Relevant bibliographies by topics / Viral and host determinants

Contents

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

Academic literature on the topic 'Viral and host determinants'

Author: Grafiati
Published: 4 June 2025
Last updated: 23 June 2025

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Journal articles on the topic "Viral and host determinants"

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Ren, Wenlin, Yunkai Zhu, Yuyan Wang, et al. "Comparative analysis reveals the species-specific genetic determinants of ACE2 required for SARS-CoV-2 entry." PLOS Pathogens 17, no. 3 (2021): e1009392. http://dx.doi.org/10.1371/journal.ppat.1009392.

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Coronavirus interaction with its viral receptor is a primary genetic determinant of host range and tissue tropism. SARS-CoV-2 utilizes ACE2 as the receptor to enter host cell in a species-specific manner. We and others have previously shown that ACE2 orthologs from New World monkey, koala and mouse cannot interact with SARS-CoV-2 to mediate viral entry, and this defect can be restored by humanization of the restrictive residues in New World monkey ACE2. To better understand the genetic determinants behind the ability of ACE2 orthologs to support viral entry, we compared koala and mouse ACE2 sequences with that of human and identified the key residues in koala and mouse ACE2 that restrict viral receptor activity. Humanization of these critical residues rendered both koala and mouse ACE2 capable of binding the spike protein and facilitating viral entry. Our study shed more lights into the genetic determinants of ACE2 as the functional receptor of SARS-CoV-2, which facilitates our understanding of viral entry.
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Peacock, Thomas P., Carol M. Sheppard, Ecco Staller, and Wendy S. Barclay. "Host Determinants of Influenza RNA Synthesis." Annual Review of Virology 6, no. 1 (2019): 215–33. http://dx.doi.org/10.1146/annurev-virology-092917-043339.

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Influenza viruses are a leading cause of seasonal and pandemic respiratory illness. Influenza is a negative-sense single-stranded RNA virus that encodes its own RNA-dependent RNA polymerase (RdRp) for nucleic acid synthesis. The RdRp catalyzes mRNA synthesis, as well as replication of the virus genome (viral RNA) through a complementary RNA intermediate. Virus propagation requires the generation of these RNA species in a controlled manner while competing heavily with the host cell for resources. Influenza virus appropriates host factors to enhance and regulate RdRp activity at every step of RNA synthesis. This review describes such host factors and summarizes our current understanding of the roles they play in viral synthesis of RNA.
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Hamid, Faysal Bin, Jinsun Kim, and Cha-Gyun Shin. "Cellular and viral determinants of retroviral nuclear entry." Canadian Journal of Microbiology 62, no. 1 (2016): 1–15. http://dx.doi.org/10.1139/cjm-2015-0350.

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Retroviruses must integrate their cDNA into the host genome to generate proviruses. Viral DNA–protein complexes interact with cellular proteins and produce pre-integration complexes, which carry the viral genome and cross the nuclear pore channel to enter the nucleus and integrate viral DNA into host chromosomal DNA. If the reverse transcripts fail to integrate, linear or circular DNA species such as 1- and 2-long terminal repeats are generated. Such complexes encounter numerous cellular proteins in the cytoplasm, which restrict viral infection and protect the nucleus. To overcome host cell defenses, the pathogens have evolved several evasion strategies. Viral proteins often contain nuclear localization signals, allowing entry into the nucleus. Among more than 1000 proteins identified as required for HIV infection by RNA interference screening, karyopherins, cleavage and polyadenylation specific factor 6, and nucleoporins have been predominantly studied. This review discusses current opinions about the synergistic relationship between the viral and cellular factors involved in nuclear import, with focus on the unveiled mysteries of the host–pathogen interaction, and highlights novel approaches to pinpoint therapeutic targets.
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Cauldwell, Anna V., Jason S. Long, Olivier Moncorgé, and Wendy S. Barclay. "Viral determinants of influenza A virus host range." Journal of General Virology 95, no. 6 (2014): 1193–210. http://dx.doi.org/10.1099/vir.0.062836-0.

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Typical avian influenza A viruses are restricted from replicating efficiently and causing disease in humans. However, an avian virus can become adapted to humans by mutating or recombining with currently circulating human viruses. These viruses have the potential to cause pandemics in an immunologically naïve human population. It is critical that we understand the molecular basis of host-range restriction and how this can be overcome. Here, we review our current understanding of the mechanisms by which influenza viruses adapt to replicate efficiently in a new host. We predominantly focus on the influenza polymerase, which remains one of the least understood host-range barriers.
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Busnadiego, Idoia, Melissa Kane, Suzannah J. Rihn, et al. "Host and Viral Determinants of Mx2 Antiretroviral Activity." Journal of Virology 88, no. 14 (2014): 7738–52. http://dx.doi.org/10.1128/jvi.00214-14.

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ABSTRACTMyxovirus resistance 2 (Mx2/MxB) has recently been uncovered as an effector of the anti-HIV-1 activity of type I interferons (IFNs) that inhibits HIV-1 at an early stage postinfection, after reverse transcription but prior to proviral integration into host DNA. The mechanistic details of Mx2 antiviral activity are not yet understood, but a few substitutions in the HIV-1 capsid have been shown to confer resistance to Mx2. Through a combination ofin vitroevolution and unbiased mutagenesis, we further map the determinants of sensitivity to Mx2 and reveal that multiple capsid (CA) surfaces define sensitivity to Mx2. Intriguingly, we reveal an unanticipated sensitivity determinant within the C-terminal domain of capsid. We also report that Mx2s derived from multiple primate species share the capacity to potently inhibit HIV-1, whereas selected nonprimate orthologs have no such activity. Like TRIM5α, another CA targeting antiretroviral protein, primate Mx2s exhibit species-dependent variation in antiviral specificity against at least one extant virus and multiple HIV-1 capsid mutants. Using a combination of chimeric Mx2 proteins and evolution-guided approaches, we reveal that a single residue close to the N terminus that has evolved under positive selection can determine antiviral specificity. Thus, the variable N-terminal region can define the spectrum of viruses inhibited by Mx2.IMPORTANCEType I interferons (IFNs) inhibit the replication of most mammalian viruses. IFN stimulation upregulates hundreds of different IFN-stimulated genes (ISGs), but it is often unclear which ISGs are responsible for inhibition of a given virus. Recently, Mx2 was identified as an ISG that contributes to the inhibition of HIV-1 replication by type I IFN. Thus, Mx2 might inhibit HIV-1 replication in patients, and this inhibitory action might have therapeutic potential. The mechanistic details of how Mx2 inhibits HIV-1 are currently unclear, but the HIV-1 capsid protein is the likely viral target. Here, we determine the regions of capsid that specify sensitivity to Mx2. We demonstrate that Mx2 from multiple primates can inhibit HIV-1, whereas Mx2 from other mammals (dogs and sheep) cannot. We also show that primate variants of Mx2 differ in the spectrum of lentiviruses they inhibit and that a single residue in Mx2 can determine this antiviral specificity.
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Van de Perre, Philippe. "Viral and host determinants of HIV-1 pathogenesis." AIDS 20, no. 6 (2006): 933–34. http://dx.doi.org/10.1097/01.aids.0000218560.67155.1c.

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Pillay, Sirika, and Jan E. Carette. "Host determinants of adeno-associated viral vector entry." Current Opinion in Virology 24 (June 2017): 124–31. http://dx.doi.org/10.1016/j.coviro.2017.06.003.

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Ketkar, Harshada, Daniella Herman, and Penghua Wang. "Genetic Determinants of the Re-Emergence of Arboviral Diseases." Viruses 11, no. 2 (2019): 150. http://dx.doi.org/10.3390/v11020150.

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Mosquito-borne diseases constitute a large portion of infectious diseases, causing more than 700,000 deaths annually. Mosquito-transmitted viruses, such as yellow fever, dengue, West Nile, chikungunya, and Zika viruses, have re-emerged recently and remain a public health threat worldwide. Global climate change, rapid urbanization, burgeoning international travel, expansion of mosquito populations, vector competence, and host and viral genetics may all together contribute to the re-emergence of arboviruses. In this brief review, we summarize the host and viral genetic determinants that may enhance infectivity in the host, viral fitness in mosquitoes and viral transmission by mosquitoes.
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LaTourrette, Katherine, and Hernan Garcia-Ruiz. "Determinants of Virus Variation, Evolution, and Host Adaptation." Pathogens 11, no. 9 (2022): 1039. http://dx.doi.org/10.3390/pathogens11091039.

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Virus evolution is the change in the genetic structure of a viral population over time and results in the emergence of new viral variants, strains, and species with novel biological properties, including adaptation to new hosts. There are host, vector, environmental, and viral factors that contribute to virus evolution. To achieve or fine tune compatibility and successfully establish infection, viruses adapt to a particular host species or to a group of species. However, some viruses are better able to adapt to diverse hosts, vectors, and environments. Viruses generate genetic diversity through mutation, reassortment, and recombination. Plant viruses are exposed to genetic drift and selection pressures by host and vector factors, and random variants or those with a competitive advantage are fixed in the population and mediate the emergence of new viral strains or species with novel biological properties. This process creates a footprint in the virus genome evident as the preferential accumulation of substitutions, insertions, or deletions in areas of the genome that function as determinants of host adaptation. Here, with respect to plant viruses, we review the current understanding of the sources of variation, the effect of selection, and its role in virus evolution and host adaptation.
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Graham, Jessica B., Jessica Swarts, Michael Mooney, and Jennifer M. Lund. "Immunogenetic determinants of HSV-2 infection and disease." Journal of Immunology 208, no. 1_Supplement (2022): 182.25. http://dx.doi.org/10.4049/jimmunol.208.supp.182.25.

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Abstract Herpes simplex virus-2 (HSV-2) is one of the most prevalent sexually transmitted infections, and can result in life-long, chronic disease. Disease severity, frequency of reactivation, and shedding rates vary between individuals, though little is known about how host genes regulate tissue-specific immune responses. We have previously used the Collaborative Cross (CC) mouse model system, which incorporates the extent of genetic variation found in the human genome, to better model the diversity of outcomes found in human viral infections, so we next probed the CC to identify host genetic regions that regulate viral shedding and disease following HSV-2 infection, as well as tissue-specific immune responses. We performed a screen of mice from different CC strains to assess viral titers and disease following vaginal HSV-2 infection, and then used this data to perform quantitative trait loci (QTL) mapping to identify chromosomal regions linked to vaginal viral shedding rates and levels, as well as virus-associated clinical disease. In parallel experiments, we assessed lymphoid, nervous system, and mucosal immune cell frequencies at innate, adaptive, and memory response timepoints. We observed a distinctive suppressive signature on vaginal Tregs compared to lymph node Tregs, at various times following HSV-2 infection. Additionally, these suppressive responses varied in mice with either higher viral titers, or more tissue inflammation, highlighting the interplay between host immune response and viral infection kinetics. Understanding host factors that contribute to HSV shedding, clinical disease, and immune responses may provide critical insights for developing new preventive strategies or interventions to HSV-2 infection. Supported by grant R21 AI152559-01 from the NIH
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Dissertations / Theses on the topic "Viral and host determinants"

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Sundaravaradan, Vasudha. "Molecular Mechanism of HIV-1 Infection: Role of Viral and Host Determinants." Diss., Tucson, Arizona : University of Arizona, 2006. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1685%5F1%5Fm.pdf&type=application/pdf.

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Sumpter, Rhea Myers Jr. "Viral and host genetic determinants of hepatitis C virus persistence and interferon resistance." Access to abstract only; dissertation is embargoed until after 5/16/2007, 2004. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=170.

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McCarthy, Kevin Raymond. "Viral and Host Determinants of Primate Lentivirus Restriction by Old World Primate TRIM5alpha Proteins." Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13065027.

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The host restriction factor TRIM5α mediates a post-entry, pre-integration block to retroviral infection that depends upon recognition of the viral capsid by the TRIM5α PRYSPRY domain. The two predominant alleles of rhesus macaque TRIM5α (rhTRIM5αQ and rhTRIM5αTFP) restrict HIV 1, but cannot restrict the macaque-adapted virus SIVmac239. To investigate how TRIM5α recognizes retroviral capsids, we exploited the differential sensitivities of these two viruses to identify gain-of-sensitivity mutations in SIVmac239, and we solved the structure of the SIVmac239 capsid N-terminal domain. When mapped onto this structure, single amino acid substitutions affecting both alleles were in the β-hairpin. In contrast, mutations specifically affecting rhTRIM5αTFP surround a highly conserved patch of amino acids that is unique to capsids of primate lentiviruses. This "patch" sits at the junction between the binding sites of multiple cellular cofactors (cyclophilin A, Nup-358 cyclophilin A-like domain, Nup-153 and CPSF6). Differential restriction of these alleles is due to a Q/TFP polymorphism in the first variable loop (V1) within the PRYSPRY domain. Q reflects the ancestral state (present in the last common ancestor of Old World primates) and has remained unmodified in all but one lineage of African monkeys, the Cercopithecinae. While Q-alleles can be found among some Cercopithecinae primates, in others Q has been replaced by a G or overwritten by a two amino acid insertion (giving rise to TFP in macaques). In one lineage, the Q to G substitution was later followed by an adjacent 20 amino acid duplication. We found that these modifications in TRIM5α specifically impart the ability to restrict Cercopithecinae SIVs without altering β-hairpin recognition. At least twice Cercopithecinae TRIM5αs independently evolved to target the same conserved patch of amino acids in capsid. Based on these findings, we propose that the β-hairpin is a retrovirus associated molecular pattern widely exploited by TRIM5α proteins, while recognition of the cofactor binding region was driven by the emergence of the ancestors of modern Cercopithecinae SIVs. Distribution on the Cercopithecinae phylogenetic tree indicates that selection for these changes in TRIM5α V1 began 11-16 million years ago, suggesting that primate lentiviruses are at least as ancient.
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Wellensiek, Brian Philip. "Molecular Mechanisms of HIV-1 Infection: Viral and Host Determinants in Transmission and Pathogenesis." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/195132.

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HIV-1 vertical transmission is the predominant cause of AIDS in children. In addition, HIV-1 infected infants have a higher viral load and progress to AIDS more rapidly than infected adults. However, the molecular mechanisms of HIV-1 vertical transmission and pathogenesis are not known. Work performed in this laboratory has shown transmission of minor genotypes with R5 phenotypes, more heterogeneity associated with transmission and a higher replication and gene expression of HIV-1 in neonatal than adult cells. In this dissertation, I have made advancements by characterizing the HIV-1 gag nucleocapsid gene, that plays a pivotal role in HIV-1 lifecycle, from six mother-infant pairs and found that there was a low degree of viral heterogeneity and a high conservation of functional domains for biological activity and CTL response. With respect to differential mechanisms of HIV-1 infection in neonatal vs. adults cells, 468 HIV-1 integration sites were characterized in the T-lymphocytes and monocyte-derived-macrophages from 5 donors of infant and adult blood. Several functional classes of genes were identified by gene ontology to be over represented, including genes for cellular components, maintenance of intracellular environment, enzyme regulation, cellular metabolism, catalytic activity and cation transport. Numerous potential transcription factors binding sites at the site of integration were identified. Furthermore, the genes at integration site, transcription factors potentially binding upstream of HIV-1 promoter and factors that assist HIV-1 integration were found to be expressed at higher levels in cord than adult cells. These results may help explain a higher HIV-1 gene expression and replication in cord compared with adult cells. Finally, I have also made progress in the development of new and novel antivirals by showing that CD4-mimetic miniproteins significantly inhibited HIV-1 entry and replication in T-cell lines and primary blood mononuclear cells. In addition, several compounds from the crude extracts of endophytic fungi found in desert plants were able to inhibit HIV-1 replication in T-cell lines. Taken together, the results from this dissertation provide new insights into understanding the mechanisms of HIV-1 vertical transmission and HIV-1 gene expression and replication in infants, as well as provide new possibilities for anti-retroviral drug development.
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Bruland, Torunn. "Studies of early retrovirus-host interactions. Viral determinants for pathogenesis and the influence of sex on the susceptibility to Friend murine leukaemia virus infection." Doctoral thesis, Norwegian University of Science and Technology, Faculty of Medicine, 2003. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-534.

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<p>The studies in the present thesis sought to define virus and host factors that can influence on the susceptibility to murine retrovirus infection. In addition, we wanted to study possible correlations between events of early infection and subsequent disease progression. For an extensive discussion of the major findings, the reader is referred to papers I-IV. The following section will give a general discussion concerning 1) some methodological aspects; 2) the course of FIS-2 infection; 3) determinants responsible for erythroleukaemia; 4) determinants responsible for immunosuppression; and, 5) does sex matter?</p>
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Mahadevan, Geetha B. "Viral suppression of host defenses." Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0507104-110551.

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Muenzner, Julia. "Viral subversion of host cell membrane trafficking." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267890.

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Enveloped viruses acquire their membrane coat from the plasma membrane or intracellular organelles and rely on cellular machinery to facilitate envelopment and egress of virus progeny. This thesis examines egress-related interactions between host cell factors and proteins of two different enveloped viruses: hepatitis D virus (HDV) and herpes simplex virus 1 (HSV-1). HDV is a small RNA virus causing fulminant hepatitis or severely aggravating cirrhosis and hepatocellular carcinoma. HSV-1 is a large DNA virus infecting epithelial and neuronal cells. Infection with HSV-1 not only triggers the development of recurring sores on oral or genital mucosa, but can also cause severe disease in neonates and immunocompromised patients. The interaction between the large antigen of HDV (HDAg-L) and the N-terminal domain (NTD) of clathrin, a protein crucial for endocytosis and intracellular vesicular trafficking, was examined by structural, biochemical and biophysical techniques. Co-crystal structures of NTD bound to HDAg-L peptides derived from different HDV genotypes revealed that HDV interacts with multiple binding sites on NTD promiscuously, prompting re-evaluation of the binding between cellular peptides and NTD. Surprisingly, co-crystal structures and pull-down capture assays showed that cellular peptides containing clathrin-binding motifs can also bind multiple sites on the surface of NTD simultaneously. In addition, the structures of viral and cellular peptides bound to NTD enabled the molecular characterization of the fourth peptide binding site on NTD, the “Royle box”, and led to the identification of a novel binding mode at the “arrestin box” peptide binding site on NTD. The work in this thesis therefore not only identifies the molecular basis of HDV:clathrin interactions, but also furthers our understanding of basic clathrin biology. Even though many HSV-1 proteins have been implicated in the envelopment and egress of viral particles, only few interactions between HSV-1 and cellular proteins promoting these processes have been described. Therefore, the HSV-1 proteins gE, UL21 and UL56 were selected and characterized bioinformatically and/or biochemically. Cellular proteins interacting with UL56 were identified by yeast two-hybrid screening and quantitative mass spectrometry. Co-immunoprecipitation and pull-down experiments confirmed the Golgi-trafficking protein GOPC, components of the mammalian trafficking protein particle complex, and the ubiquitin ligase NEDD4 as novel binding partners of UL56, thereby suggesting exciting new avenues for the investigation of cellular mechanisms contributing to HSV-1 envelopment and egress.
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Carney, Jennifer. "Viral Determinants of Flavivirus Neurotropism in Humans." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526956.

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Seaberg, Bonnie Lee. "Host factors involved in viral movement through plants." Thesis, [College Station, Tex. : Texas A&M University, 2008. http://hdl.handle.net/1969.1/ETD-TAMU-3282.

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Edge, David. "Identification of host factors controlling plant viral movement." Thesis, University of East Anglia, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398793.

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Books on the topic "Viral and host determinants"

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Koszinowski, Ulrich H., and Hartmut Hengel, eds. Viral Proteins Counteracting Host Defenses. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-59421-2.

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Pöhlmann, Stefan, and Graham Simmons, eds. Viral Entry into Host Cells. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7651-1.

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H, Koszinowski U., and Hengel H, eds. Viral proteins counteracting host defenses. Springer, 2002.

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M, Ayoub Elia, Cassell Gail H, and American Society for Microbiology, eds. Microbial determinants of virulence and host response. American Society for Microbiology, 1990.

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Neal, Nathanson, and Ahmed Rafi, eds. Viral pathogenesis and immunity. 2nd ed. Academic Press/Elsevier, 2007.

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Louis, Notkins Abner, and Oldstone Michael B. A, eds. Concepts in viral pathogenesis III. Springer-Verlag, 1989.

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Garcia, Maria Laura, and Victor Romanowski. Viral genomes: Molecular structure, diversity, gene expression mechanisms and host-virus interactions. InTech, 2012.

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Decheng, Yang, ed. RNA viruses: Host gene responses to infections. World Scientific, 2009.

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W, Dörfler, and Böhm P, eds. Adenoviruses: model and vectors in virus host interactions: Virion-structure, viral replication and host-cell interactions. Springer, 2003.

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Diamond, Michael S. West Nile encephalitis virus infection: Viral pathogenesis and the host immune response. Springer, 2009.

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Book chapters on the topic "Viral and host determinants"

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Hogle, James M., Rashid Syed, Todd O. Yeates, David Jacobson, Tod Critchlow, and David J. Filman. "Structural Determinants of Serotype Specificity and Host Range in Poliovirus." In Concepts in Viral Pathogenesis III. Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8890-6_2.

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Fujimura, R. K., P. Shapshak, D. M. Segal, et al. "Viral and Host Determinants of Neurovirulence of HIV-1 Infection." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5347-2_27.

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Anand, Vandana, Udit Yadav, and Umesh Kumar. "Host–Viral Interactions during Oncogenic Infections." In Viral Oncology. CRC Press, 2025. https://doi.org/10.1201/9781003516651-3.

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Freebern, Wendy Jo. "Viral Host Resistance Studies." In Methods in Molecular Biology. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-401-2_8.

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Nagy, Peter D., and Judit Pogany. "Host Factors Promoting Viral RNA Replication." In Viral Genome Replication. Springer US, 2009. http://dx.doi.org/10.1007/b135974_14.

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Stenglein, Mark D., April J. Schumacher, Rebecca S. LaRue, and Reuben S. Harris. "Host Factors that Restrict Retrovirus Replication." In Viral Genome Replication. Springer US, 2009. http://dx.doi.org/10.1007/b135974_15.

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Co, Man Sung, Bernard N. Fields, and Mark I. Greene. "Viral Receptors Serving Host Functions." In Concepts in Viral Pathogenesis II. Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4958-0_15.

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Grossman, Marc E., Lindy P. Fox, Carrie Kovarik, and Misha Rosenbach. "Viral Related Malignancies." In Cutaneous Manifestations of Infection in the Immunocompromised Host. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1578-8_14.

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Klenk, H. D., M. Tashiro, W. Garten, and R. Rott. "Viral Glycoproteins as Determinants of Pathogenicity." In Molecular Basis of Viral and Microbial Pathogenesis. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73214-0_3.

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Wake, Akira, and Herbert R. Morgan. "Localization of Virulence Determinants." In Host-Parasite Relationships and the Yersinia Model. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71344-6_3.

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Conference papers on the topic "Viral and host determinants"

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Skums, Pavel, Olga Glebova, David S. Campo, et al. "Algorithms for prediction of viral transmission using analysis of intra-host viral populations." In 2015 IEEE 5th International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2015. http://dx.doi.org/10.1109/iccabs.2015.7344725.

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Schuh, Andreas, Michael Morimoto, Piotr Kaszuba, et al. "Host-directed vibroacoustic biosignature of viral respiratory infection." In 2023 IEEE EMBS International Conference on Biomedical and Health Informatics (BHI). IEEE, 2023. http://dx.doi.org/10.1109/bhi58575.2023.10313464.

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Wiedemann, Dietmar G., Wolfgang Palka, and Key Pousttchi. "Understanding the Determinants of Mobile Viral Effects-Towards a Grounded Theory of Mobile Viral Marketing." In 2008 7th International Conference on Mobile Business (ICMB). IEEE, 2008. http://dx.doi.org/10.1109/icmb.2008.42.

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Bačić, D., C. Gilstrap, and N. Jukić. "Physiological and Socio-Behavioral Determinants of Viral Video User Engagement." In 2023 46th MIPRO ICT and Electronics Convention (MIPRO). IEEE, 2023. http://dx.doi.org/10.23919/mipro57284.2023.10159860.

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Xu, Yanhua, and Dominik Wojtczak. "Predicting Influenza A Viral Host Using PSSM and Word Embeddings." In 2021 IEEE Conference on Computational Intelligence in Bioinformatics and Computational Biology (CIBCB). IEEE, 2021. http://dx.doi.org/10.1109/cibcb49929.2021.9562959.

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Duncan, Matthew W. "Determinants of host use in tachinid parasitoids of stink bugs." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.112132.

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Pijlman, Gorben. "Novel viral and host factors determining arbovirus vector competence in mosquitoes." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93818.

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Zhu, Yuqing, and Deying Li. "Host Profit Maximization for Competitive Viral Marketing in Billion-Scale Networks." In IEEE INFOCOM 2018 - IEEE Conference on Computer Communications. IEEE, 2018. http://dx.doi.org/10.1109/infocom.2018.8485904.

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Ali, Sarwan, Taslim Murad, and Murray Patterson. "PCD2Vec: A Poisson Correction Distance Based Approach for Viral Host Classification." In 2023 International Joint Conference on Neural Networks (IJCNN). IEEE, 2023. http://dx.doi.org/10.1109/ijcnn54540.2023.10191311.

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Alba, E., K. I. Aronson, L. Sanso, and K. Rajwani. "Understanding the Viral and Host Factors That Influence Viral Detection Rates with Nasopharyngeal Swab Compared to Bronchoalveolar Lavage." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5218.

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Reports on the topic "Viral and host determinants"

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Citovsky, Vitaly, and Yedidya Gafni. Viral and Host Cell Determinants of Nuclear Import and Export of the Tomato Yellow Leaf Curl Virus in Tomato Plants. United States Department of Agriculture, 2002. http://dx.doi.org/10.32747/2002.7585200.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. In Israel, where TYLCV epidemics have been recorded since the 1960' s, this viral disease is well known and has been of economic significance ever since. In recent years, TYLCV outbreaks also occurred in the "New World" - Cuba, The Dominican Republic, and in the USA, in Florida, Georgia and Louisiana. Thus, TYLCV substantially hinders tomato growth throughout the world. Surprisingly, however, little is known about the molecular mechanisms of TYLCV interaction with the host tomato cells. The present proposal, a continuation of the project supported by BARD from 1994, expanded our understanding of the molecular mechanisms by which TYLCV enters the host cell nucleus for replication and transcription and exits it for the subsequent cell-to-cell spread. Our project sought two objectives: I. To study the roles of the viral capsid protein (CP) and host cell factors in TYLCV nuclear import. II. To study the roles of CP and host cell factors in TYLCV nuclear export. Our research toward these goals have produced the following major achievements: . Developed a one-hybrid assay for protein nuclear export and import (#3 in the List of Publications). . Identified a functional nuclear export signal (NES) in the capsid protein (CP) of TYLCV (#3 in the List of Publications). . Discovered homotypic interactions between intact TYLCV CP molecules and analyzed these interactions using deletion mutagenesis of TYLCV CP (#5 in the List of Publications). . Showed developmental and tissue-specific expression of the host factor required for nuclear import of TYLCV CP, tomato karyopherin alpha 1, in transgenic tomato plants (#14 in the List of Publications). . By analogy to nuclear import of TYLCV ,identified an Arabidopsis VIPI protein that participates in nuclear import of Agrobacterium T -complexes via the karyopherin alpha pathway (#4,6, and 8 in the List of Publications). These research findings provided significant insights into (i) the molecular pathway of TYLCV entry into the host cell nucleus, and (ii) the mechanism by which TYLCV is exported from the nucleus for the cell-to-cell spread of infection. Furthermore, the obtained knowledge will help to develop specific strategies to attenuate TYLCV infection, for example, by blocking viral entry into and/or exit out of the host cell nucleus. Also, as much of our findings is relevant to all geminiviruses, new anti- TYLCV approaches developed based on the results of our research will be useful to combat other members of the Geminivirus family. Finally, in addition to the study of TYLCV nuclear import and export, our research contributed to our understanding of general mechanisms for nucleocytoplasmic shuttling of proteins and nucleic acids in plant cells.
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Chejanovsky, Nor, and Suzanne M. Thiem. Isolation of Baculoviruses with Expanded Spectrum of Action against Lepidopteran Pests. United States Department of Agriculture, 2002. http://dx.doi.org/10.32747/2002.7586457.bard.

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Our long-term goal is to learn to control (expand and restrict) the host range of baculoviruses. In this project our aim was to expand the host range of the prototype baculovirus Autographa cali/arnica nuclear polyhedrosis virus (AcMNPV) towards American and Israeli pests. To achieve this objective we studied AcMNPV infection in the non-permissive hosts L. dispar and s. littoralis (Ld652Y and SL2 cells, respectively) as a model system and the major barriers to viral replication. We isolated recombinant baculoviruses with expanded infectivity towards L. dispar and S. littoralis and tested their infectivity towards other Lepidopteran pests. The restricted host range displayed by baculoviruses constitutes an obstacle to their further implementation in the control of diverse Lepidopteran pests, increasing the development costs. Our work points out that cellular defenses are major role blocks to AcMNPV replication in non- and semi-permissive hosts. Therefore a major determinant ofbaculovirus host range is the ability of the virus to effectively counter cellular defenses of host cells. This is exemplified by our findings showing tliat expressing the viral gene Ldhrf-l overcomes global translation arrest in AcMNPV -infected Ld652Y cells. Our data suggests that Ld652Y cells have two anti-viral defense pathways, because they are subject to global translation arrest when infected with AcMNPV carrying a baculovirus apoptotic suppressor (e.g., wild type AcMNPV carryingp35, or recombinant AcMNPV carrying Opiap, Cpiap. or p49 genes) but apoptose when infected with AcMNPV-Iacking a functional apoptotic suppressor. We have yet to elucidate how hrf-l precludes the translation arrest mechanism(s) in AcMNPV-infected Ld652Y cells. Ribosomal profiles of AcMNPV infected Ld652Y cells suggested that translation initiation is a major control point, but we were unable to rule-out a contribution from a block in translation elongation. Phosphorylation of eIF-2a did not appear to playa role in AcMNPV -induced translation arrest. Mutagenesis studies ofhrf-l suggest that a highly acidic domain plays a role in precluding translation arrest. Our findings indicate that translation arrest may be linked to apoptosis either through common sensors of virus infection or as a consequence of late events in the virus life-cycle that occur only if apoptosis is suppressed. ~ AcMNPV replicates poorly in SL2 cells and induces apoptosis. Our studies in AcMNPV - infected SL2ceils led us to conclude that the steady-state levels of lEI (product of the iel gene, major AcMNPV -transactivator and multifunctional protein) relative to those of the immediate early viral protein lEO, playa critical role in regulating the viral infection. By increasing the IEl\IEO ratio we achieved AcMNPV replication in S. littoralis and we were able to isolate recombinant AcMNPV s that replicated efficiently in S. lifforalis cells and larvae. Our data that indicated that AcMNPV - infection may be regulated by an interaction between IE 1 and lED (of previously unknown function). Indeed, we showed that IE 1 associates with lED by using protein "pull down" and immunoprecipitation approaches High steady state levels of "functional" IE 1 resulted in increased expression of the apoptosis suppressor p35 facilitating AcMNPV -replication in SL2 cells. Finally, we determined that lED accelerates the viral infection in AcMNPV -permissive cells. Our results show that expressing viral genes that are able to overcome the insect-pest defense system enable to expand baculovirus host range. Scientifically, this project highlights the need to further study the anti-viral defenses of invertebrates not only to maximi~e the possibilities for manipulating baculovirus genomes, but to better understand the evolutionary underpinnings of the immune systems of vertebrates towards virus infection.
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Palukaitis, Peter, Amit Gal-On, Milton Zaitlin, and Victor Gaba. Virus Synergy in Transgenic Plants. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7573074.bard.

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Transgenic plants expressing viral genes offer novel means of engendering resistance to those viruses. However, some viruses interact synergistically with other viruses and it is now known that transgenic plants expressing particular genes of one virus may also mediate synergy with a second virus. Thus, our specific objectives were to (1) determine if transgenic plants resistant to one virus showed synergy with another virus; (2) determine what viral sequences were essential for synergy; and (3) determine whether one of more mechanisms were involved i synergy. This project would also enable an evaluation of the risks of synergism associated with the use of such transgenic plants. The conclusion deriving from this project are as follows: - There is more than one mechanism of synergy. - The CMV 2b gene is required for synergistic interactions. - Synergy between a potyvirus and CMV can break natural resistance limiting CMV movement. - Synergy operates at two levels - increase in virus accumulation and increase in pathology - independently of each other. - Various sequences of CMV can interact with the host to alter pathogenicity and affect virus accumulation. - The effect of synergy on CMV satellite RNA accumulatio varies in different systems. - The HC-Pro gene may only function in host plant species to induce synergy. - The HC-Pro is a host range determinant of potyviruses. - Transgenic plants expressing some viral sequences showed synergy with one or more viruses. Transgenic plants expressing CMV RNA 1, PVY NIb and the TMV 30K gene all showed synergy with at least one unrelated virus. - Transgenic plants expressing some viral sequences showed interference with the infection of unrelated viruses. Transgenic plants expressing the TMV 30K, 54K and 126K genes, the PVY NIb gene, or the CMV 3a gene all showed some level of interference with the accumulation (and in some cases the pathology) of unrelated viruses. From our observations, there are agricultural implications to the above conclusions. It is apparent that before they are released commercially, transgenic plants expressing viral sequences for resistance to one virus need to be evaluated fro two properties: - Synergism to unrelated viruses that infect the same plant. Most of these evaluations can be made in the greenhouse, and many can be predicted from the known literature of viruses known to interact with each other. In other cases, where transgenic plants are being generated from new plant species, the main corresponding viruses from the same known interacting genera (e.g., potexviruses and cucumoviruses, potyviruses and cucumoviruses, tobamoviruses and potexviruses, etc.) should be evaluated. - Inhibition or enhancement of other resistance genes. Although it is unlikely that plants to be released would be transformed with HC-Pro or 2b genes, there may be other viral genes that can affect the expression of plant genes encoding resistance to other pathogens. Therefore, transgenic plants expressing viral genes to engender pathogen-derived resistance should be evaluated against a spectrum of other pathogens, to determine whether those resistance activities are still present, have been lost, or have been enhanced!
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, 2010. http://dx.doi.org/10.32747/2010.7592113.bard.

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The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.
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Mawassi, Munir, and Valerian Dolja. Role of RNA Silencing Suppression in the Pathogenicity and Host Specificity of the Grapevine Virus A. United States Department of Agriculture, 2010. http://dx.doi.org/10.32747/2010.7592114.bard.

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RNA silencing is a defense mechanism that functions against virus infection and involves sequence-specific degradation of viral RNA. Diverse RNA and DNA viruses of plants encode RNA silencing suppressors (RSSs), which, in addition to their role in viral counterdefense, were implicated in the efficient accumulation of viral RNAs, virus transport, pathogenesis, and determination of the virus host range. Despite rapidly growing understanding of the mechanisms of RNA silencing suppression, systematic analysis of the roles played by diverse RSSs in virus biology and pathology is yet to be completed. Our research was aimed at conducting such analysis for two grapevine viruses, Grapevine virus A (GVA) and Grapevine leafroll-associated virus-2 (GLRaV- 2). Our major achievements on the previous cycle of BARD funding are as follows. 1. GVA and GLRaV-2 were engineered into efficient gene expression and silencing vectors for grapevine. The efficient techniques for grapevine infection resulting in systemic expression or silencing of the recombinant genes were developed. Therefore, GVA and GLRaV-2 were rendered into powerful tools of grapevine virology and functional genomics. 2. The GVA and GLRaV-2 RSSs, p10 and p24, respectively, were identified, and their roles in viral pathogenesis were determined. In particular, we found that p10 functions in suppression and pathogenesis are genetically separable. 3. We revealed that p10 is a self-interactive protein that is targeted to the nucleus. In contrast, p24 mechanism involves binding small interfering RNAs in the cytoplasm. We have also demonstrated that p10 is relatively weak, whereas p24 is extremely strong enhancer of the viral agroinfection. 4. We found that, in addition to the dedicated RSSs, GVA and GLRaV-2 counterdefenses involve ORF1 product and leader proteases, respectively. 5. We have teamed up with Dr. Koonin and Dr. Falnes groups to study the evolution and function of the AlkB domain presents in GVA and many other plant viruses. It was demonstrated that viral AlkBs are RNA-specific demethylases thus providing critical support for the biological relevance of the novel process of AlkB-mediated RNA repair.
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Citovsky, Vitaly, and Yedidya Gafni. Nuclear Import of the Tomato Yellow Curl Leaf Virus in Tomato Plants. United States Department of Agriculture, 1994. http://dx.doi.org/10.32747/1994.7568765.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. In Israel the disease is well known and has an economic significance. In recent years viral symptoms were found in countries of the "New World" and since 1997, in Florida. Surprisingly, little is known about the molecular mechanisms of TYLCV interaction with the host plant cells. This proposal was aimed at expanding our understanding of the molecular mechanisms by which TYLCV enters the host cell nucleus. The main objective was to elucidate the TYLCV protein(s) involved in transport of the viral genomic DNA into the host cell nucleus. This goal was best served by collaboration between our laboratories one of which (V.C.) was already investigating the nuclear import of the T-DNA ofAgrobacterium tumefaciens, and the other (Y.G.) was studying the effect of TYLCV capsid protein (CP) in transgenic plants, hypothesizing its involvement in the viral nuclear entry. Three years of our collaborative work have provided signifcant data that strongly support our original hypothesis of the involvement of TYLCtr CP in viral nuclear import. Furthermore, our results have laid a foundation to study fundamental, but as yet practically unresolved, questions about the role ofthe host cell factors in the nuclear import of geminiviruses within their host plant. As a result, this research may lead to development of new approaches for plant protection based on control of TYLCV import to the host plant cell nucleus.
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Citovsky, Vitaly, and Yedidya Gafni. Suppression of RNA Silencing by TYLCV During Viral Infection. United States Department of Agriculture, 2009. http://dx.doi.org/10.32747/2009.7592126.bard.

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The Israeli isolate of Tomato yellow leaf curl geminivirus (TYLCV-Is) is a major tomato pathogen, causing extensive (up to 100%) crop losses in Israel and in the south-eastern U.S. (e.g., Georgia, Florida). Surprisingly, however, little is known about the molecular mechanisms of TYLCV-Is interactions with tomato cells. In the current BARD project, we have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing, and showed that V2 interacts with the tomato (L. esculentum) member of the SGS3 (LeSGS3) protein family known to be involved in RNA silencing. This proposal will use our data as a foundation to study one of the most intriguing, yet poorly understood, aspects of TYLCV-Is interactions with its host plants – possible involvement of the host innate immune system, i.e., RNA silencing, in plant defense against TYLCV-Is and the molecular pathway(s) by which TYLCV-Is may counter this defense. Our project sought two objectives: I. Study of the roles of RNA silencing and its suppression by V2 in TYLCV-Is infection of tomato plants. II. Study of the mechanism by which V2 suppresses RNA silencing. Our research towards these goals has produced the following main achievements: • Identification and characterization of TYLCV V2 protein as a suppressor of RNA silencing. (#1 in the list of publications). • Characterization of the V2 protein as a cytoplasmic protein interacting with the plant protein SlSGS3 and localized mainly in specific, not yet identified, bodies. (#2 in the list of publications). • Development of new tools to study subcellular localization of interacting proteins (#3 in the list of publications). • Characterization of TYLCV V2 as a F-BOX protein and its possible role in target protein(s) degradation. • Characterization of TYLCV V2 interaction with a tomato cystein protease that acts as an anti-viral agent. These research findings provided significant insights into (I) the suppression of RNA silencing executed by the TYLCV V2 protein and (II) characterization some parts of the mechanism(s) involved in this suppression. The obtained knowledge will help to develop specific strategies to attenuate TYLCV infection, for example, by blocking the activity of the viral suppressor of gene silencing thus enabling the host cell silencing machinery combat the virus.
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Zhao, Bingyu, Saul Burdman, Ronald Walcott, Tal Pupko, and Gregory Welbaum. Identifying pathogenic determinants of Acidovorax citrulli toward the control of bacterial fruit blotch of cucurbits. United States Department of Agriculture, 2014. http://dx.doi.org/10.32747/2014.7598168.bard.

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The specific objectives of this BARD proposal were: Use a comparative genomics approach to identify T3Es in group I, II and III strains of A. citrulli. Determine the bacterial genes contributing to host preference. Develop mutant strains that can be used for biological control of BFB. Background to the topic: Bacterial fruit blotch (BFB) of cucurbits, caused by Acidovoraxcitrulli, is a devastating disease that affects watermelon (Citrulluslanatus) and melon (Cucumismelo) production worldwide, including both Israel and USA. Three major groups of A. citrullistrains have been classified based on their virulence on host plants, genetics and biochemical properties. The host selection could be one of the major factors that shape A. citrullivirulence. The differences in the repertoire of type III‐ secreted effectors (T3Es) among the three A. citrulligroups could play a major role in determining host preferential association. Currently, there are only 11 A. citrulliT3Es predicted by the annotation of the genome of the group II strain, AAC00‐1. We expect that new A. citrulliT3Es can be identified by a combination of bioinformatics and experimental approaches, which may help us to further define the relationship of T3Es and host preference of A. citrulli. Implications, both scientific and agricultural: Enriching the information on virulence and avirulence functions of T3Es will contribute to the understanding of basic aspects of A. citrulli‐cucurbit interactions. In the long term, it will contribute to the development of durable BFB resistance in commercial varieties. In the short term, identifying bacterial genes that contribute to virulence and host preference will allow the engineering of A. citrullimutants that can trigger SAR in a given host. If applied as seed treatments, these should significantly improve the effectiveness and efficacy of BFB management in melon and atermelon production.
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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. 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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Gafni, Yedidya, and Vitaly Citovsky. Molecular interactions of TYLCV capsid protein during assembly of viral particles. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7587233.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. The present proposal, a continuation of a BARD-funded project, expanded our understanding of the molecular mechanisms by which CP molecules, as well as its pre-coat partner V2, interact with each other (CP), with the viral genome, and with cellular proteins during assembly and movement of the infectious virions. Specifically, two major objectives were proposed: I. To study in detail the molecular interactions between CP molecules and between CP and ssDNA leading to assembly of infectious TYLCV virions. II. To study the roles of host cell factors in TYLCV assembly. Our research toward these goals has produced the following major achievements: • Characterization of the CP nuclear shuttling interactor, karyopherin alpha 1, its pattern of expression and the putative involvement of auxin in regulation of its expression. (#1 in our list of publication, Mizrachy, Dabush et al. 2004). • Identify a single amino acid in the capsid protein’s sequence that is critical for normal virus life-cycle. (#2 in our list of publications, Yaakov, Levy et al. in preparation). • Development of monoclonal antibodies with high specificity to the capsid protein of TYLCV. (#3 in our list of publications, Solmensky, Zrachya et al. in press). • Generation of Tomato plants resistant to TYLCV by expressing transgene coding for siRNA targeted at the TYLCV CP. (#4 in our list of publications, Zrachya, Kumar et al. in press). •These research findings provided significant insights into (i) the molecular interactions of TYLCV capsid protein with the host cell nuclear shuttling receptor, and (ii) the mechanism by which TYLCV V2 is involved in the silencing of PTGS and contributes to the virus pathogenicity effect. Furthermore, the obtained knowledge helped us to develop specific strategies to attenuate TYLCV infection, for example, by blocking viral entry into and/or exit out of the host cell nucleus via siRNA as we showed in our publication recently (# 4 in our list of publications). Finally, in addition to the study of TYLCV nuclear import and export, our research contributed to our understanding of general mechanisms for nucleocytoplasmic shuttling of proteins and nucleic acids in plant cells. Also integration for stable transformation of ssDNA mediated by our model pathogen Agrobacterium tumefaciens led to identification of plant specific proteins involved.
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