RESUMEN
Microbial communities, including bacteria, diatoms, and fungi, colonize plastic surfaces, forming biofilms known as the "plastisphere." Recent research has revealed that plastispheres also host a wide range of viruses, sparking interest in microbial ecology and virology. This shared habitat allows viruses to replicate, interact, infect, and spread, potentially impacting the environment and human health. Consequently, viruses attached to microplastics are now recognized to have broad effects on cellular and immune responses. However, the ecology and implications of viruses hosted in plastisphere habitats remain poorly understood, highlighting their fundamental importance as a subject of study. This review explores various pathways for virus attachment to plastispheres, factors influencing these interactions, their impacts within plastisphere and host-associated environments, and associated issues. It also summarizes current research and identifies knowledge gaps. We anticipate that this paper will help improve our predictive understanding of plastisphere viruses in natural settings and emphasizes the need for more research in real-world environments to advance the field.
Asunto(s)
Virus , Plásticos , Fenómenos Fisiológicos de los Virus , Biopelículas , Ecosistema , MicroplásticosRESUMEN
Bats are special in their ability to live long and host many emerging viruses. Our previous studies showed that bats have altered inflammasomes, which are central players in aging and infection. However, the role of inflammasome signaling in combating inflammatory diseases remains poorly understood. Here, we report bat ASC2 as a potent negative regulator of inflammasomes. Bat ASC2 is highly expressed at both the mRNA and protein levels and is highly potent in inhibiting human and mouse inflammasomes. Transgenic expression of bat ASC2 in mice reduced the severity of peritonitis induced by gout crystals and ASC particles. Bat ASC2 also dampened inflammation induced by multiple viruses and reduced mortality of influenza A virus infection. Importantly, it also suppressed SARS-CoV-2-immune-complex-induced inflammasome activation. Four key residues were identified for the gain of function of bat ASC2. Our results demonstrate that bat ASC2 is an important negative regulator of inflammasomes with therapeutic potential in inflammatory diseases.
Asunto(s)
Proteínas Reguladoras de la Apoptosis , Quirópteros , Inflamasomas , Ribonucleoproteínas , Virosis , Animales , Humanos , Ratones , Proteínas Reguladoras de la Apoptosis/metabolismo , Quirópteros/inmunología , COVID-19 , Inflamasomas/inmunología , Ribonucleoproteínas/metabolismo , SARS-CoV-2 , Virosis/inmunología , Fenómenos Fisiológicos de los VirusRESUMEN
The family Simuloviridae includes tailless icosahedral viruses with an internal lipid membrane. The capsid is constructed from two major capsid proteins, both with a single jelly-roll fold. The genome is a circular dsDNA molecule of 16-19 kb. All members infect halophilic archaea in the class Halobacteria (phylum Euryarchaeota) and are temperate viruses, their proviruses residing in host cells as extrachromosomal episomes. Once the lytic life cycle is triggered, production of virions causes cell lysis. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the family Simuloviridae, which is available at ictv.global/report/simuloviridae.
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Genoma Viral , Virus , Virus/genética , Virión/genética , Fenómenos Fisiológicos de los Virus , Proteínas de la Cápside/genética , Replicación ViralRESUMEN
Viruses are obligate intracellular parasites. Despite their dependence on host cells, viruses are evolutionarily autonomous, with their own genomes and evolutionary trajectories locked in arms races with the hosts. Here, we discuss a simple functional logic to explain virus macroevolution that appears to define the course of virus evolution. A small core of virus hallmark genes that are responsible for genome replication apparently descended from primordial replicators, whereas most virus genes, starting with those encoding capsid proteins, were subsequently acquired from hosts. The oldest of these acquisitions antedate the last universal cellular ancestor (LUCA). Host gene capture followed two major routes: convergent recruitment of genes with functions that directly benefit virus reproduction and exaptation when host proteins are repurposed for unique virus functions. These forms of host protein recruitment by viruses result in different levels of similarity between virus and host homologs, with the exapted ones often changing beyond easy recognition.
Asunto(s)
Virus , Evolución Biológica , Proteínas de la Cápside/genética , Evolución Molecular , Genes Virales , Lógica , Fenómenos Fisiológicos de los Virus , Virus/genética , Virus/metabolismoAsunto(s)
Anticuerpos Monoclonales , Antineoplásicos Inmunológicos , Evolución Biológica , COVID-19 , Virus , Anticuerpos Monoclonales/uso terapéutico , Anticuerpos Antivirales/genética , Antineoplásicos Inmunológicos/uso terapéutico , COVID-19/genética , COVID-19/terapia , Humanos , SARS-CoV-2/genética , Fenómenos Fisiológicos de los Virus/genética , Virus/genética , Virus/inmunologíaRESUMEN
The intention of this Special Edition was to collect review and original research articles that illustrate and stimulate the growing efforts to highlight the mechanisms of action of gonadotropins, as well as deepen our understanding of their biological roles in health and disease, aiming at revealing novel therapeutic opportunities in reproductive and regenerative medicine [...].
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Gonadotropinas , Reproducción , Reproducción/fisiología , Fenómenos Fisiológicos de los VirusRESUMEN
Cell death by apoptosis is a major cellular response in the control of tissue homeostasis and as a defense mechanism in the case of cellular aggression such as an infection. Cell self-destruction is part of antiviral responses, aimed at limiting the spread of a virus. Although it may contribute to the deleterious effects in infectious pathology, apoptosis remains a key mechanism for viral clearance and the resolution of infection. The control mechanisms of cell death processes by viruses have been extensively studied. Apoptosis can be triggered by different viral determinants through different pathways as a result of virally induced cell stresses and innate immune responses. Zika virus (ZIKV) induces Zika disease in humans, which has caused severe neurological forms, birth defects, and microcephaly in newborns during the last epidemics. ZIKV also surprised by revealing an ability to persist in the genital tract and in semen, thus being sexually transmitted. Mechanisms of diverting antiviral responses such as the interferon response, the role of cytopathic effects and apoptosis in the etiology of the disease have been widely studied and debated. In this review, we examined the interplay between ZIKV infection of different cell types and apoptosis and how the virus deals with this cellular response. We illustrate a duality in the effects of ZIKV-controlled apoptosis, depending on whether it occurs too early or too late, respectively, in neuropathogenesis, or in long-term viral persistence. We further discuss a prospective role for apoptosis in ZIKV-related therapies, and the use of ZIKV as an oncolytic agent.
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Apoptosis/fisiología , Infección por el Virus Zika/metabolismo , Virus Zika/fisiología , Animales , Antivirales/uso terapéutico , Muerte Celular/fisiología , Interacciones Huésped-Patógeno/inmunología , Humanos , Inmunidad Innata/inmunología , Interferones/uso terapéutico , Microcefalia/virología , Fenómenos Fisiológicos de los Virus/inmunología , Replicación Viral/fisiología , Virus Zika/genética , Virus Zika/patogenicidad , Infección por el Virus Zika/virologíaRESUMEN
Multiple sclerosis (MS) is a debilitating disease that arises from immune system attacks to the protective myelin sheath that covers nerve fibers and ensures optimal communication between brain and body. Although the cause of MS is unknown, a number of factors, which include viruses, have been identified as increasing the risk of displaying MS symptoms. Specifically, the ubiquitous and highly prevalent Epstein-Barr virus, human herpesvirus 6, cytomegalovirus, varicella-zoster virus, and other viruses have been identified as potential triggering agents. In this review, we examine the specific role of proline-rich proteins encoded by these viruses and their potential role in MS at a molecular level.
Asunto(s)
Herpesviridae/fisiología , Esclerosis Múltiple/virología , Dominios Proteicos Ricos en Prolina , Proteínas Virales/química , Proteínas Virales/metabolismo , Fenómenos Fisiológicos de los Virus , Humanos , Imitación Molecular , Proteína Básica de Mielina/química , Proteína Básica de Mielina/metabolismo , Oligodendroglía/metabolismo , Fosforilación , Factores de Riesgo , Ubiquitina-Proteína Ligasas/química , Ubiquitina-Proteína Ligasas/metabolismo , Dominios WW , Dominios Homologos srcRESUMEN
Viral diseases consistently pose a substantial economic and public health burden worldwide [...].
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Antivirales/farmacología , Virosis/tratamiento farmacológico , Humanos , Virosis/virología , Fenómenos Fisiológicos de los Virus , Virus/clasificación , Virus/efectos de los fármacos , Virus/genéticaRESUMEN
Companion animals, such as cats, dogs, horses and exotic species, play an important role in society; more than 600 million cats and 900 million dogs live closely with humans worldwide [...].
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Mascotas/virología , Virosis/veterinaria , Fenómenos Fisiológicos de los Virus , Virus/aislamiento & purificación , Animales , Enfermedades de los Gatos/virología , Gatos , Enfermedades de los Perros/virología , Perros , Enfermedades de los Caballos/virología , Caballos , Virosis/virología , Virus/clasificación , Virus/genéticaRESUMEN
The principal biological function of bacterial and archaeal CRISPR systems is RNA-guided adaptive immunity against viruses and other mobile genetic elements (MGEs). These systems show remarkable evolutionary plasticity and functional versatility at multiple levels, including both the defense mechanisms that lead to direct, specific elimination of the target DNA or RNA and those that cause programmed cell death (PCD) or induction of dormancy. This flexibility is also evident in the recruitment of CRISPR systems for nondefense functions. Defective CRISPR systems or individual CRISPR components have been recruited by transposons for RNA-guided transposition, by plasmids for interplasmid competition, and by viruses for antidefense and interviral conflicts. Additionally, multiple highly derived CRISPR variants of yet unknown functions have been discovered. A major route of innovation in CRISPR evolution is the repurposing of diverged repeat variants encoded outside CRISPR arrays for various structural and regulatory functions. The evolutionary plasticity and functional versatility of CRISPR systems are striking manifestations of the ubiquitous interplay between defense and "normal" cellular functions.
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Archaea/genética , Bacterias/genética , Evolución Molecular , Inmunidad Adaptativa , Archaea/inmunología , Bacterias/inmunología , Repeticiones Palindrómicas Cortas Agrupadas y Regularmente Espaciadas , Plásmidos , Fenómenos Fisiológicos de los Virus , VirusRESUMEN
Risky research on lab-modified self-spreading viruses has yet to present credible paths to upsides.
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Animales Salvajes , Organismos Modificados Genéticamente , Control Biológico de Vectores , Vacunas Atenuadas , Vacunas Virales , Virus , Animales , Evolución Molecular , Humanos , Cooperación Internacional , Políticas , Fenómenos Fisiológicos de los Virus , Virus/genéticaRESUMEN
Hunting can fundamentally alter wildlife population dynamics but the consequences of hunting on pathogen transmission and evolution remain poorly understood. Here, we present a study that leverages a unique landscape-scale quasi-experiment coupled with pathogen-transmission tracing, network simulation and phylodynamics to provide insights into how hunting shapes feline immunodeficiency virus (FIV) dynamics in puma (Puma concolor). We show that removing hunting pressure enhances the role of males in transmission, increases the viral population growth rate and increases the role of evolutionary forces on the pathogen compared to when hunting was reinstated. Changes in transmission observed with the removal of hunting could be linked to short-term social changes while the male puma population increased. These findings are supported through comparison with a region with stable hunting management over the same time period. This study shows that routine wildlife management can have impacts on pathogen transmission and evolution not previously considered.
Asunto(s)
Virus de la Inmunodeficiencia Felina , Puma , Animales , Animales Salvajes , Femenino , Virus de la Inmunodeficiencia Felina/fisiología , Masculino , Conducta Predatoria , Puma/fisiología , Puma/virología , Fenómenos Fisiológicos de los VirusAsunto(s)
Virus , Animales , Antivirales/farmacología , Farmacorresistencia Viral/efectos de los fármacos , Farmacorresistencia Viral/genética , Interacciones Huésped-Patógeno , Humanos , Análisis de Secuencia de ARN , Proteínas Virales/genética , Proteínas Virales/metabolismo , Zoonosis Virales/virología , Fenómenos Fisiológicos de los Virus , Virus/efectos de los fármacos , Virus/genética , Virus/metabolismoRESUMEN
The chikungunya virus has spread globally with a remarkably high attack rate. Infection causes arthralgic sequelae that can last for years. Nevertheless, there are no specific drugs or vaccines to contain the virus. Understanding the biology of the virus, such as its replication cycle, is a powerful tool to identify new drugs and comprehend virus-host interactions. Even though the chikungunya virus has been known for a long time (it was first described in 1952), many aspects of the replication cycle remain unclear. Furthermore, part of the cycle is based on observations of other alphaviruses. In this study, we used electron and scanning microscopy, as well as biological assays, to analyze and investigate the stages of the chikungunya virus replication cycle. Based on our data, we found infection cellular activities other than those usually described for the chikungunya virus replication cycle, i.e., we show particles enveloping intracellularly without budding in a membrane-delimited morphogenesis area, and we also observed virion release by membrane protrusions. Our work provides novel details regarding the biology of chikungunya virus and fills gaps in our knowledge of its replication cycle. These findings may contribute to a better understanding of virus-host interactions and support the development of antivirals. IMPORTANCE The understanding of virus biology is essential to containing virus dissemination, and exploring the virus replication cycle is a powerful tool to do this. There are many points in the biology of the chikungunya virus that need to be clarified, especially regarding its replication cycle. Our incomplete understanding of chikungunya virus infection stages is based on studies with other alphaviruses. We systematized the chikungunya virus replication cycle using microscopic imaging in the order of infection stages, as follows: entry, replication, protein synthesis, assembly/morphogenesis, and release. The imaging evidence shows novel points in the replication cycle of enveloping without budding, as well as particle release by cell membrane protrusion.
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Fiebre Chikungunya/virología , Virus Chikungunya/fisiología , Virus Chikungunya/ultraestructura , Fenómenos Fisiológicos de los Virus , Replicación Viral , Animales , Células Cultivadas , Chlorocebus aethiops , Efecto Citopatogénico Viral , Vacuolas/ultraestructura , Células Vero , Liberación del VirusRESUMEN
Viruses can provide new biological functions to plants and animals. Some viruses persisting at low levels in plants might confer resistance to stress and parasites. In animals, more numerous examples of genes originating from viruses and used by different organisms have been described. For examples these genes might contribute to protect from new infections, or to ensure communication between neurons or to enable placenta development. In parasitic wasps, a complex viral machinery has been conserved as an endogenous virus dispersed in the wasp genome, which produces virions. These virions infect the parasitized host resulting in the production of virulence factors that inhibit defense mechanisms against the parasite. Different organisms have used the same viral functions repeatedly during animal evolution.
Title: Des virus bénéfiques pour les plantes et les animaux. Abstract: Les virus peuvent apporter de nouvelles fonctions aux organismes qui les portent. Chez les plantes, des virus, présents à des niveaux d'infection faibles, confèrent des propriétés de résistance aux stress et aux parasites. Chez les animaux, de plus nombreux exemples d'appropriation de gènes viraux, qui participent en particulier à la protection contre de nouvelles infections, à la communication entre les neurones, ou à la morphogenèse du placenta, ont été décrits. Chez les guêpes parasites, une machinerie virale complexe est conservée sous la forme d'un virus endogène dispersé dans le génome, leur permettant d'infecter l'hôte parasité et de lui faire exprimer des protéines inhibant ses propres mécanismes de défense. Les processus d'appropriation des mêmes fonctions virales se sont souvent répétés au cours de l'évolution. Cette revue aborde des exemples de symbioses virales (c'est-à-dire, des cas où le virus exploite un organisme-hôte en lui étant par ailleurs bénéfique), où l'apport positif des virus est bien documenté.
Asunto(s)
Polydnaviridae , Virus , Avispas , Animales , Polydnaviridae/fisiología , Virus/genética , Virión/fisiología , Fenómenos Fisiológicos de los Virus , Factores de VirulenciaRESUMEN
Better methods to predict and prevent the emergence of zoonotic viruses could support future efforts to reduce the risk of epidemics. We propose a network science framework for understanding and predicting human and animal susceptibility to viral infections. Related approaches have so far helped to identify basic biological rules that govern cross-species transmission and structure the global virome. We highlight ways to make modelling both accurate and actionable, and discuss the barriers that prevent researchers from translating viral ecology into public health policies that could prevent future pandemics.