Relevant bibliographies by topics / Host-virus relationships

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

Academic literature on the topic 'Host-virus relationships'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Host-virus relationships"

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Lal, Sunil K. "Influenza A Virus: Host–Virus Relationships." Viruses 12, no. 8 (August 9, 2020): 870. http://dx.doi.org/10.3390/v12080870.

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We are in the midst of a pandemic where the infective agent has been identified, but how it causes mild disease in some and fatally severe disease in other infected individuals remains a mystery [...]
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Mansour, A., and A. Al-Musa. "Cucumber Vein Yellowing Virus; Host Range and Virus Vector Relationships." Journal of Phytopathology 137, no. 1 (January 1993): 73–78. http://dx.doi.org/10.1111/j.1439-0434.1993.tb01327.x.

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López‐Lastra, Marcelo. "Host–virus relationships: a sum of many battles." FEBS Open Bio 12, no. 6 (June 2022): 1094–95. http://dx.doi.org/10.1002/2211-5463.13420.

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Dusi, A. N., and D. Peters. "Beet mosaic virus: its Vector and Host Relationships." Journal of Phytopathology 147, no. 5 (May 1999): 293–98. http://dx.doi.org/10.1111/j.1439-0434.1999.tb03833.x.

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Xu, Feng, Chen Zhao, Yuhua Li, Jiang Li, Youping Deng, and Tieliu Shi. "Exploring virus relationships based on virus-host protein-protein interaction network." BMC Systems Biology 5, Suppl 3 (2011): S11. http://dx.doi.org/10.1186/1752-0509-5-s3-s11.

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MANSOUR, A., and A. AL-MUSA. "Tomato yellow leaf curl virus: host range and virus-vector relationships." Plant Pathology 41, no. 2 (April 1992): 122–25. http://dx.doi.org/10.1111/j.1365-3059.1992.tb02328.x.

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Scharninghausen, Jerrold J., Michael Faulde, and Semra Cavaljuga. "Hantavirus host/virus interactions within Southeast Europe." Bosnian Journal of Basic Medical Sciences 4, no. 4 (November 20, 2004): 13–18. http://dx.doi.org/10.17305/bjbms.2004.3353.

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Viral studies have historically approached their phylogenetic analysis without consideration of the impact of the role the host plays in evolution. Our study examines host/viral interactions through analysis of the phylogenetic relationship between hantavirus genetic sequences and host cytochrome B sequences. Phylogenetic analysis of known Hantavirus genetic sequences were performed using PAUP 3.1.1 (vers. 4.0.0d64). Only sequences available through GENBANK were analyzed. Phylogenetic analysis of hantavirus sequences revealed distinct patterns based upon geographic area. These patterns coincided with the known ranges of reservoir hosts. Multiple hosts for individual viruses and multiple viruses in a single host species for hantaviruses have been described. This may be due to accidental exposure, host-switching, co-speciation, or broad co-accommodation. Since the host is the actual environment that the virus survives in, changes in the host over time could potentially directly influence changes in the virus. Multiple viruses and hosts collide in Southeastern Europe increasing the prospect of finding distinct viral/host relationships. Rodent Cytochrome B is very well conserved and can be used to tract host lineage. By tracking the relationship of infected hosts, we theorize that patterns in host DNA will emerge that will mirror patterns in viral sequences. This analysis of the host DNA could provide an understanding into the causes of variation in hantaviral sequences, pathogenicity, transmissibility, infectivity, viral range and expand our knowledge of viral/host interactions. Surveillance for viruses in the field should include analysis of the host DNA in combination with the viral analysis.
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Hunziker, Lukas, Mike Recher, Adrian Ciurea, Marianne M. A. Martinic, Bernhard Odermatt, Hans Hengartner, and Rolf M. Zinkernagel. "Antagonistic Variant Virus Prevents Wild-type Virus-induced Lethal Immunopathology." Journal of Experimental Medicine 196, no. 8 (October 21, 2002): 1039–46. http://dx.doi.org/10.1084/jem.20012045.

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Altered peptide ligands (APLs) and their antagonistic or partial agonistic character–influencing T cell activation have mainly been studied in vitro Some studies have shown APLs as a viral escape mechanism from cytotoxic CD8+ T cell responses in vivo. However, whether infection or superinfection with a virus displaying an antagonistic T cell epitope can alter virus–host relationships via inhibiting T cell–mediated immunopathology is unclear. Here, we evaluated a recently described CD4+ T cell escape lymphocytic choriomeningitis virus (LCMV) variant that in vitro displayed antagonistic characteristics for the major histocompatibility complex class II–restricted mutated epitope. Mice transgenic for the immunodominant LCMV-specific T helper epitope that usually succumb to wild-type LCMV-induced immunopathology, survived if they were simultaneously coinfected with antagonistic variant but not with control virus. The results illustrate that a coinfecting APL-expressing virus can shift an immunopathological virus–host relationships in favor of host survival. This may play a role in poorly cytopathic long-lasting virus carrier states in humans.
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Brown, J. K. "Host Range and Vector Relationships of Cotton Leaf Crumple Virus." Plant Disease 71, no. 6 (1987): 522. http://dx.doi.org/10.1094/pd-71-0522.

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McLeish, Michael, Soledad Sacristán, Aurora Fraile, and Fernando García-Arenal. "Scale dependencies and generalism in host use shape virus prevalence." Proceedings of the Royal Society B: Biological Sciences 284, no. 1869 (December 20, 2017): 20172066. http://dx.doi.org/10.1098/rspb.2017.2066.

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Processes that generate the distribution of pathogens and their interactions with hosts are not insensitive to changes in spatial scale. Spatial scales and species traits are often selected intentionally, based on practical considerations, ignoring biases that the scale and type of observation may introduce. Specifically, these biases might change the interpretation of disease–diversity relationships that are reported as either ‘dilution’ or ‘amplification’ effects. Here, we combine field data of a host–pathogen community with empirical models to test the effects that (i) spatial scale and (ii) host range have on the relationship between plant–virus infection prevalence and diversity. We show that prevalence–diversity relationships are scale-dependent and can produce opposite effects associated with different habitats at sub-ecosystem scales. The total number of host species of each virus reflected generalism at the ecosystem scale. However, plasticity in host range resembled habitat-specific specialization and also changed model predictions. We show that habitat heterogeneity, ignored at larger (ecosystem) spatial scales, influences pathogen distributions. Hence, understanding disease distributions and the evolution of pathogens requires reconciling specific hypotheses of the study with an appropriate spatial scale, or scales, and consideration of traits, such as host range, that might strongly contribute to biotic interactions.
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Dissertations / Theses on the topic "Host-virus relationships"

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Wang, Pui, and 王培. "Study of the host factors interacting with H5N1 influenza virus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085210.

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Wang, Pui. "Study of the host factors interacting with H5N1 influenza virus." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085210.

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Baldridge, Gerald Don. "Molecular biology of Bunyavirus-host interactions." Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184934.

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Ribonuclease T1 oligonucleotide fingerprint (ONF) analysis was used to study genomic stability of La Crosse virus (Bunyaviridae) during vertical and horizontal transmission in the laboratory. No RNA genomic changes were detected in vertebrate cell culture-propagated virus isolated (following oral ingestion and replication) from the natural mosquito host, Aedes triseriatus. Genomic changes were not detected during transovarial passage of virus through two generations of mosquitoes or in virus isolated from suckling mice infected by transovarially infected mosquitoes. These results demonstrate that the La Crosse virus genome can remain relatively stable during transovarial transmission (TOT) in the insect host and during transfer between insect and vertebrate hosts. ONF analysis was used to demonstrate TOT of reassortant California serogroup bunyaviruses in Aedes treiseriatus. Mosquitoes were simultaneously inoculated with temperature sensitive mutants of La Crosse and Snowshoe hare viruses able to replicate at 33°C but not at 40°C. Putative reassortants, selected by replication at 40°C, were isolated from progeny mosquitoes and mice infected by these mosquitoes. ONF analysis confirmed that they were reassortants. Approximately 75% of the M segment and 25% of the L segment nucleotide sequences of Inkoo virus (Bunyaviridae) were determined by Sanger dideoxynucleotide sequencing of cDNA clones. Comparison of the M segment nucleotide and deduced amino acid sequences with those of four other bunyaviruses, representing two serogroups, revealed greater conservation of nucleotide than of amino acid sequence between serogroups. Areas of the sequences representing nonstructural protein(s) were less conserved than glycoprotein regions. The L segment nucleotide sequence begins with the known 3' end of the viral L segment and contains an open reading frame encoding the amino terminal 505 amino acids of the viral L protein. The amino acid sequence contains the glycine-aspartate-aspartate motif which is conserved in many RNA-dependent RNA polymerases. Comparison of the L segment sequences with those in the GEN Bank Data Base revealed no significant similarities with any other sequence.
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Burgess, Shane Campbell. "Investigations into host cell-virus relationships and tumour immunity in Marek's disease." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324271.

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Crill, Wayne Douglass. "Experimental evolution and molecular basis of host-specific viral adaptation /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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Hadi, Buyung Asmara Ratna Flanders Kathy L. Bowen Kira L. "Aphid vectors and grass hosts of barley yellow dwarf virus and cereal yellow dwarf virus in Alabama and western Florida." Auburn, Ala., 2009. http://hdl.handle.net/10415/2018.

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Li, Tin-wai Olive. "Influenza polymerase subunit compatibility between human H1 and H5 viruses." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41896890.

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Brown, J. K., and M. R. Nelson. "Transmission, Host Range and Virus-Vector Relationships of Chino del Tomate Virus (CdTV), a New Whitefly-transmitted Geminivirus of Tomato." College of Agriculture, University of Arizona (Tucson, AZ), 1988. http://hdl.handle.net/10150/214160.

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The transmission properties, host range, and virus- vector relationships of chino del tomate virus (CdTV), a new whitefly-transmitted geminivirus of tomato, are described. The virus is transmitted by B. tabaci, the sweet potato whitefly, but not by seed or sap. The virus infects members of the Asclepiadaceae, Leguminosae, Malvaceae, and Solanaceae. In virus-vector studies, minimum AAF and IAF times were 1 hour and 2 hours, respectively. The virus was retained by its whitefly vector for 4.5 and 7.3 days following 24- and 72-hr AAF respectively. Relative efficiencies of transmission for 1, 5, 10 and 20 B. tabaci were 15, 49, 84 and 100 percent, respectively. The chino del tomate (CdT), or leaf curl disease of tomato (Lycopersicon esculentum Mill.), was first reported in cultivated tomato fields in Sinaloa, Mexico in 1970-71 (4). Presently, it occurs in tomato production areas of the west coast of Sinaloa and may affect 100 percent of the plants in a field (1). The disease is characterized by curled and rolled leaves, thickened veins, a bright-to-subdued-yellow mosaic which varies with time of the year, stunting, and a reduced fruit set (1,3). Recently, a whitefly -transmitted geminivirus, CdT virus (CdTV), was implicated as the causal agent of the disease (1,3), but information concerning the biological nature of the virus is lacking. Here, we present the results of studies involving virus transmission, experimental host range, and virus -vector relationships.
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Maekawa, Akiko Medical Sciences Faculty of Medicine UNSW. "Characterisation of the immune co-receptor function of CD4." Publisher:University of New South Wales. Medical Sciences, 2007. http://handle.unsw.edu.au/1959.4/40498.

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CD4 is a co-receptor for binding of T cells to antigen-presenting cells (APC) and the primary receptor for human immunodeficiency virus-I. The disulfide bond in the second extracellular domain (D2) of CD4 is reduced on the cell surface, which leads to formation of disulfide-linked homodimers. A large conformational change must take place in D2 to allow for formation of the disulfide-linked dimer. Domain swapping of D2 is the most likely candidate for the conformational change leading to formation of two disulfide-bonds between Cysl30 in one monomer and Cysl59 in the other one (Cys133 and Cysl62 in the mouse CD4). Thus, we hypothesized that the domain swapping of D2 in CD4 regulates its co-receptor function of antigenspecific T cell activation. We found that mild reduction of the extracellular part of human CD4 resulted in formation of disulfide-linked dimers. We then tested the functional significance of dimer formation for co-receptor function using the engineered Jurkat T cell system by expressing wild-type or disulfide-bond mutant mouse CD4. Eliminating the D2 disulfide bond markedly impaired CD4's coreceptor function as assessed by antigen-specific IL-2 production. Exogenous wild type thioredoxin, but not redox-inactive thioredoxin, could inhibit the CD4-mediated IL-2 production, suggesting that the redox state of D2 disulfide bond is controlled by this oxidoreductase. Furthermore, structural modeling of the complex ofthe T cell receptor and domain-swapped CD4 dimer bound to class II major histocompatibility complex and antigen supports the domain-swapped dimer as the immune co-receptor. The known involvement of D4 residues Lys318 and Gln344 in dimer formation isalso accommodated by this model. These findings imply that disulfide-linked dimeric CD4 is the preferred functional co-receptor for binding to APC. Strategies to promote dimerisation of CD4 should, therefore, enhance the immune response, while inhibiting dimer formation is predicted to be immunosuppressive.
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Knez, Jozo Capone John P. "Characterization of the role of herpes simplex virus protein VP16 in viral gene expression through interactions with the virion host shutoff protein (VHS) and HCF-1/." *McMaster only, 2003.

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Books on the topic "Host-virus relationships"

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Bailer, Susanne M., and Diana Lieber. Virus-host interactions: Methods and protocols. New York: Humana Press, 2013.

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Sether, D. M. Tomato spotted wilt virus host list and bibliography. Corvallis, Or: Agricultural Experiment Station, Oregon State University, 1992.

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Grigorʹevich, Reĭfman Vladimir, and Biologo-pochvennyĭ institut (Akademii͡a︡ nauk SSSR), eds. Vzaimootnoshenii͡a︡ virusov s kletkami rastenii͡a︡-khozi͡a︡ina: Sbornik nauchnykh rabot. Vladivostok: DVNT͡S︡ AN SSSR, 1985.

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Fey, Jeanette. Untersuchungen zur persistierenden Sendai-Virus Infektion in Zellkultur: Nachweis von Mutationen im Nukleokapsid- und Fusionsprotein. Gauting bei München: A.S Intemann und C.C. Intemann, 1987.

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Danielová, Vlasta. Relationships of mosquitoes to Ťahyňa virus as determinant factors of its circulation in nature. Prague: Academia, Publishing House of the Czechoslovak Academy of Sciences, 1992.

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

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

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Sompayrac, Lauren. How pathogenic viruses think: Making sense of virology. 2nd ed. Burlington, Mass: Jones & Bartlett Learning, 2013.

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1933-, Doerfler Walter, and Böhm P, eds. Virus strategies: Molecular biology and pathogenesis. Weinheim: VCH, 1993.

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Eckard, Wimmer, ed. Cellular receptors for animal viruses. Plainview , N.Y: Cold Spring Harbor Laboratory Press, 1994.

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Book chapters on the topic "Host-virus relationships"

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Martelli, Giovanni P., and Marcello Russo. "Virus-Host Relationships." In The Plant Viruses, 163–205. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4937-2_6.

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Frezza, D., A. Fruscalzo, A. Pucci, F. Felici, G. Gualandi, D. Caporossi, P. Vernole, G. Ragona, B. Nicoletti, and E. Calef. "Changes in virus-host genome relationship in two sublines of the same Burkitt’s lymphoma." In Epstein-Barr Virus and Human Disease • 1988, 333–39. Totowa, NJ: Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4508-7_50.

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Gordon, Y. Jerold. "Pathogenesis and Latency of Herpes Simplex Virus Type 1 (HSV-1): An Ophthalmologist’s View of the Eye as a Model for the Study of the Virus-Host Relationship." In Immunobiology and Prophylaxis of Human Herpesvirus Infections, 205–9. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5853-4_21.

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Crawford, Dorothy H. "Lifelong Residents." In Viruses, 122–45. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780192845030.003.0006.

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This chapter assesses some of the more intransigent persistent virus infections. Persistent viruses tend to strike up stable relationships with their respective hosts as they skilfully evade immune response and exploit the host to ensure their own long-term survival. This is an incredibly successful lifestyle for a virus, and generally causes little harm to the host. However, there can still be problems. The most obvious of these is seen with immunosuppression of the host leading to virus reactivation and disease, but there are also more subtle, long-term effects. The chapter then considers herpesviruses, such as varicella zoster virus (VZV) and herpes simplex virus (HSV); human papilloma virus (HPV) and cytomegalovirus (CMV); retroviruses; human immunodeficiency virus-1 (HIV-1); and hepatitis viruses.
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Kuno, Goro. "The Boundaries of Arboviruses: Complexities Revealed in Their Host Ranges, Virus-Host Interactions and Evolutionary Relationships." In Arboviruses: Molecular Biology, Evolution and Control, 219–68. Caister Academic Press, 2016. http://dx.doi.org/10.21775/9781910190210.14.

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Virelizier, Jean-Louis. "The immune system: an update for virologists." In Immune Responses, Virus Infections and Disease, 1–14. Oxford University PressOxford, 1990. http://dx.doi.org/10.1093/oso/9780199630301.003.0001.

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Abstract Virologists are often puzzled by the immunological literature, even that which deals with immunity to virus infections. They are sometimes repelled by the odd vocabulary, the variable nomenclature and the many controversies in this field of research. They tend to believe that immunology is essentially a theoretical science, as opposed to the more exact and precise field of virology. Although immunology, especially in the past, may have deserved this bad image, things are changing and immunological approaches are becoming more molecular, drawing closer to virology. Infectious diseases may be considered as the encounter of two genomes, that of the virus and that part of the host’s which is responsible for responses in immunocompetent cells. Analysis of the functioning of genes, whether cellular or viral, implies very similar approaches, so that immunologists and virologists will soon be speaking the same language. This is timely indeed, because knowledge of immunology is needed more than ever by virologists interested in host-virus relationships in vitro and in vivo to provide a necessary basis for the understanding of the pathogenesis of any viral disease. The present communication does not intend to review all aspects of immunity to viruses, but rather to discuss, in the light of recent findings, present knowledge in the three main compartments of host defence mechanisms against viruses, namely natural immunity, antibody production and cell-mediated immunity.
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Stow, Nigel D. "Molecular interactions in herpes simplex virus DNA replication." In DNA Virus Replication, 66–104. Oxford University PressOxford, 2000. http://dx.doi.org/10.1093/oso/9780199637133.003.0003.

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Abstract The family Herpesviridae comprises a diverse and interesting group of viruses characterized by their distinctive virion morphology and the possession of large linear double-stranded DNA genomes which range in size from approximately 120-250 kb (for review see refs 1, 2). Many vertebrate species are natural hosts to herpesviruses including fish, amphibians, reptiles, birds, marsupials, and mammals, and eight viruses that infect man have been identified. The family has historically been sub-divided into the Alpha-, Beta-, and Gammaherpesvirinae subfamilies on the basis of bio-logical properties; a classification largely (but not completely) supported by our rapidly advancing understanding of the genetic relationships amongst these viruses based upon DNA sequencing studies. The prototype and most extensively studied herpesvirus is herpes simplex virus type 1 (HSV-1), a human pathogen belonging to the Alphaherpesvirinae which is most frequently responsible for cold-sore lesions around the lips and mouth. In common with most other herpesviruses, HSV-1 is able to enter a latent state in its natural host. The latent viral genomes reside in a quiescent form within neuronal cells of the sensory ganglia but a variety of stimuli can trigger sporadic reactivation of viral replication giving rise to the recurrent symptoms of disease.
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Sağnıç, Saliha. "Human Papillomavirus and Cervical Cancer." In Cervical Cancer - A Global Public Health Treatise [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98490.

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Cervical cancer is one of the leading female cancers especially in developing countries and a common cause of death among middle-aged women. The main role of Human Papillomavirus (HPV) in both cervical cancer and pre-invasive lesions of the cervix has been proven in studies. Reducing the incidence of the disease can be achieved by the regular cervical screening of women and vaccination of appropriate age groups. The disease can be better controlled by better elucidating the details of HPV carcinogenesis, the interaction between the host and the virus, and determinants of the systemic and cellular immune response to the viral infection. HPV causes oropharyngeal and anogenital diseases in both men and women and is usually sexually transmitted. Most infections are transient and could be cleared spontaneously by the host immune system. After the first encounter with HPV infection, it takes years to progress to cervical cancer, which gives clinicians a long period to follow these patients in terms of precancerous lesions and to investigate the pathogenesis of the disease. HPV plays a major role in the development of cervical cancer, but histological types have different relationships with HPV genotypes. HPV can remain latent for a long time and the most important thing determining the persistence is the type of HPV. HPV vaccination provides a direct benefit to both men and women by providing safe protection against cancers that may result from persistent HPV infection.
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Shahid, Imran, and Qaiser Jabeen. "HCV-Host Interactions: A Plethora of Genes and their Intricate Interplay Part 1: Virus Specific Factors." In Hepatitis C Virus-Host Interactions and Therapeutics: Current Insights and Future Perspectives, 1–25. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123432123010004.

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Hepatitis C virus (HCV) interaction with host cells is pivotal for natural disease course starting from asymptomatic acute infection to progress into persistent chronic infection and subsequent extrahepatic manifestations, including fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The HCV infection biology in infected host cells via virus attachment, virus genome replication, mRNA translation, new virion formation, and egress from infected cells involves highly coordinated participation of the virus- and host-specific proteins, a plethora of genes, and cell signaling cascade. The progression of persistent chronic hepatitis C (CHC) infection to hepatic fibrosis, cirrhosis, and HCC involves viral invasion strategies against host immune system defense mechanisms as well as impeding healthy metabolic and signaling networks of the liver cells. Thereby, HCV-induced liver injury via chronic inflammatory processes that fail to resolve is responsible for decompensated cirrhosis and on occasion, hepatocarcinogenesis in infected individuals. With the latest advancement and rapid expansion of our knowledge in hepatology, the human liver is deciphered as an immunologically distinct organ with its specialized physiological niche. The relationship between human hepatocytes and different components of the immune system is quite complex and dynamic. The immunopathogenesis of various viral infections demonstrates that the immune system plays an essential role to determine the progression of many hepatic diseases through immune cell communication and cell signaling networks. In this book chapter, we overview HCV host interactions and their intricate interplay with complex crosstalk to propagate less fetal acute HCV infection to CHC and subsequent hepatocarcinogenesis (i.e. HCC) in infected individuals.
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Narayan Talukdar, Sattya, and Masfique Mehedi. "Respiratory Syncytial Virus." In RNA Viruses Infection [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104771.

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Respiratory Syncytial Virus (RSV)-driven bronchiolitis is one of the most common causes of pediatric hospitalization. Every year, we face 33.1 million episodes of RSV-driven lower respiratory tract infection without any available vaccine or cost-effective therapeutics since the discovery of RSV eighty years before. RSV is an enveloped RNA virus belonging to the pneumoviridae family of viruses. This chapter aims to elucidate the structure and functions of the RSV genome and proteins and the mechanism of RSV infection in host cells from entry to budding, which will provide current insight into the RSV-host relationship. In addition, this book chapter summarizes the recent research outcomes regarding the structure of RSV and the functions of all viral proteins along with the RSV life cycle and cell-to-cell spread.
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Reports on the topic "Host-virus relationships"

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Ullman, Diane, James Moyer, Benjamin Raccah, Abed Gera, Meir Klein, and Jacob Cohen. Tospoviruses Infecting Bulb Crops: Evolution, Diversity, Vector Specificity and Control. United States Department of Agriculture, September 2002. http://dx.doi.org/10.32747/2002.7695847.bard.

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Objectives. The overall goal of the proposed research was to develop a mechanistic understanding of tospovirus evolution, diversity and vector specificity that could be applied to development of novel methods for limiting virus establishment and spread. Our specific objectives were: 1) To characterize newly intercepted tospoviruses in onion, Hippeastrum and other bulb crops and compare them with the known tomato spotted wilt virus (TSWV) and its isolates; 2) To characterize intra- and interspecific variation in the virus transmission by thrips of the new and distinct tospoviruses. and, 3) To determine the basis of vector specificity using biological, cellular and molecular approaches. Background. New tospoviruses infecting bulb crops were detected in Israel and the US in the mid-90s. Their plant host ranges and relationships with thrips vectors showed they differed from the type member of the Tospovirus genus, tomato spotted wilt virus (TSWV). Outbreaks of these new viruses caused serious crop losses in both countries, and in agricultural and ornamental crops elsewhere. In the realm of plant infecting viruses, the tospoviruses (genus: Tospovirus , family: Bunyaviridae ) are among the most aggressive emerging viruses. Tospoviruses are transmitted by several species of thrips in a persistent, propagative fashion and the relationships between the viruses and their thrips vectors are often specific. With the emergence of new tospoviruses, new thrips vector/tospovirus relationships have also arisen and vector specificities have changed. There is known specificity between thrips vector species and particular tospoviruses, although the cellular and molecular bases for this specificity have been elusive. Major conclusions, solutions and achievements. We demonstrated that a new tospovirus, iris yellow spot virus (IYSV) caused "straw bleaching" in onion (Allium cepa) and lisianthus necrosis in lisianthus (Eustoma russellianum). Characterization of virus isolates revealed genetic diversity among US, Brazilian, Dutch and Israeli isolates. IYSV was not seed transmitted, and in Israel, was not located in bulbs of infected plants. In the US, infected plants were generated from infected bulbs. The relationship between IYSV and Thrips tabaci was shown to be specific. Frankliniella occidentalis, the primary vector of many other tospoviruses, did not transmit IYSV isolates in Israel or the US. Furthermore, 1': tabaci populations varied in their transmission ability. Transmission was correlated to IYSV presence in thrips salivary glands. In Israel, surveys in onion fields revealed that the onion thrips, Thrips tabaci Lindeman was the predominant species and that its incidence was strongly related to that of IYSV infection. In contrast, in the U.S., T. tabaci and F. occidentalis were present in high numbers during the times sampled. In Israel, insecticides reduced onion thrips population and caused a significant yield increase. In the US, a genetic marker system that differentiates non-thrips transmissible isolates from thrips transmissible isolate demonstrated the importance of the M RNA to thrips transmission of tospoviruses. In addition, a symbiotic Erwinia was discovered in thrips and was shown to cause significant artifacts in certain types of virus binding experiments. Implications, scientific and agricultural. Rapid emergence of distinct tospoviruses and new vector relationships is profoundly important to global agriculture. We advanced the understanding of IYSV in bulb crops and its relationships with thrips vector species. The knowledge gained provided growers with new strategies for control and new tools for studying the importance of particular viral proteins in thrips specificity and transmission efficiency.
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Valverde, Rodrigo A., Aviv Dombrovsky, and Noa Sela. Interactions between Bell pepper endornavirus and acute viruses in bell pepper and effect to the host. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598166.bard.

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Based on the type of relationship with the host, plant viruses can be grouped as acute or persistent. Acute viruses are well studied and cause disease. In contrast, persistent viruses do not appear to affect the phenotype of the host. The genus Endornavirus contains persistent viruses that infect plants without causing visible symptoms. Infections by endornaviruses have been reported in many economically important crops, such as avocado, barley, common bean, melon, pepper, and rice. However, little is known about the effect they have on their plant hosts. The long term objective of the proposed project is to elucidate the nature of the symbiotic interaction between Bell pepper endornavirus (BPEV) and its host. The specific objectives include: a) to evaluate the phenotype and fruit yield of endornavirus-free and endornavirus-infected bell pepper near-isogenic lines under greenhouse conditions; b) to conduct gene expression studies using endornavirus-free and endornavirus-infected bell pepper near-isogenic lines; and c) to study the interactions between acute viruses, Cucumber mosaic virus Potato virus Y, Pepper yellow leaf curl virus, and Tobacco etch virus and Bell pepper endornavirus. It is likely that BPEV in bell pepper is in a mutualistic relationship with the plant and provide protection to unknown biotic or abiotic agents. Nevertheless, it is also possible that the endornavirus could interact synergistically with acute viruses and indirectly or directly cause harmful effects. In any case, the information that will be obtained with this investigation is relevant to BARD’s mission since it is related to the protection of plants against biotic stresses.
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