniques, AI-driven models, and enhanced data integration practices. By providing a comprehensive synthesis of existing knowledge, this review is designed to guide future research and contribute to more informed approaches in the surveillance, prevention, and control of viral infectious diseases, particularly within the context of the expanding big-data landscape.
Big Data ; Humans ; Virus Diseases/virology* ; Artificial Intelligence

The innate immune response is the first line of defense for the host against viral infections. Targeted degradation of pathogenic microorganisms through autophagy, in conjunction with pattern recognition receptors synergistically inducing the production of interferon (IFN), constitutes an important pathway for the body to resist viral infections. Rubicon, a Run domain Beclin 1-interacting and cysteine-rich domain protein, has an inhibitory effect on autophagy and IFN production. On the one hand, Rubicon, as a component of the phosphoinositide 3-kinase (PI3K) complex, interacts with different domains of vacuolar protein sorting 34 (Vps34), ultraviolet radiation resistance associated gene (UVRAG), guanosine triphosphate (GTP) kinase, and RAS oncogene family member 7 (Rab7) to mediate the inhibition of autophagy maturation; on the other hand, Rubicon inhibits the ubiquitination of nuclear factor κB essential modulator (NEMO) and the dimerization of interferon regulatory factor 3 (IRF3), thereby blocking the signal transduction related to IFN production. Research has revealed that various viruses, such as Kaposi's sarcoma-associated herpesvirus (KSHV), hepatitis B virus (HBV), Sendai virus (SeV), and hepatitis C virus (HCV), achieve innate immune evasion by regulating the expression or function of Rubicon. Rubicon is expected to be a new target for antiviral therapy.
Humans ; Autophagy/immunology* ; Immunity, Innate ; Interferons/immunology* ; Immune Evasion ; Animals ; Virus Diseases/virology* ; Signal Transduction ; Viruses/immunology* ; Intracellular Signaling Peptides and Proteins/immunology* ; Autophagy-Related Proteins

Mitochondria are one of the oldest and most important endomembrane systems in eukaryotic cells and serve as the hubs of multiple cellular processes. Mitophagy (mitochondrial autophagy), a major way to maintain mitochondrial homeostasis, is closely linked to antiviral immune regulation. Depending on whether ubiquitination is required for the involved receptors or adaptors, mitophagy can be classified into ubiquitin-dependent and ubiquitin-independent types. Viruses can directly or indirectly regulate mitophagy and mitochondrial dynamics through various pathways. Through these processes, they can affect innate and adaptive immunity, so as to achieve immune escape, aggravate cell damage or promote the formation of adaptive immunity. This review summarizes the latest research progress on the role of viral infection-regulated mitophagy in the regulation of immune response.
Mitophagy/immunology* ; Humans ; Animals ; Virus Diseases/immunology* ; Mitochondria/metabolism* ; Immunity, Innate ; Adaptive Immunity

Virus-induced senescence (VIS) is a significant biological phenomenon, which is associated with declining immune function, accelerating aging process and causing aging-related diseases. A variety of common viruses, including RNA viruses (such as SARS-CoV-2), DNA viruses (such as herpesviruses and hepatitis B virus), and prions can cause VIS in host cells. The primary mechanisms include abnormal activation of the cGAS-STING signaling pathway, DNA damage response, and potential correlations with the integrated stress response due to intracellular phase separation. Viral infection and cellular senescence influence each other: cellular senescence serves as a defense to restrict viral replication and transmission, while some viruses exploit cellular senescence to enhance their infectivity and replication. Understanding the mechanisms of VIS is conducive to the development of therapeutic strategies for viral infections and promotion of healthy aging. However, there is lack of research on therapeutic targets and drug development in this field so far. Although senolytics may be effective for anti-senescent cells therapy, their efficacy for VIS needs evidence from further clinical trials. This article reviews the research progress on the connection between viral infection and cellular senescence, to provide insights for the prevention and treatment of aging related diseases.
Humans ; Cellular Senescence/physiology* ; Virus Diseases/physiopathology* ; Signal Transduction ; Nucleotidyltransferases/metabolism* ; DNA Damage ; Virus Replication ; COVID-19 ; Membrane Proteins/metabolism* ; SARS-CoV-2

A growing interest in the comprehensive pathogenic mechanisms of psychiatric disorders from the perspective of the microbiome has been witnessed in recent decades; the intrinsic link between microbiota and brain function through the microbiota-gut-brain axis or other pathways has gradually been realized. However, little research has focused on viruses-entities characterized by smaller dimensions, simpler structures, greater diversity, and more intricate interactions with their surrounding milieu compared to bacteria. To date, alterations in several populations of bacteriophages and viruses have been documented in both mouse models and patients with psychiatric disorders, including schizophrenia, major depressive disorder, autism spectrum disorder, and Alzheimer's disease, accompanied by metabolic disruptions that may directly or indirectly impact brain function. In addition, eukaryotic virus infection-mediated brain dysfunction provides insights into the psychiatric pathology involving viruses. Efforts towards virus-based diagnostic and therapeutic approaches have primarily been documented. However, limitations due to the lack of large-scale cohort studies, reliability, clinical applicability, and the unclear role of viruses in microbiota interactions pose a challenge for future studies. Nevertheless, it is conceivable that investigations into viruses herald a new era in the field of precise psychiatry.
Humans ; Mental Disorders/virology* ; Animals ; Brain/virology* ; Gastrointestinal Microbiome/physiology* ; Viruses ; Virus Diseases/complications*

The protein kinase A/protein kinase G/protein kinase C-family (AGC kinase family) of eukaryotes is involved in regulating numerous biological processes. The 3-phosphoinositide- dependent protein kinase 1 (PDK1), is a conserved serine/threonine kinase in eukaryotes. To understand the roles of PDK1 homologous genes in cell death and immunity in tetraploid Nicotiana tabacum, the previuosly generated transgenic CRISPR/Cas9 lines, in which 5-7 alleles of the 4 homologous PDK1 genes (NtPDK1a/1b/1c/1d homologs) simultaneously knocked out, were used in this study. Our results showed that the hypersensitive response (HR) triggered by transient overexpression of active Pto (Pto^Y207D) or soybean GmMEKK1 was significantly delayed, whereas the resistance to Pseudomonas syrangae pv. tomato DC3000 (Pst DC3000) and tobacco mosaic virus (TMV) was significantly elevated in these partial knockout lines. The elevated resistance to Pst DC3000 and TMV was correlated with the elevated activation of NtMPK6, NtMPK3, and NtMPK4. Taken together, our results indicated that NtPDK1s play a positive role in cell death but a positive role in disease resistance, likely through negative regulation of the MAPK signaling cascade.
Nicotiana/virology* ; Disease Resistance/genetics* ; Plant Diseases/immunology* ; Plants, Genetically Modified/genetics* ; Gene Knockout Techniques ; Plant Proteins/genetics* ; CRISPR-Cas Systems ; Protein Serine-Threonine Kinases/genetics* ; 3-Phosphoinositide-Dependent Protein Kinases/genetics* ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase ; Tobacco Mosaic Virus/pathogenicity*

Porcine epidemic diarrhea virus (PEDV) is an intestinal coronavirus that can cause porcine epidemic diarrhea, leading to diarrhea, vomiting, weight loss, and even death in piglets. Due to the diversity of PEDV strains, traditional vaccines are difficult to sustainably and effectively prevent and control PEDV. This article reviews the strategies and mechanisms of active substances in regulating intracellular signaling pathways, viral proteins, and microbial metabolites to enhance the host immune function against PEDV. It emphasizes the prevention of PEDV resistance and the potential harm of PEDV breaking through interspecies barriers to the human society, aiming to provide reliable theoretical support for the development of new antiviral drugs or vaccines.
Porcine epidemic diarrhea virus/immunology* ; Animals ; Swine ; Swine Diseases/prevention & control* ; Antiviral Agents/pharmacology* ; Coronavirus Infections/virology* ; Viral Vaccines/immunology* ; Humans ; Signal Transduction

Viral infections are one of the main causes of deaths and economic losses around the globe, and effective virus detection methods are essential for epidemic prevention and control. Most existing detection methods have problems such as high false negative/positive rates, slow responses, high costs, and dependence on professional equipment and personnel, which are not conducive to the rapid and accurate detection of viruses. Field effect transistor (FET) biosensors have attracted widespread attention due to their advantages of label-free detection, high sensitivity, fast responses, real-time measurement, low power consumption, and small sizes for portability. This article first briefly describes the basic situation of viruses and the structure and detection principle of FET biosensors. Subsequently, it delves into the research achievements in the application of FET biosensors in the detection of influenza viruses, hepatitis viruses, human immunodeficiency virus, and severe acute respiratory syndrome coronavirus 2. Finally, we make a comprehensive summary and reasonable outlook on the role played by FET biosensors in biomedicine.
Biosensing Techniques/instrumentation* ; Transistors, Electronic ; Humans ; SARS-CoV-2/isolation & purification* ; Viruses/isolation & purification* ; Orthomyxoviridae/isolation & purification* ; Hepatitis Viruses/isolation & purification* ; Virus Diseases/virology* ; HIV/isolation & purification* ; COVID-19/diagnosis*