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Molecular Plant-microbe Interactions :... Mar 2016Satellite RNAs and satellite viruses are extraviral components that can affect either the pathogenicity, the accumulation, or both of their associated viruses while... (Review)
Review
Satellite RNAs and satellite viruses are extraviral components that can affect either the pathogenicity, the accumulation, or both of their associated viruses while themselves being dependent on the associated viruses as helper viruses for their infection. Most of these satellite RNAs are noncoding RNAs, and in many cases, have been shown to alter the interaction of their helper viruses with their hosts. In only a few cases have the functions of these satellite RNAs in such interactions been studied in detail. In particular, work on the satellite RNAs of Cucumber mosaic virus and Turnip crinkle virus have provided novel insights into RNAs functioning as noncoding RNAs. These effects are described and potential roles for satellite RNAs in the processes involved in symptom intensification or attenuation are discussed. In most cases, models describing these roles involve some aspect of RNA silencing or its suppression, either directly or indirectly involving the particular satellite RNA.
Topics: Cucumber Mosaic Virus Satellite; Cucumovirus; Gene Expression Regulation, Viral; RNA, Satellite; Satellite Viruses
PubMed: 26551994
DOI: 10.1094/MPMI-10-15-0232-FI -
Journal of Translational Internal... 2015Hepatitis outbreaks in hemodialysis (HD) patients and staff were reported in the late 1960s, and a number of hepatotropic viruses transmitted by blood and other body... (Review)
Review
Hepatitis outbreaks in hemodialysis (HD) patients and staff were reported in the late 1960s, and a number of hepatotropic viruses transmitted by blood and other body fluids have been identified. Hepatitis B virus (HBV) was the first significant hepatotropic virus to be identified in HD centers. HBV infection has been effectively controlled by active vaccination, screening of blood donors, the use of erythropoietin and segregation of HBV carriers. Hepatitis delta virus is a defective virus that can only infect HBV-positive individuals. Hepatitis C virus (HCV) is the most significant cause of non-A, non-B hepatitis and is mainly transmitted by blood transfusion. The introduction in 1990 of routine screening of blood donors for HCV contributed significantly to the control of HCV transmission. An effective HCV vaccine remains an unsolved challenge; however, pegylation of interferon-alfa has made it possible to treat HCV-positive dialysis patients. Unexplained sporadic outbreaks of hepatitis by the mid-1990s prompted the discovery of hepatitis G virus, hepatitis GB virus C and the TT virus. The vigilant observation of guidelines on universal precaution and regular virologic testing are the cornerstones of the effective control of chronic hepatitis in the setting of HD. Major recent advances in the viral diagnosis technology and the development of new oral, direct-acting antiviral agents allow early diagnosis and better therapeutic response. The current update will review the recent developments, controversies and new treatment of viral hepatitis in HD patients.
PubMed: 27847896
DOI: 10.1515/jtim-2015-0018 -
Cells Jan 2022The novel coronavirus SARS-CoV-2 has caused a pandemic resulting in millions of deaths worldwide. While multiple vaccines have been developed, insufficient vaccination... (Review)
Review
The novel coronavirus SARS-CoV-2 has caused a pandemic resulting in millions of deaths worldwide. While multiple vaccines have been developed, insufficient vaccination combined with adaptive mutations create uncertainty for the future. Here, we discuss novel strategies to control COVID-19 relying on Defective Interfering Particles (DIPs) and related particles that arise naturally during an infection. Our intention is to encourage and to provide the basis for the implementation of such strategies by multi-disciplinary teams. We therefore provide an overview of SARS-CoV-2 for a multi-disciplinary readership that is specifically tailored to these strategies, we identify potential targets based on the current knowledge of the properties and functions of coronaviruses, and we propose specific strategies to engineer DIPs and other interfering or therapeutic nanoparticles.
Topics: COVID-19; Defective Interfering Viruses; Humans; Nanoparticles; Pandemics; SARS-CoV-2
PubMed: 35053418
DOI: 10.3390/cells11020302 -
Current Opinion in Virology Dec 2018Individual virions typically fail to infect cells. Such decoupling between virions and infectious units is most evident in multicomponent and other segmented viruses,... (Review)
Review
Individual virions typically fail to infect cells. Such decoupling between virions and infectious units is most evident in multicomponent and other segmented viruses, but is also frequent in non-segmented viruses. Despite being a well-known observation, the causes and implications of low single-virion infectivity often remain unclear. In principle, this can originate from intrinsic genetic and/or structural virion defects, but also from host infection barriers that limit early viral proliferation. Hence, viruses may have evolved strategies to increase the per-virion likelihood of establishing successful infections. This can be achieved by adopting spread modes that elevate the multiplicity of infection at the cellular level, including direct cell-to-cell viral transfer, encapsulation of multiple virions in microvesicles or other intercellular vehicles, virion aggregation, and virion binding to microbiota. In turn, increasing the multiplicity of infection could favor the evolution of defective viruses, hence modifying the fitness value of these spread modes.
Topics: Microbial Interactions; Virus Diseases; Virus Internalization; Virus Physiological Phenomena; Virus Replication
PubMed: 30015082
DOI: 10.1016/j.coviro.2018.06.001 -
Current Opinion in Virology Apr 2017During RNA virus infection of a host, error-prone viral replication will give rise to a cloud of genetically-linked mutants, as well as truncated, defective genomes. In... (Review)
Review
During RNA virus infection of a host, error-prone viral replication will give rise to a cloud of genetically-linked mutants, as well as truncated, defective genomes. In this review, we describe the dynamics of viral diversity during infection, illustrating that the viral population fluctuates greatly in number of genomes and composition of mutants, in relation with the existence of physical barriers or immune pressures. We illustrate the importance of generating diversity by analyzing the case of fidelity variants, largely attenuated in vivo. Recombination is also considered in its various roles: redistribution of mutations on full-length genomes, and production of highly-immunostimulatory defective genomes. We cover these notions by underlining, when they exist, the differences between acute and persistent infections.
Topics: Genetic Variation; Genetics, Population; Population Dynamics; RNA Virus Infections; Viruses
PubMed: 28456056
DOI: 10.1016/j.coviro.2017.03.013 -
Cell Dec 2021RNA viruses generate defective viral genomes (DVGs) that can interfere with replication of the parental wild-type virus. To examine their therapeutic potential, we...
RNA viruses generate defective viral genomes (DVGs) that can interfere with replication of the parental wild-type virus. To examine their therapeutic potential, we created a DVG by deleting the capsid-coding region of poliovirus. Strikingly, intraperitoneal or intranasal administration of this genome, which we termed eTIP1, elicits an antiviral response, inhibits replication, and protects mice from several RNA viruses, including enteroviruses, influenza, and SARS-CoV-2. While eTIP1 replication following intranasal administration is limited to the nasal cavity, its antiviral action extends non-cell-autonomously to the lungs. eTIP1 broad-spectrum antiviral effects are mediated by both local and distal type I interferon responses. Importantly, while a single eTIP1 dose protects animals from SARS-CoV-2 infection, it also stimulates production of SARS-CoV-2 neutralizing antibodies that afford long-lasting protection from SARS-CoV-2 reinfection. Thus, eTIP1 is a safe and effective broad-spectrum antiviral generating short- and long-term protection against SARS-CoV-2 and other respiratory infections in animal models.
Topics: Administration, Intranasal; Animals; Antiviral Agents; Broadly Neutralizing Antibodies; COVID-19; Capsid Proteins; Cell Line; Defective Interfering Viruses; Disease Models, Animal; Genome, Viral; Humans; Influenza, Human; Interferons; Male; Mice; Mice, Inbred C57BL; Poliovirus; Respiratory Tract Infections; SARS-CoV-2; Virus Replication
PubMed: 34852237
DOI: 10.1016/j.cell.2021.11.023 -
Current Opinion in HIV and AIDS Mar 2018To provide an overview of recent research of how HIV integration relates to productive and latent infection and implications for cure strategies. (Review)
Review
PURPOSE OF REVIEW
To provide an overview of recent research of how HIV integration relates to productive and latent infection and implications for cure strategies.
RECENT FINDINGS
How and where HIV integrates provides new insights into how HIV persists on antiretroviral therapy (ART). Clonal expansion of infected cells with the same integration site demonstrates that T-cell proliferation is an important factor in HIV persistence, however, the driver of proliferation remains unclear. Clones with identical integration sites harbouring defective provirus can accumulate in HIV-infected individuals on ART and defective proviruses can express RNA and produce protein. HIV integration sites differ in clonally expanded and nonexpanded cells and in latently and productively infected cells and this influences basal and inducible transcription. There is a growing number of cellular proteins that can alter the pattern of integration to favour latency. Understanding these pathways may identify new interventions to eliminate latently infected cells.
SUMMARY
Using advances in analysing HIV integration sites, T-cell proliferation of latently infected cells is thought to play a major role in HIV persistence. Clonal expansion has been demonstrated with both defective and intact viruses. Production of viral RNA and protein from defective viruses may play a role in driving chronic immune activation. The site of integration may determine the likelihood of proliferation and the degree of basal and induced transcription. Finally, host factors and gene expression at the time of infection may determine the integration site. Together these new insights may lead to novel approaches to elimination of latently infected cells.
Topics: Animals; HIV Infections; HIV-1; Humans; T-Lymphocytes; Virus Integration
PubMed: 29206656
DOI: 10.1097/COH.0000000000000438 -
Epidemiology and Infection Oct 2018Hepatitis delta virus (HDV) is a defective RNA virus that depends on the presence of hepatitis B virus (HBV) for the creation of new virions and propagation of the... (Review)
Review
Hepatitis delta virus (HDV) is a defective RNA virus that depends on the presence of hepatitis B virus (HBV) for the creation of new virions and propagation of the infection to hepatocytes. Chronic infection with HDV is usually associated with a worsening of HBV infection, leading more frequently to cirrhosis, increased risk of liver decompensation and hepatocellular carcinoma (HCC) occurrence. In spite of a progressive declining prevalence of both acute and chronic HDV infection observed over several years, mainly due to increased global health policies and mass vaccination against HBV, several European countries have more recently observed stable HDV prevalence mainly due to migrants from non-European countries. Persistent HDV replication has been widely demonstrated as associated with cirrhosis development and, as a consequence, development of liver decompensation and occurrence of HCC. Several treatment options have been attempted with poor results in terms of HDV eradication and improvement of long-term prognosis. A global effort is deemed urgent to enhance the models already existing as well as to learn more about HDV infection and correlated tumourigenesis mechanisms.
Topics: Carcinoma, Hepatocellular; Hepatitis D; Hepatitis D, Chronic; Hepatitis Delta Virus; Humans; Liver Neoplasms
PubMed: 29991359
DOI: 10.1017/S0950268818001942 -
Clinical Medicine (London, England) Jul 2023Hepatitis D virus (HDV), also referred to as hepatitis delta virus, is the smallest virus capable of causing human disease. It is unable to replicate on its own and can... (Review)
Review
Hepatitis D virus (HDV), also referred to as hepatitis delta virus, is the smallest virus capable of causing human disease. It is unable to replicate on its own and can only propagate in the presence of hepatitis B virus (HBV). Infection with both HBV and HDV frequently results in more severe disease than HBV alone, with higher instances of cirrhosis, liver failure and hepatocellular carcinoma (HCC). Thus, there is a need for effective treatment for HDV; however, currently approved treatment options are very limited both in terms of their efficacy and availability. This makes the management of HDV a challenge for physicians. In this review, we look at the background, diagnosis and treatment of HDV, informed by our hospital data, to set out the optimal management of HDV; we also explore novel treatment options for this disease.
Topics: Humans; Hepatitis Delta Virus; Antiviral Agents; Carcinoma, Hepatocellular; Liver Neoplasms; Hepatitis B virus
PubMed: 37353306
DOI: 10.7861/clinmed.2022-0556 -
Trends in Microbiology Jul 2020Viral defective interfering particles (DIPs) were intensely studied several decades ago but research waned leaving open many critical questions. New technologies and... (Review)
Review
Viral defective interfering particles (DIPs) were intensely studied several decades ago but research waned leaving open many critical questions. New technologies and other advances led to a resurgence in DIP studies for negative-strand RNA viruses. While DIPs have long been recognized, their exact contribution to the outcome of acute or persistent viral infections has remained elusive. Recent studies have identified defective viral genomes (DVGs) in human infections, including respiratory syncytial virus and influenza, and growing evidence indicates that DVGs influence disease severity and may contribute to viral persistence. Further, several studies have advanced our understanding of key viral and host factors that regulate DIP formation and activity. Here we review these discoveries and highlight key questions moving forward.
Topics: Defective Viruses; Gene Deletion; Genome, Viral; Orthomyxoviridae; Respiratory Syncytial Viruses; Viral Interference; Virus Replication
PubMed: 32544442
DOI: 10.1016/j.tim.2020.02.006