Relevant bibliographies by topics / Alphavirus

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Alphavirus'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 December 2023

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Journal articles on the topic "Alphavirus"

1

Mostafavi, Helen, Eranga Abeyratne, Ali Zaid, and Adam Taylor. "Arthritogenic Alphavirus-Induced Immunopathology and Targeting Host Inflammation as A Therapeutic Strategy for Alphaviral Disease." Viruses 11, no. 3 (March 22, 2019): 290. http://dx.doi.org/10.3390/v11030290.

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Arthritogenic alphaviruses are a group of medically important arboviruses that cause inflammatory musculoskeletal disease in humans with debilitating symptoms, such as arthralgia, arthritis, and myalgia. The arthritogenic, or Old World, alphaviruses are capable of causing explosive outbreaks, with some viruses of major global concern. At present, there are no specific therapeutics or commercially available vaccines available to prevent alphaviral disease. Infected patients are typically treated with analgesics and non-steroidal anti-inflammatory drugs to provide often inadequate symptomatic relief. Studies to determine the mechanisms of arthritogenic alphaviral disease have highlighted the role of the host immune system in disease pathogenesis. This review discusses the current knowledge of the innate immune response to acute alphavirus infection and alphavirus-induced immunopathology. Therapeutic strategies to treat arthritogenic alphavirus disease by targeting the host immune response are also examined.
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Landers, V. Douglas, Daniel W. Wilkey, Michael L. Merchant, Thomas C. Mitchell, and Kevin J. Sokoloski. "The Alphaviral Capsid Protein Inhibits IRAK1-Dependent TLR Signaling." Viruses 13, no. 3 (February 27, 2021): 377. http://dx.doi.org/10.3390/v13030377.

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Alphaviruses are arthropod-borne RNA viruses which can cause either mild to severe febrile arthritis which may persist for months, or encephalitis which can lead to death or lifelong cognitive impairments. The non-assembly molecular role(s), functions, and protein–protein interactions of the alphavirus capsid proteins have been largely overlooked. Here we detail the use of a BioID2 biotin ligase system to identify the protein–protein interactions of the Sindbis virus capsid protein. These efforts led to the discovery of a series of novel host–pathogen interactions, including the identification of an interaction between the alphaviral capsid protein and the host IRAK1 protein. Importantly, this capsid–IRAK1 interaction is conserved across multiple alphavirus species, including arthritogenic alphaviruses SINV, Ross River virus, and Chikungunya virus; and encephalitic alphaviruses Eastern Equine Encephalitis virus, and Venezuelan Equine Encephalitis virus. The impact of the capsid–IRAK1 interaction was evaluated using a robust set of cellular model systems, leading to the realization that the alphaviral capsid protein specifically inhibits IRAK1-dependent signaling. This inhibition represents a means by which alphaviruses may evade innate immune detection and activation prior to viral gene expression. Altogether, these data identify novel capsid protein–protein interactions, establish the capsid–IRAK1 interaction as a common alphavirus host–pathogen interface, and delineate the molecular consequences of the capsid–IRAK1 interaction on IRAK1-dependent signaling.
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Kaelber, Jason T., David Chmielewski, Wah Chiu, and Albert J. Auguste. "Alphavirus Particles Can Assemble with an Alternate Triangulation Number." Viruses 14, no. 12 (November 27, 2022): 2650. http://dx.doi.org/10.3390/v14122650.

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Alphaviruses are spherical, enveloped RNA viruses primarily transmitted by mosquitoes, and cause significant arthritogenic and neurotropic disease in humans and livestock. Previous reports have shown that—in contrast to prototypical icosahedral viruses—alphaviruses incorporate frequent defects, and these may serve important functions in the viral life cycle. We confirm the genus-wide pleomorphism in live viral particles and extend our understanding of alphavirus assembly through the discovery of an alternate architecture of Eastern equine encephalitis virus (EEEV) particles. The alternate T = 3 icosahedral architecture differs in triangulation number from the classic T = 4 icosahedral organization that typifies alphaviruses, but the alternate architecture maintains the quasi-equivalence relationship of asymmetric units. The fusion spike glycoproteins are more loosely apposed in the T = 3 form with corresponding changes in the underlying capsid protein lattice. This alternate architecture could potentially be exploited in engineering alphavirus-based particles for delivery of alphaviral or other RNA.
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Bedoui, Yosra, Dauriane De Larichaudy, Matthieu Daniel, Franck Ah-Pine, Jimmy Selambarom, Pascale Guiraud, and Philippe Gasque. "Deciphering the Role of Schwann Cells in Inflammatory Peripheral Neuropathies Post Alphavirus Infection." Cells 12, no. 1 (December 26, 2022): 100. http://dx.doi.org/10.3390/cells12010100.

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Old world alphaviruses (e.g., chikungunya) are known to cause severe acute and chronic debilitating arthralgia/arthritis. However, atypical neurological manifestations and, in particular, unexpected cases of acute inflammatory Guillain–Barre syndrome (GBS) have been associated with the arthritogenic alphaviruses. The pathogenesis of alphavirus-associated GBS remains unclear. We herein addressed for the first time the role of Schwann cells (SC) in peripheral neuropathy post-alphaviral infection using the prototypical ONNV alphavirus model. We demonstrated that human SC expressed the recently identified alphavirus receptor MxRA8 and granting viral entry and robust replication. A canonical innate immune response was engaged by ONNV-infected SC with elevated gene expression for RIG-I, MDA5, IFN-β, and ISG15 and inflammatory chemokine CCL5. Transcription levels of prostaglandin E2-metabolizing enzymes including cPLA2α, COX-2, and mPGES-1 were also upregulated in ONNV-infected SC. Counterintuitively, we found that ONNV failed to affect SC regenerative properties as indicated by elevated expression of the pro-myelinating genes MPZ and MBP1 as well as the major pro-myelin transcription factor Egr2. While ONNV infection led to decreased expression of CD55 and CD59, essential to control complement bystander cytotoxicity, it increased TRAIL expression, a major pro-apoptotic T cell signal. Anti-apoptotic Bcl2 transcription levels were also increased in infected SC. Hence, our study provides new insights regarding the remarkable immunomodulatory role of SC of potential importance in the pathogenesis of GBS following alphavirus infection.
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Cherkashchenko, Liubov, Kai Rausalu, Sanjay Basu, Luke Alphey, and Andres Merits. "Expression of Alphavirus Nonstructural Protein 2 (nsP2) in Mosquito Cells Inhibits Viral RNA Replication in Both a Protease Activity-Dependent and -Independent Manner." Viruses 14, no. 6 (June 17, 2022): 1327. http://dx.doi.org/10.3390/v14061327.

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Alphaviruses are positive-strand RNA viruses, mostly being mosquito-transmitted. Cells infected by an alphavirus become resistant to superinfection due to a block that occurs at the level of RNA replication. Alphavirus replication proteins, called nsP1-4, are produced from nonstructural polyprotein precursors, processed by the protease activity of nsP2. Trans-replicase systems and replicon vectors were used to study effects of nsP2 of chikungunya virus and Sindbis virus on alphavirus RNA replication in mosquito cells. Co-expressed wild-type nsP2 reduced RNA replicase activity of homologous virus; this effect was reduced but typically not abolished by mutation in the protease active site of nsP2. Mutations in the replicase polyprotein that blocked its cleavage by nsP2 reduced the negative effect of nsP2 co-expression, confirming that nsP2-mediated inhibition of RNA replicase activity is largely due to nsP2-mediated processing of the nonstructural polyprotein. Co-expression of nsP2 also suppressed the activity of replicases of heterologous alphaviruses. Thus, the presence of nsP2 inhibits formation and activity of alphavirus RNA replicase in protease activity-dependent and -independent manners. This knowledge improves our understanding about mechanisms of superinfection exclusion for alphaviruses and may aid the development of anti-alphavirus approaches.
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Souza-Souza, Kauê F. C., Cassiano F. Gonçalves-de-Albuquerque, Cláudio Cirne-Santos, Izabel C. N. P. Paixão, and Patrícia Burth. "Alphavirus Replication: The Role of Cardiac Glycosides and Ion Concentration in Host Cells." BioMed Research International 2020 (May 9, 2020): 1–7. http://dx.doi.org/10.1155/2020/2813253.

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Alphaviruses are arthropod-borne viruses that can cause fever, rash, arthralgias, and encephalitis. The mosquito species Aedes aegypti and Aedes albopictus are the most frequent transmitters of alphaviruses. There are no effective vaccines or specific antivirals available for the treatment of alphavirus-related infections. Interestingly, changes in ion concentration in host cells have been characterized as critical regulators of the alphavirus life cycle, including fusion with the host cell, glycoprotein trafficking, genome translation, and viral budding. Cardiac glycosides, which are classical inhibitors of the Na+ K+ ATPase (NKA), can inhibit alphavirus replication although their mechanisms of action are poorly understood. Nonetheless, results from multiple studies suggest that inhibition of NKA may be a suitable strategy for the development of alphavirus-specific antiviral treatments. This review is aimed at exploring the role of changes in ion concentration during alphavirus replication and at considering the possibility of NKA as a potential therapeutic target for antiviral drugs.
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Powers, Ann M., Aaron C. Brault, Yukio Shirako, Ellen G. Strauss, WenLi Kang, James H. Strauss, and Scott C. Weaver. "Evolutionary Relationships and Systematics of the Alphaviruses." Journal of Virology 75, no. 21 (November 1, 2001): 10118–31. http://dx.doi.org/10.1128/jvi.75.21.10118-10131.2001.

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ABSTRACT Partial E1 envelope glycoprotein gene sequences and complete structural polyprotein sequences were used to compare divergence and construct phylogenetic trees for the genus Alphavirus. Tree topologies indicated that the mosquito-borne alphaviruses could have arisen in either the Old or the New World, with at least two transoceanic introductions to account for their current distribution. The time frame for alphavirus diversification could not be estimated because maximum-likelihood analyses indicated that the nucleotide substitution rate varies considerably across sites within the genome. While most trees showed evolutionary relationships consistent with current antigenic complexes and species, several changes to the current classification are proposed. The recently identified fish alphaviruses salmon pancreas disease virus and sleeping disease virus appear to be variants or subtypes of a new alphavirus species. Southern elephant seal virus is also a new alphavirus distantly related to all of the others analyzed. Tonate virus and Venezuelan equine encephalitis virus strain 78V3531 also appear to be distinct alphavirus species based on genetic, antigenic, and ecological criteria. Trocara virus, isolated from mosquitoes in Brazil and Peru, also represents a new species and probably a new alphavirus complex.
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Lundstrom, Kenneth. "Alphaviruses in Immunotherapy and Anticancer Therapy." Biomedicines 10, no. 9 (September 13, 2022): 2263. http://dx.doi.org/10.3390/biomedicines10092263.

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Alphaviruses have been engineered as expression vectors for vaccine development and gene therapy. Due to the feature of RNA self-replication, alphaviruses can provide exceptional direct cytoplasmic expression of transgenes based on the delivery of recombinant particles, naked or nanoparticle-encapsulated RNA or plasmid-based DNA replicons. Alphavirus vectors have been utilized for the expression of various antigens targeting different types of cancers, and cytotoxic and antitumor genes. The most common alphavirus vectors are based on the Semliki Forest virus, Sindbis virus and Venezuelan equine encephalitis virus, but the oncolytic M1 alphavirus has also been used. Delivery of immunostimulatory cytokine genes has been the basis for immunotherapy demonstrating efficacy in different animal tumor models for brain, breast, cervical, colon, lung, ovarian, pancreatic, prostate and skin cancers. Typically, therapeutic effects including tumor regression, tumor eradication and complete cure as well as protection against tumor challenges have been observed. Alphavirus vectors have also been subjected to clinical evaluations. For example, therapeutic responses in all cervical cancer patients treated with an alphavirus vector expressing the human papilloma virus E6 and E7 envelope proteins have been achieved.
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Rao, Shambhavi, and Adam Taylor. "Arthritogenic Alphavirus Capsid Protein." Life 11, no. 3 (March 11, 2021): 230. http://dx.doi.org/10.3390/life11030230.

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In the past two decades Old World and arthritogenic alphavirus have been responsible for epidemics of polyarthritis, causing high morbidity and becoming a major public health concern. The multifunctional arthritogenic alphavirus capsid protein is crucial for viral infection. Capsid protein has roles in genome encapsulation, budding and virion assembly. Its role in multiple infection processes makes capsid protein an attractive target to exploit in combating alphaviral infection. In this review, we summarize the function of arthritogenic alphavirus capsid protein, and describe studies that have used capsid protein to develop novel arthritogenic alphavirus therapeutic and diagnostic strategies.
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Nguyen, LeAnn P., Kelly S. Aldana, Emily Yang, Zhenlan Yao, and Melody M. H. Li. "Alphavirus Evasion of Zinc Finger Antiviral Protein (ZAP) Correlates with CpG Suppression in a Specific Viral nsP2 Gene Sequence." Viruses 15, no. 4 (March 24, 2023): 830. http://dx.doi.org/10.3390/v15040830.

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Certain re-emerging alphaviruses, such as chikungunya virus (CHIKV), cause serious disease and widespread epidemics. To develop virus-specific therapies, it is critical to understand the determinants of alphavirus pathogenesis and virulence. One major determinant is viral evasion of the host interferon response, which upregulates antiviral effectors, including zinc finger antiviral protein (ZAP). Here, we demonstrated that Old World alphaviruses show differential sensitivity to endogenous ZAP in 293T cells: Ross River virus (RRV) and Sindbis virus (SINV) are more sensitive to ZAP than o’nyong’nyong virus (ONNV) and CHIKV. We hypothesized that the more ZAP-resistant alphaviruses evade ZAP binding to their RNA. However, we did not find a correlation between ZAP sensitivity and binding to alphavirus genomic RNA. Using a chimeric virus, we found the ZAP sensitivity determinant lies mainly within the alphavirus non-structural protein (nsP) gene region. Surprisingly, we also did not find a correlation between alphavirus ZAP sensitivity and binding to nsP RNA, suggesting ZAP targeting of specific regions in the nsP RNA. Since ZAP can preferentially bind CpG dinucleotides in viral RNA, we identified three 500-bp sequences in the nsP region where CpG content correlates with ZAP sensitivity. Interestingly, ZAP binding to one of these sequences in the nsP2 gene correlated to sensitivity, and we confirmed that this binding is CpG-dependent. Our results demonstrate a potential strategy of alphavirus virulence by localized CpG suppression to evade ZAP recognition.
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Dissertations / Theses on the topic "Alphavirus"

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Berglund, Peter. "Alphavirus vectors as recombinant vaccines /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2657-3.

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Skoging, Nyberg Ulrica. "Protein interactions involved in alphavirus assembly /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4329-x/.

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Shabman, Reed Solomon Heise Mark T. "Alphavirus evasion of type I interferons." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1879.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.
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Lim, Elisa X. "Host-pathogen interactions during alphavirus infection." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/410163.

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Arthritogenic alphavirus infection causes debilitating pain in the joints and muscles with many patients experiencing such symptoms chronically. However, there is insufficient evidence to explain the underlying causes behind symptoms of persistent arthralgia and myalgia. Joint-associated tissues are the main site of inflammation during alphavirus infection, and it has been shown that alphaviruses induce damage to the cartilage and synovium. Therefore, the cell types present in these tissues play critical roles in disease pathogenesis. The findings described in this thesis contribute to the general understanding of host-pathogen interactions during alphavirus infection of joint-associated cell types. Here, the analysis of murine joints revealed chondrocytes as a target of RRV infection (Chapter 1). Further evaluation of human primary chondrocytes and skeletal muscle cells through short-term in vitro cell culture showed that these cell types could support productive RRV infection. Our study presents the first evidence of the role of chondrocytes in alphavirus disease pathogenesis. Currently, there are gaps in our understanding of chronic alphavirus disease, especially in the absence of detectable viraemia after recovery from infection. Here, we have investigated the r sponses of several cell types in joint-associated tissues during chronic infection. Human primary cells and their corresponding cell line counterparts for chondrocytes, muscle cells and fibroblast-like synoviocytes (FLS) were infected with four alphaviruses of clinical importance, namely Ross River virus (RRV), Barmah Forest virus (BFV), chikungunya virus (CHIKV) and o’nyong’nyong virus (ONNV). We found that all cell types studied were able to retain residual alphaviral nucleic acids after recovery from infection despite several passages in culture (up to 10 weeks), indicating the potential of these cell types as reservoirs for the virus and/or viral RNA (Chapter 2). Regretfully, we were unable to determine the roles of the lingering viral nucleic acids though we hypothesise that they may play roles in causing chronic inflammation. During this study, we also established persistent alphavirus infection in chondrocyte C28/I2 and muscle RD cell lines (Chapter 2) and hypothesise that these two cell types could act as potential harbours for virus evasion from the immune system. The characterisation of genetic variants present in samples from persistent infections led to the identification of several mutations which could potentially be important for alphavirus persistence. We speculate that C28/I2 and RD cell lines are suitable candidates for exploring alphavirus evolution through selective pressures applied by in vitro serial passaging of infected cells. Our findings indicate that infected chondrocytes, muscle cells and FLS contribute to alphavirus disease pathogenesis through increased expression of pro-inflammatory cytokines associated with clinical disease such as IL-6, MCP-1 and IL-8 (Chapter 1 and 2). However, further studies are required to determine if the presence of residual alphaviral nucleic acids serves as PAMPs that are responsible for eliciting chronic inflammatory responses. While we have shown that RRV-infected chondrocytes play a role in causing alphavirus-induced inflammation, we also observed that these cells cause cartilage damage through disruption of ECM homeostasis. As the main cell type of the cartilage, chondrocytes are responsible for the regulation of ECM synthesis and degradation. During RRV-infection of chondrocytes, we observed reduced gene expression of key ECM constituents COL1A1, COL2A1 and ACAN and elevated gene expression of ECM breakdown enzymes like HPSE, ADAMTS4 and MMP9 (Chapter 1, 2 and 3). We also observed evidence of this through our transcriptomic analysis of RRVinfected and uninfected bystander chondrocytes. This is also the first study that investigates the direct and indirect responses to alphavirus infection of chondrocyte (Chapter 3). As an avascular tissue type, chondrocytes are not easily accessible to virus infection. However, we found evidence of RRV RNA in the chondrocytes of infected mice (Chapter 1) and have shown that these cells are susceptible to alphavirus infection (Chapters 1-4). Therefore, we can only speculate on the possible routes of alphavirus infection of chondrocytes. The use of in vitro chondrocyte models with complex ECM architecture allows for greater physiological relevance in the study of cartilage and their responses to alphavirus infection. The synovium is a neighbouring tissue with access to the blood supply network and provides nutrients to the cartilage. Therefore, it is possible that chondrocytes can acquire alphavirus infection via the synovium. Fibroblast-like synoviocytes (FLS) are the main resident cell type of the synovium and maintains the synovial fluid through the expression of ECM components and breakdown enzymes like MMP3. We found that interactions between chondrocytes and FLS result in increased viral infectivity profiles (Chapter 4). Our study also demonstrates that the ECM surrounding the chondrocytes acts as a physical barrier that prevents access to virus particles. Treatment of cells with MMP3 was able to loosen the interactions of the ECM and expose the chondrocytes to virus infection, resulting in greater virus attachment and infectivity compared to non-treated cells. Taken together, this thesis presents key findings on the possible mechanisms involved in alphavirus disease pathogenesis and the roles of cell types of joint-associated tissues in causing the chronic symptoms of joint and muscle pain felt by the majority of infected patients.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Griffith Health
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Li, Ke-Jun. "Semliki forest virus-derived packaging system for production of retroviral vectors /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3268-9/.

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Gershy-Damet, Guy-Michel. "Etude épidémiologue et virologique des infections à arbovirus en Côte d'Ivoire : aspects ultrastructuraux de l'infection expérimentale du nourrisson par la souche vaccinale antiamarile." Aix-Marseille 2, 1985. http://www.theses.fr/1985AIX21901.

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Nubgan, Amer S. "The role of the deubiquitylase MYSM1 during alphavirus infection." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3015357/.

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The members of the genus Alphavirus are positive-sense RNA viruses and it is one of two within the family Togaviridae. Most alphaviruses are predominantly transmitted to susceptible vertebrates by a mosquito vector. Alphavirus disease in humans can be severely debilitating, and depending on the particular viral species, infection may result in encephalitis and possibly life threatening symptoms. Chikungunya virus (CHIKV) is the aetiological agent represents a substantial health burden to affected populations, with clinical symptoms that include severe joint and muscle pain, rashes, and fever, as well as prolonged periods of disability in some patients. In recent years, CHIKV has received significant attention from public health authorities as a consequence of the dramatic emergence infections in the Indian Ocean islands and the Caribbean as well as the recent emergence of CHIKV in the Americas. Infections have also been reported around Europe such as in Italy, France and Greece. Currently, no safe, approved or effective vaccine or treatment exists for CHIKV infection. The ubiquitin-proteasome system (UPS), the major intracellular proteolytic pathway, mediates different kinds of cellular processes, which may be targeted by viruses to aid their replication within cells. In recent years it has been well established that both the forward reaction of ubiquitination, and the reverse reaction of deubiquitination are targeted during virus infection to enhance their replication, either by targeting of cellular proteins or encoding viral homologues of key pathway proteins. The reverse reaction is undertaken by a large family of enzymes termed deubiquitylases or DUBs, and many of these have been shown to play a crucial role, not only in virus replication but also in the regulation of the immune system and vesicle trafficking. The DUBs are attractive drug targets and have increasingly been implicated in cellular processes germane to malignancy which makes the continued characterisation of the role of DUBs during virus infection a worthwhile objective. In on-going experiments in the research group a DUB siRNA pools library screen identified 12 DUBs (USP1, USP4, USP5, USP34, USP45, USP46, OTUD6A, UCHL1, JOSD2, BRCC3 and MYSM1). Depletion of these hits in HeLa cells lead to an increase in cell viability following Semiliki Forest Virus (SFV) infection (and predicted to be pro-viral) and thus could potential be candidate antiviral targets. Inroads into understanding the role of the DUB hits during the alphavirus infection, focusing initial on the BSL2 model virus SFV, and extending this to CHIKV (at BSL3). In the present study, further screening focused on the deconvolution siRNA pools for the DUB hits. Investigation of the subsequent follow up experiments with one strong candidate DUB from this list, MYSM1. Two different approaches were taken. Firstly, the effect of depletion of MYSM1 by siRNA treatment was further investigated in HeLa cells. Secondly, the analysis was extended to investigate the role of MYSM1 in fibroblasts utilising MYSM1 genetic knockout murine embryo fibroblasts. Results from this study indicate that depletion of MYSM1 in HeLa cells by siRNAs resulted in a reduction in both SFV and CHIKV replication, as assayed by measuring RNA levels and plaque formation. It was also found that MYSM1 genetic knockout in MEF cells lead to increase in both SFV and CHIKV replication. In addition, depletion of MYSM1 by siRNAs in MRC-5 cells lead to increase in SFV replication. In conclusion, MYSM1 generated interesting data, implying a role during virus infection that appeared to depend on the cell type being infected. Up to now it is unclear what the effector mechanisms are that contribute to these observations, subject to further mechanistic and functional studies, may increase the options available for targeting this vital DUB during Alphavirus infections.
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Plaskon, Nicole Elyse. "The Development of New Tools to Investigate Alphavirus Replication Kinetics." Thesis, Virginia Tech, 2009. http://hdl.handle.net/10919/34787.

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Members of the alphavirus genus pose a serious or potential threat to public health in many areas of the world. Nearly all alphaviruses are maintained in nature by transmission cycles that involve alternating replication in a susceptible vertebrate and invertebrate host. The maintenance of this transmission cycle depends on the establishment of a life-long persistent infection in the invertebrate vector host. Although alphavirus replication has been extensively studied in vertebrate models, the strand-specific replication kinetics of alphaviruses during persistent infections of the invertebrate host have not been reported. We investigated the strand-specific replication of different alphavirus genotypes in invertebrate cells.

By comparing different detection strategies and chemistries, we identified an optimal ssqPCR assay design for strand-specific quantification of viral RNAs in infected cells and tissues. We found that primer sets incorporating the use of a non-target tag sequence were able to avoid real-time PCR detection of amplicons that were falsely-primed during reverse-transcription. We also determined that DNA hydrolysis probes increased the sensitivity of ssqPCR assays when compared to a double-stranded DNA-specific dye, SYBR Green.

Using this information, we determined the replication kinetics of two different genotypes of o'nyong nyong virus (ONNV) and chikungunya virus (CHIKV) in infected mosquito cells. We found that (-) strand viral RNAs persisted in invertebrate cells for up to 21 days after infection. We also found that significantly less (-) strand RNA was present in cells infected with opal variants of both ONNV and CHIKV than sense variants at several time points post infection, suggesting that the opal codon has a functional role in (-) strand RNA regulation. We also report the development of an ONNV replicon expression system.

In total, the tools we developed for this report will facilitate future replication studies in the mosquito that may shed light on questions regarding the regulatory role of the opal codon and the persistence of (-) strand RNAs during long-term infections. The strand-specific replication kinetics of ONNV and CHIKV genotypes reported here will serve as a foundation for such investigations.


Master of Science in Life Sciences
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Belarbi, Essia. "Etude de la physiopathologie des infections à alphavirus arthritogènes par une approche d’imagerie in vivo." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS073.

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Les alphavirus arthritogènes de la rivière Ross (RRV) et du chikungunya (CHIKV) sont des arbovirus à l’origine de maladies inflammatoires musculosquelettiques chez l'homme. Ils sont largement distribués dans le monde et provoquent périodiquement des épidémies explosives. Les principaux signes cliniques lors d’une infection par un alphavirus arthritogène sont les myalgies, polyarthrites et arthralgies intenses pouvant persister plusieurs mois après l'infection. Les mécanismes de développement de l’infection et des manifestations persistantes sont peu connus. Pour étudier la pathogenèse de l'infection par RRV, nous avons généré un virus recombinant exprimant une nouvelle luciférase brillante et brillante. Nous avons montré que les monocytes humains, malgré une faible susceptibilité à l'infection in vitro par RRV, étaient capables de maintenir une réplication virale jusqu'à 45 jours post infection indiquant leur rôle potentiel dans les formes chroniques. Grâce un modèle expérimental de l’infection par RRV, nous avons suivi les phases aiguë et chronique de la maladie in vivo. Nous avons montré que les cinétiques de réplication du virus recombinant étaient proches de celles du virus parental. Nous avons également observé un tropisme musculaire et articulaire et une corrélation entre le signal bioluminescent et la charge virale confirmant ainsi la relevance de ce modèle. En étudiant la dissémination virale, nous avons montré que le Bindarit, une molécule anti-inflammatoire diminuant le développement de la maladie dans le modèle murin, induit une plus grande réplication dans le tissu cardiaque. Enfin, nous avons pu observer une réplication virale dans les tissus musculaires durant la phase chronique de la maladie et avons montré le rôle de la dose inoculée dans le développement de la persistance virale. Suite à un traitement immunosuppresseur, nous avons observé une légère augmentation du signal bioluminescent indiquant un contrôle de la réplication virale persistante par la réponse immunitaire adaptative. Ce nouveau modèle d’imagerie in vivo permet un suivi en temps réel de la dissémination virale permettant des études de pathogenèse et l'évaluation de stratégies thérapeutiques
Ross River virus (RRV) and chikungunya virus (CHIKV) are mosquito-transmitted viruses that cause musculoskeletal inflammatory diseases in humans. They are widely distributed and periodically cause explosive epidemics. After infection with RRV, patients experience fever, maculopapular rash, myalgia and intense pain in the peripheral joints. Approximately 30% of patients develop a chronic form of the disease with myalgia and poly-arthralgia persisting for months to years after infection. The mechanisms underlying these persistent symptoms remain unclear. To study the dynamics and pathogenesis of RRV infection in vitro and in living animals, we generated a recombinant virus expressing a novel small and bright luciferase. First we showed that human monocytes, despite a low susceptibility to RRV infection, were able to maintain viral replication in vitro up to 45 days post infection. Then, using a murine model of RRV infection, we monitored the acute and chronic phases of the disease. We observed near native replication kinetics and a muscular/articular tropism after infection with our recombinant virus. Moreover, the bioluminescent signal correlated with the viral load further confirming the relevance of this new imaging model. After monitoring of the viral dissemination in live mice, we showed that Bindarit, an anti-inflammatory molecule known to prevent the development of the alphaviral disease in a mouse model, induces a higher replication in the cardiac tissue; thereby indicating that caution must be used before treatment of patients. We were also able to observe viral replication in the muscles during the chronic stage of the disease when using a low inoculation dose. Finally, following an immunosuppressive treatment, we observed a slight increase in the bioluminescent signal indicating a control of remnant viral replication by the adaptive immune response. This new model provides a non-invasive real-time assessment of viral replication and dissemination allowing pathogenesis studies and therapeutic strategies evaluation
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Castro, Ceyla Maria Oeiras de. "Análise metabolômica de alterações induzidas pelo vírus mayaro em células vero." Faculdade de Medicina de São José do Rio Preto, 2015. http://hdl.handle.net/tede/373.

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This study aimed at assessing the extracellular metabolic profile of Vero cells infected by Mayaro virus. In this metabolomic study, the use of nuclear magnetic resonance associated to multivariate analytical methods, devices of standard recognition, showed metabolic variations which can be attributed to the effect of Mayaro virus infection. Vero cells were infected and incubated for 2, 6 and 12 hour periods. Differentiated variations in the levels of several metabolites such as amino acids, organic acids, guanidine compound, monoamine, carbohydrates and fatty acids have occurred in each period. These organic compounds are metabolites involved in the glycolysis pathway, tricarboxylic acid cycle, pentose phosphate pathway, and the oxidation pathway of fatty acids (via the β-oxidation). This study demonstrates footprinting analysis representing the effect of the virus action on the Vero cell metabolism, furthermore, these analyzes point out the intracellular metabolic state, improving the knowledge of the microorganism influence on cellular metabolism.
O presente estudo tem como objetivo avaliar o perfil metabólico extracelular de células Vero infectadas pelo vírus Mayaro. Neste estudo metabolômico o uso da ressonância magnética nuclear combinado a métodos analíticos multivariados, ferramentas de reconhecimento padrão que demonstraram variações metabólicas que podem ser atribuídas ao efeito da infecção do vírus Mayaro. As células Vero foram infectadas e incubadas em períodos de 2, 6 e 12 horas. Em cada período ocorrem variações diferenciadas nos níveis de vários metabólitos, como aminoácidos, ácidos orgânicos, composto de guanidina, monoamina, carboidratos e ácidos graxos. Esses compostos orgânicos são metabólitos envolvidos na via da glicólise, ciclo do ácido tricarboxílico, via das pentoses-fosfato, e via da oxidação dos ácidos graxos (via da β-oxidação). Este estudo demonstra footprinting analysis que representa o efeito da ação do vírus no metabolismo da célula Vero, além disso, essas análises indicaram o estado metabólico intracelular, e contribuem para o conhecimento da influência do microorganismo no metabolismo celular.
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Books on the topic "Alphavirus"

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Tavani, Romolo, and Peter Georgas-Frey. Alphavirus. Independently Published, 2020.

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DiCiommo, David P. A novel, DNA-based alphavirus gene expression system for rapid recombinant protein purification and virus-based gene delivery to retina and retinoblastoma tumor cells. 2002.

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Alphaviruses: Current Biology. Caister Academic Press, 2016. http://dx.doi.org/10.21775/9781910190159.

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Depa, Larisse, Larissa Depa, Crhisllane Vasconcelos, Vagner Fonseca, and Diego Frias. Estudo do uso de códons nos vírus da Dengue, Zika e Chikungunya com foco em terapia por inibição seletiva de tRNAs contra arboviroses. Edited by Diego Mariano. Alfahelix, 2021. http://dx.doi.org/10.51780/978-6-5992753-3-3.

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O vírus da dengue (DENV), o vírus da Zika (ZIKV) e o vírus da chikungunya (CHIKV) são espécies que apresentam relevância clínica para a saúde pública. Porém, ainda não existe um tratamento específico ou vacina disponível para esses arbovírus. Nesse contexto, é fundamental encontrar novos alvos terapêuticos que possam auxiliar estratégias e tratamentos mais eficientes. A metodologia de codon usage tem demonstrado bons resultados para encontrar alvos para terapias que visam inibidores de tradução. Este estudo buscou analisar o uso de códons e o equilíbrio entre a abundância relativa dos RNAs transportadores (tRNAs) para encontrar alvos terapêuticos que irão estimular novas alternativas de tratamento para infecções causadas pelos DENV, ZIKV e CHIKV. Para tanto, foi replicada uma estratégia computacional, assumindo uma terapia hipotética de inibição seletiva de tRNA (Selective Transport RNA Inhibition Therapy - STRIT), onde foi estabelecido um índice de potencial terapêutico (T-score) para encontrar potenciais espécies de tRNA que poderiam ser inibidas seletivamente para atenuar a replicação viral na célula hospedeira. Foram identificados os cinco códons com maior frequência relativa vírus/hospedeiro (mais relevantes para o vírus) nas seis espécies de arbovírus, notando que todos terminam com purinas A ou G. Os códons GGA (Glicina), AGA (Arginina) e ATA (Isoleucina) são relevantes em todos os flavivirus (ZIKV, DENV-1, DENV-2, DENV-3, DENV-4), mas não no alphavirus CHIKV, onde os códons ACG (Treonina) e CCG (Prolina) são os mais relevantes. Posteriormente, selecionando os cinco códons com maiores T-score nas seis espécies virais (30 códons em total) encontramos apenas 11 códons diferentes, todos terminados com A ou G. Agrupados segundo o nucleotídeo na primeira posição do códon estes 11 códons são: (AGA, ACA, ATA, ACG), (GGA, GCA, GTA, GCG), (CTA, CCG) e (TGG). No agrupamento, notamos outro fato intrigante: que 10 dos 11 códons mais bem ranqueados por T-score, terminam com GA, CA, TA ou CG. Nosso método identificou as espécies de tRNA (através da identificação do códon cognato com maior T-score), cuja inibição funcional por qualquer método específico a anticódon, poderia ter potenciais efeitos terapêuticos em células infectadas pelo vírus da Dengue, Zika e Chikungunya causando a inibição da tradução das proteínas do vírus sem ter um efeito deletério na sobrevivência das células hospedeiras durante o período da infeção. A predominância absoluta dos nucleotídeos A e G na terceira posição dos 11 códons com maior T-score, que por sua vez indica uma preferência dos arbovírus por 11 espécies de tRNA com C ou T na primeira posição do anticódon, abre um novo espaço de pesquisa na interação vírus-hospedeiro.
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Book chapters on the topic "Alphavirus"

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Stollar, Victor. "Alphavirus‡." In The Springer Index of Viruses, 1859–66. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-95919-1_304.

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Harrison, Stephen C. "Alphavirus Structure." In The Togaviridae and Flaviviridae, 21–34. Boston, MA: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-0785-4_2.

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Lundstrom, Kenneth. "Alphavirus-Based Vaccines." In Viral Vectors in Veterinary Vaccine Development, 169–80. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51927-8_11.

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Garoff, Henrik, and Kejun Li. "Alphavirus-Retrovirus Vectors." In Gene Therapy, 61–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72160-1_6.

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Lundstrom, Kenneth. "Alphavirus-Based Vaccines." In Vaccine Design, 313–28. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3389-1_22.

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Lundstrom, Kenneth. "Alphavirus-Based Vectors." In Neuromethods, 95–111. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-610-8_5.

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Lundstrom, Kenneth. "Alphavirus-Based Vaccines." In Methods in Molecular Biology, 225–42. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6869-5_13.

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Griffin, Diane E. "Alphavirus Pathogenesis and Immunity." In The Togaviridae and Flaviviridae, 209–49. Boston, MA: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-0785-4_8.

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Rice, Charles M. "Alphavirus-Based Expression Systems." In Advances in Experimental Medicine and Biology, 31–40. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1382-1_5.

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Shafferman, A., S. Lustig, Y. Inbar, M. Halevy, P. Schneider, T. Bino, M. Leitner, et al. "Alphavirus Hybrid Virion Vaccines." In Advances in Experimental Medicine and Biology, 41–47. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1382-1_6.

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Conference papers on the topic "Alphavirus"

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Cao, Yanran, Stene Anne, Lars Christian Gansel, Stig Atle Tuene, Grete Hansen Aas, and Anne Synnove Rosvik. "Natural infection induced immune response against salmonid alphavirus in farmed salmon." In OCEANS 2017 - Aberdeen. IEEE, 2017. http://dx.doi.org/10.1109/oceanse.2017.8084664.

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CONT, R. N., and G. B. CABRAL. "DIAGNÓSTICO SOROLÓGICO DE CHIKUNGUNYA EM REGIÕES DE CO-CIRCULAÇÃO DE ARBOVIROSES." In III Mostra Dos Trabalhos De Conclusão De Curso Da Especialização Em Vigilância Laboratorial Em Saúde Pública. Agron Science, 2022. http://dx.doi.org/10.53934/10105-2.

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A febre Chikungunya, é a doença causada pela infecção do vírus Chikungunya, um alphavirus, da família Togaviridae, transmitida por mosquitos Aedes aegypti e Aedes albopictus, que circula no Brasil desde 2014. No ano vigente, até setembro, ocorreram 87.748 casos prováveis, e 10 óbitos confirmados por critérios laboratoriais. A co-circulação de arboviroses, como Dengue e Zika, é uma realidade em muitas regiões, o que dificulta o diagnóstico clínico, devido a semelhança dos sintomas entre essas doenças. Para um diagnóstico mais específico, utiliza-se os testes laboratoriais. Entretanto, um dos desafios primários na interpretação dos testes sorológicos de infecções agudas por arboviroses, são os resultados falsos-positivos devido a reatividade-cruzada. Através de uma revisão bibliográfica, demonstrou-se a ocorrência de reação-cruzada nos testes sorológicos de Chikungunya em diversos estudos, variando de 1% a 37%, dependendo do kit comercial e da quantidade de amostras utilizados. Além disso, apresentamos estudos para o desenvolvimento de testes capazes de minimizar essa ocorrência.
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Rocha, Vinicius, Breno Barreto, Larissa Fonseca, Jesse Erasmus, Amit Khandhar, Steve Reed, Roberto Badaró, Milena Soares, and Bruna Machado. "An alphavirus-derived replicon polyvalent RNA vaccine induces neutralizing antibodies in mice against omicron SARS-CoV-2 variant of concern." In International Symposium on Immunobiologicals. Instituto de Tecnologia em Imunobiológicos, 2023. http://dx.doi.org/10.35259/isi.2023_57936.

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Silva, Victor Luiz Luciano da, URSULA RAIANNY LACERDA DA SILVA, AMANDA MARIA SANTANA DA COSTA, ITALO MATHEUS DA SILVA PEQUENO, and FRANCISCO ISRAEL MAGALHÃES FEIJAO. "CHIKUNGUNYA NO BRASIL: UM ESTUDO OBSERVACIONAL TRANSVERSAL COMPARANDO AS 16 PRIMEIRAS SEMANAS EPIDEMIOLÓGICAS DE 2021 E 2022." In I Congresso Brasileiro de Estudos Epidemiológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/epidemion/7622.

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Introdução: A chikungunya é uma arbovirose que consiste em uma doença febril, ocasionada pelo vírus de RNA chikungunya (CHIKV), do gênero Alphavirus cuja transmissão ocorre, principalmente, através da picada de fêmeas dos mosquitos Aedes aegypti e Aedes albopictus infectados. Objetivo: O objetivo do estudo é analisar as estatísticas da doença no Brasil, no período correspondente às 16 primeiras semanas epidemiológicas de 2021 e 2022, a fim de entender o cenário epidemiológico em sua totalidade. Material e Métodos: Realizou-se um estudo descritivo a partir de dados extraídos de Boletins Epidemiológicos da Secretaria de Vigilância em Saúde do Ministério da Saúde. Foram utilizadas técnicas de estatística descritiva e inferência estatística para analisar as informações coletadas. Resultados: Notou-se um aumento significativo dos casos de chikungunya no Brasil comparando-se as 16 primeiras semanas epidemiológicas de 2021 e 2022, especificamente nas regiões Centro-oeste, Norte e Nordeste, ao mesmo tempo que aconteceu uma redução dos casos nas regiões Sul e Sudeste. Além disso, o número de óbitos por chikungunya no Brasil nesse período mais que dobrou. Conclusão: Os dados apontaram para um alarmante aumento do número de casos e de óbitos por chikungunya no período analisado, evidenciando a necessidade da intensificação de ações para a contenção do mosquito vetor. Constatou-se também um maior aumento do número de casos na região Nordeste, fato que pode estar relacionado ao fenômeno La Niña, responsável por alterações climáticas que podem ter favorecido a proliferação do vetor na região, somado a fatores sociais como a pandemia da COVID-19 que abalou o setor de saúde.
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Silva, Victor Luiz Luciano da, URSULA RAIANNY LACERDA DA SILVA, AMANDA MARIA SANTANA DA COSTA, ITALO MATHEUS DA SILVA PEQUENO, and FRANCISCO ISRAEL MAGALHÃES FEIJAO. "CHIKUNGUNYA NO BRASIL: UM ESTUDO OBSERVACIONAL TRANSVERSAL COMPARANDO AS 16 PRIMEIRAS SEMANAS EPIDEMIOLÓGICAS DE 2021 E 2022." In I Congresso Brasileiro de Estudos Epidemiológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/epidemion/7622.

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Introdução: A chikungunya é uma arbovirose que consiste em uma doença febril, ocasionada pelo vírus de RNA chikungunya (CHIKV), do gênero Alphavirus cuja transmissão ocorre, principalmente, através da picada de fêmeas dos mosquitos Aedes aegypti e Aedes albopictus infectados. Objetivo: O objetivo do estudo é analisar as estatísticas da doença no Brasil, no período correspondente às 16 primeiras semanas epidemiológicas de 2021 e 2022, a fim de entender o cenário epidemiológico em sua totalidade. Material e Métodos: Realizou-se um estudo descritivo a partir de dados extraídos de Boletins Epidemiológicos da Secretaria de Vigilância em Saúde do Ministério da Saúde. Foram utilizadas técnicas de estatística descritiva e inferência estatística para analisar as informações coletadas. Resultados: Notou-se um aumento significativo dos casos de chikungunya no Brasil comparando-se as 16 primeiras semanas epidemiológicas de 2021 e 2022, especificamente nas regiões Centro-oeste, Norte e Nordeste, ao mesmo tempo que aconteceu uma redução dos casos nas regiões Sul e Sudeste. Além disso, o número de óbitos por chikungunya no Brasil nesse período mais que dobrou. Conclusão: Os dados apontaram para um alarmante aumento do número de casos e de óbitos por chikungunya no período analisado, evidenciando a necessidade da intensificação de ações para a contenção do mosquito vetor. Constatou-se também um maior aumento do número de casos na região Nordeste, fato que pode estar relacionado ao fenômeno La Niña, responsável por alterações climáticas que podem ter favorecido a proliferação do vetor na região, somado a fatores sociais como a pandemia da COVID-19 que abalou o setor de saúde.
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Ryabov, Vladimir, Peter Pushko, Irina Tretyakova, Rikka Saito, Richard B. Alexander, and Elena N. Klyushnenkova. "Abstract 2880: Novel alphavirus-based vaccine targets dendritic cells and efficiently breaks immunological tolerance to “self” tumor-associated antigen (PSA) in an HLA-DR mouse model of prostate cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2880.

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Abraham, Rachy, Aravinth Jayabalan, Robert L. McPherson, Anthony K. L. Leung, and Diane E. Griffin. "UNDERSTANDING OF “X DOMAIN” FUNCTION IN ALPHAVIRUSES." In Viruses: Discovering Big in Small. TORUS PRESS, 2019. http://dx.doi.org/10.30826/viruses-2019-04.

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Crosby, EJ, WR Gwin, S. Chang, HT Maecker, V. Lubkov, JC Snyder, G. Broadwater, et al. "Abstract P2-09-16: CD8 T cells induced by novel alphaviral vector predict improved progression free survival in advanced HER2+ breast cancer patients." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p2-09-16.

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Reports on the topic "Alphavirus"

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Strauss, James. Molecular Studies of Alphavirus Immunogenicity. Fort Belvoir, VA: Defense Technical Information Center, December 1992. http://dx.doi.org/10.21236/ada264058.

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Loy, J. Dustin, Mark Mogler, Jill Gander, Kurt I. Kamrud, and D. L. Hank Harris. Development of an Alphavirus Replicon Classical Swine Fever Virus Vaccine Candidate. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-1256.

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Chen, Qi, Ryan Vander Veen, Darin M. Madson, and D. L. Hank Harris. Immunization for Influenza A Virus by Intranasal Administration of Alphavirus Replicon Particles. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-29.

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Mogler, Mark, Kurt I. Kamrud, Jill Gander, and D. L. Hank Harris. Expression and Immunogenicity of an Alphavirus Replicon African Swine Fever Virus Vaccine Candidate in Swine. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-861.

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Wang, X. F., and M. Schuldiner. Systems biology approaches to dissect virus-host interactions to develop crops with broad-spectrum virus resistance. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134163.bard.

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More than 60% of plant viruses are positive-strand RNA viruses that cause billion-dollar losses annually and pose a major threat to stable agricultural production, including cucumber mosaic virus (CMV) that infects numerous vegetables and ornamental trees. A highly conserved feature among these viruses is that they form viral replication complexes (VRCs) to multiply their genomes by hijacking host proteins and remodeling host intracellular membranes. As a conserved and indispensable process, VRC assembly also represents an excellent target for the development of antiviral strategies that can be used to control a wide-range of viruses. Using CMV and a model virus, brome mosaic virus (BMV), and relying on genomic tools and tailor-made large-scale resources specific for the project, our original objectives were to: 1) Identify host proteins that are required for viral replication complex assembly. 2) Dissect host requirements that determine viral host range. 3) Provide proof-of-concept evidence of a viral control strategy by blocking the viral replication complex-localized phospholipid synthesis. We expect to provide new ways and new concepts to control multiple viruses by targeting a conserved feature among positive-strand RNA viruses based on our results. Our work is going according to the expected timeline and we are progressing well on all aims. For Objective 1, among ~6,000 yeast genes, we have identified 96 hits that were possibly play critical roles in viral replication. These hits are involved in cellular pathways of 1) Phospholipid synthesis; 2) Membrane-shaping; 3) Sterol synthesis and transport; 4) Protein transport; 5) Protein modification, among many others. We are pursuing several genes involved in lipid metabolism and transport because cellular membranes are primarily composed of lipids and lipid compositional changes affect VRC formation and functions. For Objective 2, we have found that CPR5 proteins from monocotyledon plants promoted BMV replication while those from dicotyledon plants inhibited it, providing direct evidence that CPR5 protein determines the host range of BMV. We are currently examining the mechanisms by which dicot CPR5 genes inhibit BMV replication and expressing the dicot CPR5 genes in monocot plants to control BMV infection. For Objective 3, we have demonstrated that substitutions in a host gene involved in lipid synthesis, CHO2, prevented the VRC formation by directing BMV replication protein 1a (BMV 1a), which remodels the nuclear membrane to form VRCs, away from the nuclear membrane, and thus, no VRCs were formed. This has been reported in Journal of Biological Chemistry. Based on the results from Objective 3, we have extended our plan to demonstrate that an amphipathic alpha-helix in BMV 1a is necessary and sufficient to target BMV 1a to the nuclear membrane. We further found that the counterparts of the BMV 1a helix from a group of viruses in the alphavirus-like superfamily, such as CMV, hepatitis E virus, and Rubella virus, are sufficient to target VRCs to the designated membranes, revealing a conserved feature among the superfamily. A joint manuscript describing these exciting results and authored by the two labs will be submitted shortly. We have also successfully set up systems in tomato plants: 1) to efficiently knock down gene expression via virus-induced gene silencing so we could test effects of lacking a host gene(s) on CMV replication; 2) to overexpress any gene transiently from a mild virus (potato virus X) so we could test effects of the overexpressed gene(s) on CMV replication. In summary, we have made promising progress in all three Objectives. We have identified multiple new host proteins that are involved in VRC formation and may serve as good targets to develop antiviral strategies; have confirmed that CPR5 from dicot plants inhibited viral infection and are generating BMV-resistance rice and wheat crops by overexpressing dicot CPR5 genes; have demonstrated to block viral replication by preventing viral replication protein from targeting to the designated organelle membranes for the VRC formation and this concept can be further employed for virus control. We are grateful to BARD funding and are excited to carry on this project in collaboration.
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