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For:	Taylor JM. Replication of human hepatitis delta virus: recent developments. Trends Microbiol 2003;11:185-90. [PMID: 12706997 DOI: 10.1016/s0966-842x(03)00045-3] [Citation(s) in RCA: 73] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]

Number

Cited by Other Article(s)

The unique carnation stunt-associated pararetroviroid. Virus Res 2022;312:198709. [DOI: 10.1016/j.virusres.2022.198709] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/25/2021] [Revised: 02/07/2022] [Accepted: 02/12/2022] [Indexed: 12/12/2022]

Badar U, Venkataraman S, AbouHaidar M, Hefferon K. Molecular interactions of plant viral satellites. Virus Genes 2020;57:1-22. [PMID: 33226576 DOI: 10.1007/s11262-020-01806-9] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/02/2019] [Accepted: 10/24/2020] [Indexed: 12/18/2022]

Hongjaisee S, Khamduang W, Sripan P, Choyrum S, Thepbundit V, Ngo-Giang-Huong N, Tangmunkongvorakul A. Prevalence and factors associated with hepatitis B and D virus infections among migrant sex workers in Chiangmai, Thailand: A cross-sectional study in 2019. Int J Infect Dis 2020;100:247-254. [PMID: 32898671 DOI: 10.1016/j.ijid.2020.09.004] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2020] [Accepted: 09/02/2020] [Indexed: 12/20/2022] Open

Statin inhibits large hepatitis delta antigen-Smad3 -twist-mediated epithelial-to-mesenchymal transition and hepatitis D virus secretion. J Biomed Sci 2020;27:65. [PMID: 32434501 PMCID: PMC7240974 DOI: 10.1186/s12929-020-00659-6] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/08/2020] [Accepted: 05/14/2020] [Indexed: 01/01/2023] Open

Volloch V, Olsen BR, Rits S. AD "Statin": Alzheimer's Disorder is a "Fast" Disease Preventable by Therapeutic Intervention Initiated Even Late in Life and Reversible at the Early Stages. ANNALS OF INTEGRATIVE MOLECULAR MEDICINE 2020;2:75-89. [PMID: 32201863 PMCID: PMC7083596 DOI: 10.33597/aimm.02-1006] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]

Abstract

The present study posits that Alzheimer's disorder is a "fast" disease. This is in sharp contrast to a view, prevailing until now, that Alzheimer's Disease (AD) is a quintessential "slow" disease that develops throughout the life as one prolonged process. According to this view, beta-amyloid (Aβ) is produced and secreted solely by the beta-amyloid precursor protein (βAPP) proteolytic/secretory pathway. As its extracellular levels increase, it triggers neurodegeneration starting relatively early in life. Damages accumulate and manifest, late in life in sporadic Alzheimer's Disease (SAD) cases, as AD symptoms. In familial AD (FAD) cases, where mutations in βAPP gene or in presenilins increase production of either common Aβ isoform or of its more toxic isoforms, neurodegeneration reaches critical threshold sooner and AD symptoms occur earlier in life, mostly in late 40s and 50s. There are currently no preventive AD therapies but if they were available, according to this viewpoint it would be largely futile to intervene late in life in case of potential SAD or at mid-age in cases of FAD because, although AD symptoms have not yet manifested, the damage has already occurred during the preceding decades. In this paradigm, to be effective, preventive therapeutic intervention should be initiated early in life. The outlook suggested by the present study is radically different. According to it, Alzheimer's disease evolves in two stages. The first stage is a slow process of intracellular beta-amyloid accumulation. It occurs via βAPP proteolytic/secretory pathway and cellular uptake of secreted Aβ common to Homo sapiens, including healthy humans, and to non-human mammals, and results neither in significant damage, nor in manifestation of the disease. The second stage occurs exclusively in humans, commences shortly before symptomatic onset of the disease, sharply accelerates the production and increases intracellular levels of Aβ that is not secreted but is retained intracellularly, generates significant damages, triggers AD symptoms, and is fast. It is driven by an Aβ generation pathway qualitatively and quantitatively different from βAPP proteolytic process and entirely independent of beta-amyloid precursor protein, and results in rapid and substantial intracellular accumulation of Aβ, consequent significant neurodegeneration, and symptomatic AD. In this paradigm, a preventive therapy for AD, an AD "statin", would be effective when initiated at any time prior to commencement of the second stage. Moreover, there are good reasons to believe that with a drug blocking βAPP-independent Aβ production pathway in the second stage, it would be possible not only to preempt the disease but also to stop and to reverse it even when early AD symptoms have already manifested. The present study posits a notion of AD as a Fast Disease, offers evidence for the occurrence of the AD-specific Aβ production pathway, describes cellular and molecular processes constituting an engine that drives Alzheimer's disease, and explains why non-human mammals are not susceptible to AD and why only a subset of humans develop the disease. It establishes that Alzheimer's disease is preventable by therapeutic intervention initiated even late in life, details a powerful mechanism underlying the disease, suggests that Aβ produced in the βAPP-independent pathway is retained intracellularly, elaborates why neither BACE inhibition nor Aβ immunotherapy are effective in treatment of AD and why intracellularly retained beta-amyloid could be the primary agent of neuronal death in Alzheimer's disease, necessitates generation of a novel animal AD model capable of producing Aβ via βAPP-independent pathway, proposes therapeutic targets profoundly different from previously pursued components of the βAPP proteolytic pathway, and provides conceptual rationale for design of drugs that could be used not only preemptively but also for treatment and reversal of the early stages of the disease.

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Volloch V, Olsen B, Rits S. Alzheimer's Disease is Driven by Intraneuronally Retained Beta-Amyloid Produced in the AD-Specific, βAPP-Independent Pathway: Current Perspective and Experimental Models for Tomorrow. ANNALS OF INTEGRATIVE MOLECULAR MEDICINE 2020;2:90-114. [PMID: 32617536 PMCID: PMC7331974 DOI: 10.33597/aimm.02-1007] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]

Abstract

A view of the origin and progression of Alzheimer's disease, AD, prevailing until now and formalized as the Amyloid Cascade Hypothesis theory, maintains that the disease is initiated by overproduction of beta-amyloid, Aβ, which is generated solely by the Aβ precursor protein, βAPP, proteolytic pathway and secreted from the cell. Consequent extracellular accumulation of Aβ triggers a cascade of molecular and cellular events leading to neurodegeneration that starts early in life, progresses as one prolonged process, builds up for decades, and culminates in symptomatic manifestations of the disease late in life. In this paradigm, a time window for commencement of therapeutic intervention is small and accessible only early in life. The outlook introduced in the present study is fundamentally different. It posits that the βAPP proteolytic/secretory pathway of Aβ production causes AD in humans no more than it does in either short- or long-lived non-human mammals that share this pathway with humans, accumulate beta-amyloid as they age, but do not develop the disease. Alzheimer's disease, according to this outlook, is driven by an additional powerful AD-specific pathway of Aβ production that operates in affected humans, is completely independent of the βAPP precursor, and is not available in non-human mammals. The role of the βAPP proteolytic pathway in the disease in humans is activation of this additional AD-specific Aβ production pathway. This occurs through accumulation of intracellular Aβ, primarily via ApoE-assisted cellular uptake of secreted beta-amyloid, but also through retention of a fraction of Aβ produced in the βAPP proteolytic pathway. With time, accumulated intracellular Aβ triggers mitochondrial dysfunction. In turn, cellular stresses associated with mitochondrial dysfunction, including ER stress, activate a second, AD-specific, Aβ production pathway: Asymmetric RNA-dependent βAPP mRNA amplification; animal βAPP mRNA is ineligible for this process. In this pathway, every conventionally produced βAPP mRNA molecule serves potentially as a template for production of severely 5'-truncated mRNA encoding not the βAPP but its C99 fragment (hence "asymmetric"), the immediate precursor of Aβ. Thus produced, N-terminal signal peptide-lacking C99 is processed not in the secretory pathway on the plasma membrane, but at the intracellular membrane sites, apparently in a neuron-specific manner. The resulting Aβ is, therefore, not secreted but is retained intraneuronally and accumulates rapidly within the cell. Increased levels of intracellular Aβ augment mitochondrial dysfunction, which, in turn, sustains the activity of the βAPP mRNA amplification pathway. These self-propagating mutual Aβ overproduction/mitochondrial dysfunction feedback cycles constitute a formidable two-stroke engine, an engine that drives Alzheimer's disease. The present outlook envisions Alzheimer's disorder as a two-stage disease. The first stage is a slow process of intracellular beta-amyloid accumulation. It results neither in significant neurodegenerative damage, nor in manifestation of the disease. The second stage commences with the activation of the βAPP mRNA amplification pathway shortly before symptomatic onset of the disease, sharply increases the rate of Aβ generation and the extent of its intraneuronal accumulation, produces significant damages, triggers AD symptoms, and is fast. In this paradigm, the time window of therapeutic intervention is wide open, and preventive treatment can be initiated any time, even late in life, prior to commencement of the second stage of the disease. Moreover, there are good reasons to believe that with a drug blocking the βAPP mRNA amplification pathway, it would be possible not only to preempt the disease but also to stop and to reverse it even when early AD symptoms have already manifested. There are numerous experimental models of AD, all based on a notion of the exceptionality of βAPP proteolytic/secretory pathway in Aβ production in the disease. However, with no drug even remotely effective in Alzheimer's disease, a long list of candidate drugs that succeeded remarkably in animal models, yet failed utterly in human clinical trials of potential AD drugs, attests to the inadequacy of currently employed AD models. The concept of a renewable supply of beta-amyloid, produced in the βAPP mRNA amplification pathway and retained intraneuronally in Alzheimer's disease, explains spectacular failures of both BACE inhibition and Aβ-immunotherapy in human clinical trials. This concept also forms the basis of a new generation of animal and cell-based experimental models of AD, described in the present study. These models incorporate Aβ- or C99-encoding mRNA amplification pathways of Aβ production, as well as intracellular retention of their product, and can support not only further investigation of molecular mechanisms of AD but also screening for and testing of candidate drugs aimed at therapeutic targets suggested by the present study.

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Makhlouf NA, Morsy KH, Mahmoud AA. Hepatitis D virus infection among hepatitis B virus surface antigen positive individuals in Upper Egypt: Prevalence and clinical features. J Infect Public Health 2019;12:350-356. [PMID: 30833193 DOI: 10.1016/j.jiph.2018.12.001] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/27/2018] [Revised: 05/25/2018] [Accepted: 12/03/2018] [Indexed: 11/21/2022] Open

Volloch V, Rits-Volloch S. News from Mars: Two-Tier Paradox, Intracellular PCR, Chimeric Junction Shift, Dark Matter mRNA and Other Remarkable Features of Mammalian RNA-Dependent mRNA Amplification. Implications for Alzheimer's Disease, RNA-Based Vaccines and mRNA Therapeutics. ACTA ACUST UNITED AC 2019;2:131-173. [PMID: 33942036 DOI: 10.33597/aimm.02-1009] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/25/2022]

Abstract

Molecular Biology, a branch of science established to examine the flow of information from "letters" encrypted into DNA structure to functional proteins, was initially defined by a concept of DNA-to-RNA-to-Protein information movement, a notion termed the Central Dogma of Molecular Biology. RNA-dependent mRNA amplification, a novel mode of eukaryotic protein-encoding RNA-to-RNA-to-Protein genomic information transfer, constitutes the extension of the Central Dogma in the context of mammalian cells. It was shown to occur in cellular circumstances requiring exceptionally high levels of production of specific polypeptides, e.g. globin chains during erythroid differentiation or defined secreted proteins in the context of extracellular matrix deposition. Its potency is reflected in the observed cellular levels of the resulting amplified mRNA product: At the peak of the erythroid differentiation, for example, the amount of globin mRNA produced in the amplification pathway is about 1500-fold higher than the amount of its conventionally generated counterpart in the same cells. The cellular enzymatic machinery at the core of this process, RNA-dependent RNA polymerase activity (RdRp), albeit in a non-conventional form, was shown to be constitutively and ubiquitously present, and RNA-dependent RNA synthesis (RdRs) appeared to regularly occur, in mammalian cells. Under most circumstances, the mammalian RdRp activity produces only short antisense RNA transcripts. Generation of complete antisense RNA transcripts and amplification of mRNA molecules require the activation of inducible components of the mammalian RdRp complex. The mechanism of such activation is not clear. The present article suggests that it is triggered by a variety of cellular stresses and occurs in the context of stress responses in general and within the framework of the integrated stress response (ISR) in particular. In this process, various cellular stresses activate, in a stress type-specific manner, defined members of the mammalian translation initiation factor 2α, eIF2α, kinase family: PKR, GCN2, PERK and HRI. Any of these kinases, in an activated form, phosphorylates eIF2α. This results in suppression of global cellular protein synthesis but also in activation of expression of select group of transcription factors including ATF4, ATF5 and CHOP. These transcription factors either function as inducible components of the RdRp complex or enable their expression. The assembly of the competent RdRp complex activates mammalian RNA-dependent mRNA amplification, which appears to be a two-tier process. Tier One is a "chimeric" pathway, named so because it results in an amplified chimeric mRNA molecule containing a fragment of the antisense RNA strand at its 5' terminus. Tier Two further amplifies one of the two RNA end products of the chimeric pathway and constitutes the physiologically occurring intracellular polymerase chain reaction, iPCR. Depending on the structure of the initial mRNA amplification progenitor, the chimeric pathway, Tier One, may result in multiple outcomes including chimeric mRNA that produces either a polypeptide identical to the original, conventional mRNA progenitor-encoded protein or only its C-terminal fragment, CTF. The chimeric RNA end product of Tier One may also produce a polypeptide that is non-contiguously encoded in the genome, activate translation from an open reading frame, which is "silent" in a conventionally transcribed mRNA, or initiate an abortive translation. In sharp contrast, regardless of the outcome of Tier One, the mRNA end product of Tier Two of mammalian mRNA amplification, the iPCR pathway, always produces a polypeptide identical to a conventional mRNA progenitor-encoded protein. This discordance is referred to as the Two-Tier Paradox and discussed in detail in the present article. On the other hand, both Tiers are similar in that they result in heavily modified mRNA molecules resistant to reverse transcription, undetectable by reverse transcription-based methods of sequencing and therefore constituting a proverbial "Dark Matter" mRNA, despite being highly ubiquitous. It appears that in addition to their other functions, the modifications of the amplified mRNA render it compatible, unlike the bulk of cellular mRNA, with phosphorylated eIF2α in translation, implying that in addition to being extraordinarily abundant due to the method of its generation, amplified mRNA is also preferentially translated under the ISR conditions, thus augmenting the efficiency of the amplification process. The vital importance of powerful mechanisms of amplification of protein-encoding genomic information in normal physiology is self-evident. Their malfunctions or misuse appear to be associated with two types of abnormalities, the deficiency of a protein normally produced by these mechanisms and the mRNA amplification-mediated overproduction of a protein normally not generated by such a process. Certain classes of beta-thalassemia exemplify the first type, whereas the second type is represented by overproduction of beta-amyloid in Alzheimer's disease. Moreover, the proposed mechanism of Alzheimer's disease allows a crucial and verifiable prediction, namely that the disease-causing intraneuronally retained variant of beta-amyloid differs from that produced conventionally by βAPP proteolysis in that it contains the additional methionine or acetylated methionine at its N-terminus. Because of its extraordinary evidential value as a natural reporter of the mRNA amplification pathway, this feature, if proven, would, arguably, constitute the proverbial Holy Grail not only for Alzheimer's disease but also for the mammalian RNA-dependent mRNA amplification field in general. Both examples are discussed in detail in the present article, which summarizes and systematizes our current understanding of the field and describes two categories of reporter constructs, one for the chimeric Tier of mRNA amplification, another for the iPCR pathway; both reporter types are essential for elucidating underlying molecular mechanisms. It also suggests, in light of the recently demonstrated feasibility of RNA-based vaccines, that the targeted intracellular amplification of exogenously introduced amplification-eligible antigen-encoding mRNAs via the induced or naturally occurring RNA-dependent mRNA amplification pathway could be of substantial benefit in triggering a fast and potent immune response and instrumental in the development of future vaccines. Similar approaches can also be effective in achieving efficient and sustained expression of exogenous mRNA in mRNA therapeutics.

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Thio CL, Hawkins C. Hepatitis B Virus and Hepatitis Delta Virus. MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 2015:1815-1839.e7. [DOI: 10.1016/b978-1-4557-4801-3.00148-x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]

Persistent hepatitis D virus mono-infection in humanized mice is efficiently converted by hepatitis B virus to a productive co-infection. J Hepatol 2014;60:538-44. [PMID: 24280293 DOI: 10.1016/j.jhep.2013.11.010] [Citation(s) in RCA: 68] [Impact Index Per Article: 6.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/26/2013] [Revised: 11/01/2013] [Accepted: 11/17/2013] [Indexed: 12/14/2022]

Ma W, Yu C, Zhang W. Circularity and self-cleavage as a strategy for the emergence of a chromosome in the RNA-based protocell. Biol Direct 2013;8:21. [PMID: 23971788 PMCID: PMC3765326 DOI: 10.1186/1745-6150-8-21] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/27/2013] [Accepted: 08/21/2013] [Indexed: 12/23/2022] Open

Abstract

Background

It is now popularly accepted that an “RNA world” existed in early evolution. During division of RNA-based protocells, random distribution of individual genes (simultaneously as ribozymes) between offspring might have resulted in gene loss, especially when the number of gene types increased. Therefore, the emergence of a chromosome carrying linked genes was critical for the prosperity of the RNA world. However, there were quite a few immediate difficulties for this event to occur. For example, a chromosome would be much longer than individual genes, and thus more likely to degrade and less likely to replicate completely; the copying of the chromosome might start at middle sites and be only partial; and, without a complex transcription mechanism, the synthesis of distinct ribozymes would become problematic.

Results

Inspired by features of viroids, which have been suggested as “living fossils” of the RNA world, we supposed that these difficulties could have been overcome if the chromosome adopted a circular form and small, self-cleaving ribozymes (e.g. the hammer head ribozymes) resided at the sites between genes. Computer simulation using a Monte-Carlo method was conducted to investigate this hypothesis. The simulation shows that an RNA chromosome can spread (increase in quantity and be sustained) in the system if it is a circular one and its linear “transcripts” are readily broken at the sites between genes; the chromosome works as genetic material and ribozymes “coded” by it serve as functional molecules; and both circularity and self-cleavage are important for the spread of the chromosome.

Conclusions

In the RNA world, circularity and self-cleavage may have been adopted as a strategy to overcome the immediate difficulties for the emergence of a chromosome (with linked genes). The strategy suggested here is very simple and likely to have been used in this early stage of evolution. By demonstrating the possibility of the emergence of an RNA chromosome, this study opens on the prospect of a prosperous RNA world, populated by RNA-based protocells with a number of genes, showing complicated functions.

Reviewers

This article was reviewed by Sergei Kazakov (nominated by Laura Landweber), Nobuto Takeuchi (nominated by Anthony Poole), and Eugene Koonin.

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Freitas N, Cunha C. Searching for nuclear export elements in hepatitis D virus RNA. World J Virol 2013;2:123-135. [PMID: 24255883 PMCID: PMC3832856 DOI: 10.5501/wjv.v2.i3.123] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/06/2013] [Revised: 07/26/2013] [Accepted: 08/09/2013] [Indexed: 02/05/2023] Open

Bishal AK, Mukherjee R, Chakraborty C. Synonymous codon usage pattern analysis of Hepatitis D virus. Virus Res 2013;173:350-3. [DOI: 10.1016/j.virusres.2013.01.007] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/23/2012] [Revised: 01/15/2013] [Accepted: 01/15/2013] [Indexed: 11/24/2022]

RNA polymerase II acts as an RNA-dependent RNA polymerase to extend and destabilize a non-coding RNA. EMBO J 2013;32:781-90. [PMID: 23395899 DOI: 10.1038/emboj.2013.18] [Citation(s) in RCA: 40] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/23/2012] [Accepted: 01/03/2013] [Indexed: 11/09/2022] Open

Sartakhti JS, Zangooei MH, Mozafari K. Hepatitis disease diagnosis using a novel hybrid method based on support vector machine and simulated annealing (SVM-SA). COMPUTER METHODS AND PROGRAMS IN BIOMEDICINE 2012;108:570-579. [PMID: 21968203 DOI: 10.1016/j.cmpb.2011.08.003] [Citation(s) in RCA: 52] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 05/15/2011] [Revised: 07/15/2011] [Accepted: 08/20/2011] [Indexed: 05/31/2023]

Hepatitis D virus isolates with low replication and epithelial-mesenchymal transition-inducing activity are associated with disease remission. J Virol 2012;86:9044-54. [PMID: 22674995 DOI: 10.1128/jvi.00130-12] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open

Shen L, Gu Y, Sun L, Yang Y, Wang F, Li Y, Bi S. Development of a hepatitis delta virus antibody assay for study of the prevalence of HDV among individuals infected with hepatitis B virus in China. J Med Virol 2012;84:445-9. [DOI: 10.1002/jmv.23212] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]

Samuel CE. ADARs: viruses and innate immunity. Curr Top Microbiol Immunol 2012;353:163-95. [PMID: 21809195 PMCID: PMC3867276 DOI: 10.1007/82_2011_148] [Citation(s) in RCA: 62] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

Theise ND, Bodenheimer HC, Ferrell LD. Acute and chronic viral hepatitis. MACSWEEN'S PATHOLOGY OF THE LIVER 2012:361-401. [DOI: 10.1016/b978-0-7020-3398-8.00007-6] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]

Host response to polyomavirus infection is modulated by RNA adenosine deaminase ADAR1 but not by ADAR2. J Virol 2011;85:8338-47. [PMID: 21632755 DOI: 10.1128/jvi.02666-10] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023] Open

Samuel CE. Adenosine deaminases acting on RNA (ADARs) are both antiviral and proviral. Virology 2011;411:180-93. [PMID: 21211811 PMCID: PMC3057271 DOI: 10.1016/j.virol.2010.12.004] [Citation(s) in RCA: 248] [Impact Index Per Article: 17.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/03/2010] [Accepted: 12/04/2010] [Indexed: 12/18/2022]

Gellatly D, Mirhadi K, Venkataraman S, AbouHaidar MG. Structural and sequence integrity are essential for the replication of the viroid-like satellite RNA of lucerne transient streak virus. J Gen Virol 2011;92:1475-1481. [PMID: 21346030 DOI: 10.1099/vir.0.029801-0] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022] Open

George CX, Gan Z, Liu Y, Samuel CE. Adenosine deaminases acting on RNA, RNA editing, and interferon action. J Interferon Cytokine Res 2010;31:99-117. [PMID: 21182352 DOI: 10.1089/jir.2010.0097] [Citation(s) in RCA: 91] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022] Open

Zaidi G, Idrees M, Malik FA, Amin I, Shahid M, Younas S, Hussain R, Awan Z, Tariq A, Parveen K. Prevalence of hepatitis delta virus infection among hepatitis B virus surface antigen positive patients circulating in the largest province of Pakistan. Virol J 2010;7:283. [PMID: 20977704 PMCID: PMC2988018 DOI: 10.1186/1743-422x-7-283] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/23/2010] [Accepted: 10/26/2010] [Indexed: 11/19/2022] Open

de Sousa BC, Cunha C. Development of mathematical models for the analysis of hepatitis delta virus viral dynamics. PLoS One 2010;5:e12512. [PMID: 20862328 PMCID: PMC2940762 DOI: 10.1371/journal.pone.0012512] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2010] [Accepted: 08/09/2010] [Indexed: 12/12/2022] Open

Abstract

BACKGROUND

Mathematical models have shown to be extremely helpful in understanding the dynamics of different virus diseases, including hepatitis B. Hepatitis D virus (HDV) is a satellite virus of the hepatitis B virus (HBV). In the liver, production of new HDV virions depends on the presence of HBV. There are two ways in which HDV can occur in an individual: co-infection and super-infection. Co-infection occurs when an individual is simultaneously infected by HBV and HDV, while super-infection occurs in persons with an existing chronic HBV infection.

METHODOLOGY/PRINCIPAL FINDINGS

In this work a mathematical model based on differential equations is proposed for the viral dynamics of the hepatitis D virus (HDV) across different scenarios. This model takes into consideration the knowledge of the biology of the virus and its interaction with the host. In this work we will present the results of a simulation study where two scenarios were considered, co-infection and super-infection, together with different antiviral therapies. Although, in general the predicted course of HDV infection is similar to that observed for HBV, we observe a faster increase in the number of HBV infected cells and viral load. In most tested scenarios, the number of HDV infected cells and viral load values remain below corresponding predicted values for HBV.

CONCLUSIONS/SIGNIFICANCE

The simulation study shows that, under the most commonly used and generally accepted therapy approaches for HDV infection, such as lamivudine (LMV) or ribavirine, peggylated alpha-interferon (IFN) or a combination of both, LMV monotherapy and combination therapy of LMV and IFN were predicted to more effectively reduce the HBV and HDV viral loads in the case of super-infection scenarios when compared with the co-infection. In contrast, IFN monotherapy was found to reduce the HDV viral load more efficiently in the case of super-infection while the effect on the HBV viral load was more pronounced during co-infection. The results suggest that there is a need for development of high efficacy therapeutic approaches towards the specific inhibition of HDV replication. These approaches may additionally be directed to the reduction of the half-life of infected cells and life-span of newly produced circulating virions.

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Shih HH, Shih C, Wang HW, Su CW, Sheen IJ, Wu JC. Pro-205 of large hepatitis delta antigen and Pro-62 of major hepatitis B surface antigen influence the assembly of different genotypes of hepatitis D virus. J Gen Virol 2009;91:1004-12. [PMID: 19940060 DOI: 10.1099/vir.0.017541-0] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022] Open

Mota S, Mendes M, Freitas N, Penque D, Coelho AV, Cunha C. Proteome analysis of a human liver carcinoma cell line stably expressing hepatitis delta virus ribonucleoproteins. J Proteomics 2008;72:616-27. [PMID: 19136081 DOI: 10.1016/j.jprot.2008.12.003] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/14/2008] [Revised: 12/03/2008] [Accepted: 12/04/2008] [Indexed: 01/26/2023]

Artsimovitch I, Vassylyev DG. Merging the RNA and DNA worlds. Nat Struct Mol Biol 2008;14:1122-3. [PMID: 18059450 DOI: 10.1038/nsmb1207-1122] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]

Motard J, Bolduc F, Thompson D, Perreault JP. The peach latent mosaic viroid replication initiation site is located at a universal position that appears to be defined by a conserved sequence. Virology 2008;373:362-75. [PMID: 18190946 DOI: 10.1016/j.virol.2007.12.010] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/15/2007] [Revised: 11/18/2007] [Accepted: 12/10/2007] [Indexed: 10/22/2022]

Changes in the proteome of Huh7 cells induced by transient expression of hepatitis D virus RNA and antigens. J Proteomics 2008;71:71-9. [PMID: 18541475 DOI: 10.1016/j.jprot.2007.12.002] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/26/2007] [Revised: 12/13/2007] [Accepted: 12/14/2007] [Indexed: 02/06/2023]

Quer J, Martell M, Rodriguez F, Bosch A, Jardi R, Buti M, Esteban J. The Impact of Rapid Evolution of Hepatitis Viruses. ORIGIN AND EVOLUTION OF VIRUSES 2008:303-349. [DOI: 10.1016/b978-0-12-374153-0.00015-1] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/03/2025]

Molecular basis of RNA-dependent RNA polymerase II activity. Nature 2007;450:445-9. [PMID: 18004386 DOI: 10.1038/nature06290] [Citation(s) in RCA: 100] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/18/2007] [Accepted: 09/21/2007] [Indexed: 12/28/2022]

Behzadian F, Sabahi F, Sadeghizadeh M, Maghsoudi N, Fotouhi F, Chahooki FF, Karimi M. In vitro replication of hepatitis D virus using a new construct containing a cDNA dimer of HDV genome. Intervirology 2007;50:387-93. [PMID: 17975319 DOI: 10.1159/000110650] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/23/2007] [Accepted: 08/02/2007] [Indexed: 01/12/2023] Open

Alves C, Freitas N, Cunha C. Characterization of the nuclear localization signal of the hepatitis delta virus antigen. Virology 2007;370:12-21. [PMID: 17897693 DOI: 10.1016/j.virol.2007.07.034] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/27/2007] [Revised: 06/05/2007] [Accepted: 07/31/2007] [Indexed: 12/18/2022]

Canny MD, Jucker FM, Pardi A. Efficient ligation of the Schistosoma hammerhead ribozyme. Biochemistry 2007;46:3826-34. [PMID: 17319693 PMCID: PMC3203546 DOI: 10.1021/bi062077r] [Citation(s) in RCA: 40] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]

Wang SY, Wu JC, Chiang TY, Huang YH, Su CW, Sheen IJ. Positive selection of hepatitis delta antigen in chronic hepatitis D patients. J Virol 2007;81:4438-44. [PMID: 17301143 PMCID: PMC1900184 DOI: 10.1128/jvi.02847-06] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open

Toth AM, Zhang P, Das S, George CX, Samuel CE. Interferon action and the double-stranded RNA-dependent enzymes ADAR1 adenosine deaminase and PKR protein kinase. ACTA ACUST UNITED AC 2007;81:369-434. [PMID: 16891177 DOI: 10.1016/s0079-6603(06)81010-x] [Citation(s) in RCA: 72] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [MESH Headings] [Grants] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]

Ding B, Itaya A. Viroid: a useful model for studying the basic principles of infection and RNA biology. MOLECULAR PLANT-MICROBE INTERACTIONS : MPMI 2007;20:7-20. [PMID: 17249418 DOI: 10.1094/mpmi-20-0007] [Citation(s) in RCA: 75] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/13/2023]

Coupling of transcription termination to RNAi. J Theor Biol 2006;245:278-89. [PMID: 17157879 DOI: 10.1016/j.jtbi.2006.10.026] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/22/2006] [Revised: 10/21/2006] [Accepted: 10/25/2006] [Indexed: 11/28/2022]

Abstract

In metazoans, the mechanisms of transcriptional termination by RNA polymerase II (Pol II) and accelerated decay of messenger RNA (mRNA) following transcription shutdown are linked by sharing the same sequence elements and mRNA elongation, processing and termination factors. This begs the question, how could one process have two opposite outcomes, making or degrading mRNA? An integrated "allosteric-GENEi-torpedo" model that could explain this paradox predicts participation of two novel factors: (1) An allosteric factor, regulated by a physiological repressor, binds to a unique sequence element of a gene near the site of cleavage and polyadenylation, poly(A) site, and acts on the homologous site on the nascent transcript to cause its cleavage. The conformational changes of this factor determine the fate of nascent RNA, either to get cleaved and processed to mature mRNA for directing protein synthesis, or not to get cleaved and become template for double-stranded (ds) RNA synthesis. (2) A general transcription termination factor, recruited by transcribing Pol II at the poly(A) site, allostrically alters and induces Pol II to switch template from DNA to nascent RNA several hundred nucleotides downstream of the poly(A) site. The template switch disengages Pol II from DNA and effectively terminates transcription. The Pol II with newly acquired RNA-dependent RNA polymerase activity retraces its path, back along the nascent RNA, so generating dsRNA. The extent to which it can retrace this path is determined by the factors influencing the cleavage of the pre-mRNA at the site of polyA addition. If cleavage and polyadenylation occur, the retracing is cut short, the 3' RNA is degraded by an exonuclease and the polymerase is liberated to reinitiate transcription. If the cleavage is inhibited, then a full-length dsRNA can be produced. This can then be subject to cleavage by "Dicer", which generates fragments of approximately 22bp that guide degradation of the cognate mRNA via the RNA interference (RNAi) pathway. This model complements the current "allosteric-torpedo" model of transcription termination, and could explain the apparent paradox of the divergent results of a common biological process.

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Protein Prenylation: An (Almost) Comprehensive Overview on Discovery History, Enzymology, and Significance in Physiology and Disease. MONATSHEFTE FUR CHEMIE 2006. [DOI: 10.1007/s00706-006-0534-9] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]

Wu JC. Functional and clinical significance of hepatitis D virus genotype II infection. Curr Top Microbiol Immunol 2006;307:173-86. [PMID: 16903226 DOI: 10.1007/3-540-29802-9_9] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]

Abstract

Hepatitis D virus (HDV) infection is one of the important etiologies of fulminant hepatitis and may aggravate the clinical course of chronic HBV infection to cirrhosis and liver failure. HDV was classified into three genotypes. Recent molecular phylogenetic analysis of HDV suggests at least seven major clades. The genotype I HDV is widely spread, genotype II is found in East Asia and genotype III HDV is prevalent in South America. The genomic size is 1682-1685 nucleotides (nt) for genotype II, and 1676 nt for genotype IV (IIb). The divergence in HDV nucleic acid sequences between genotype II and other genotypes varies from 13.8% to 35.3%. The divergences in the HDAg-coding region may range from 17.8% to 29.8% between genotype II and other genotypes. There is no genotypic or size restriction on the interactions of either the small or the large hepatitis delta antigens (HDAgs) between genotypes I and II, and there is also no genotypic incompatibility during co-package of HDAgs of different genotypes into virus like particles. There appears no apparent universal genotypic restriction of the transactivation of genotype I HDV RNA replication by small HDAg of genotype II. In contrast, there appears more genotypic restriction for genotype I small HDAgs to transactivate genotype II HDV RNA replication. Of the functional domains of HDAg, the 19 amino acids at the carboxyl-end of the large HDAg show the greatest divergences (70%-80%) between genotypes I and II. The viral packaging efficiencies of genotype I HDV isolates are usually higher than those of genotype II. The 19 amino acids at the carboxyl-end seem to be the most important determinant for viral packaging efficiencies. The editing efficiencies of the genotype I HDV are also higher than those of the genotype II. Genotype II HDV infection is relatively less frequently associated with fulminant hepatitis at the acute stage and less unfavorable outcomes [cirrhosis or hepatocellular carcinoma (HCC)] at the chronic stage as compared to genotype I. It appears that the clinical manifestations and outcomes of patients with genotype IV (IIb) HDV infection are more like those of patients with genotype II HDV infection. Persistent replication of HBV or HDV was associated with higher adverse outcomes (cirrhosis, HCC or mortality) compared to those who cleared both viruses from the sera. HBV of the genotype C is also a significant factor associated with adverse outcomes (cirrhosis, HCC or mortality) in patients with chronic hepatitis D in addition to genotype I HDV and age. However, most patients with chronic HDV infection have low or undetectable hepatitis B virus DNA levels. During longitudinal follow-up, genotype I HDV is the most important determinant associated with survival.

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Taylor JM. Structure and replication of hepatitis delta virus RNA. Curr Top Microbiol Immunol 2006;307:1-23. [PMID: 16903218 DOI: 10.1007/3-540-29802-9_1] [Citation(s) in RCA: 38] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]

Zhong X, Leontis N, Qian S, Itaya A, Qi Y, Boris-Lawrie K, Ding B. Tertiary structural and functional analyses of a viroid RNA motif by isostericity matrix and mutagenesis reveal its essential role in replication. J Virol 2006;80:8566-81. [PMID: 16912306 PMCID: PMC1563885 DOI: 10.1128/jvi.00837-06] [Citation(s) in RCA: 64] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/23/2006] [Accepted: 06/19/2006] [Indexed: 02/07/2023] Open

Huang IC, Chien CY, Huang CR, Lo SJ. Induction of hepatitis D virus large antigen translocation to the cytoplasm by hepatitis B virus surface antigens correlates with endoplasmic reticulum stress and NF-kappaB activation. J Gen Virol 2006;87:1715-1723. [PMID: 16690938 DOI: 10.1099/vir.0.81718-0] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023] Open

Rocheleau L, Pelchat M. The Subviral RNA Database: a toolbox for viroids, the hepatitis delta virus and satellite RNAs research. BMC Microbiol 2006;6:24. [PMID: 16519798 PMCID: PMC1413538 DOI: 10.1186/1471-2180-6-24] [Citation(s) in RCA: 54] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/02/2005] [Accepted: 03/06/2006] [Indexed: 12/11/2022] Open

Bielawski KP, Zietkowski D, Charmuszko U, Sikorska K, Stalke P. Hepatitis delta virus infection in chronically HBV-infected patients from northern Poland. Arch Virol 2006;151:1207-15. [PMID: 16385395 DOI: 10.1007/s00705-005-0700-0] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/29/2005] [Accepted: 11/25/2005] [Indexed: 12/18/2022]

Rizzetto M. Hepatitis D. ZAKIM AND BOYER'S HEPATOLOGY 2006:687-692. [DOI: 10.1016/b978-1-4160-3258-8.50038-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 09/02/2023]

Tang S, Lai KN. Chronic viral hepatitis in hemodialysis patients. Hemodial Int 2005;9:169-79. [PMID: 16191066 DOI: 10.1111/j.1492-7535.2005.01129.x] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]

Abstract

Ever since the first outbreaks of hepatitis in hemodialysis units in the late 1960s, a number of hepatotropic viruses transmitted by blood and other body fluids have been identified. This review summarizes the current state of knowledge regarding these blood-borne agents from an epidemiologic and preventive perspective. Data source and study selection were obtained from research and review articles related to the epidemiology of viral hepatitis in hemodialysis and indexed on Medline and Embase from 1965 to 2004. Hepatitis B virus (HBV) was the first significant hepatotropic virus to be identified in hemodialysis centers. HBV infection has been effectively controlled by active vaccination, screening of blood donors, the use of erythropoietin, and segregation of HBV carriers. To date, HBV remains an important cause of morbidity in endemic areas. Hepatitis delta virus is a defective virus that can only infect HBV-positive individuals. Hepatitis C virus 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-alpha 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 and hepatitis GB virus C in 1995 and the TT virus in 1997. Although epidemiologic analyses revealed high prevalence rates of both viruses in the hemodialysis population, their exact role in liver disease has yet to be determined. 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 hemodialysis.

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Ivanovska I, Hardwick JM. Viruses activate a genetically conserved cell death pathway in a unicellular organism. ACTA ACUST UNITED AC 2005;170:391-9. [PMID: 16061692 PMCID: PMC2171480 DOI: 10.1083/jcb.200503069] [Citation(s) in RCA: 76] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]

Chang J, Gudima SO, Tarn C, Nie X, Taylor JM. Development of a novel system to study hepatitis delta virus genome replication. J Virol 2005;79:8182-8. [PMID: 15956563 PMCID: PMC1143748 DOI: 10.1128/jvi.79.13.8182-8188.2005] [Citation(s) in RCA: 49] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022] Open