Journal articles: 'Host-virus interplay'

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Krupovic, M., and D. H. Bamford. "Revealing Virus-Host Interplay." Science 333, no. 6038 (June 30, 2011): 45–46. http://dx.doi.org/10.1126/science.1208557.

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Atanasova, Nina S., Dennis H. Bamford, and Hanna M. Oksanen. "Virus-host interplay in high salt environments." Environmental Microbiology Reports 8, no. 4 (April 28, 2016): 431–44. http://dx.doi.org/10.1111/1758-2229.12385.

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Wu, Chunyan, Yuchen Nan, and Yan-Jin Zhang. "New insights into hepatitis E virus virus–host interaction: interplay with host interferon induction." Future Virology 10, no. 4 (April 2015): 439–48. http://dx.doi.org/10.2217/fvl.15.17.

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Li, Changfei, Jun Hu, Junli Hao, Bao Zhao, Bo Wu, Lu Sun, Shanxin Peng, George F. Gao, and Songdong Meng. "Competitive virus and host RNAs: the interplay of a hidden virus and host interaction." Protein & Cell 5, no. 5 (April 12, 2014): 348–56. http://dx.doi.org/10.1007/s13238-014-0039-y.

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Gallo, Giovanna Lucrecia, Nora López, and María Eugenia Loureiro. "The Virus–Host Interplay in Junín Mammarenavirus Infection." Viruses 14, no. 6 (May 24, 2022): 1134. http://dx.doi.org/10.3390/v14061134.

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Junín virus (JUNV) belongs to the Arenaviridae family and is the causative agent of Argentine hemorrhagic fever (AHF), a severe human disease endemic to agricultural areas in Argentina. At this moment, there are no effective antiviral therapeutics to battle pathogenic arenaviruses. Cumulative reports from recent years have widely provided information on cellular factors playing key roles during JUNV infection. In this review, we summarize research on host molecular determinants that intervene in the different stages of the viral life cycle: viral entry, replication, assembly and budding. Alongside, we describe JUNV tight interplay with the innate immune system. We also review the development of different reverse genetics systems and their use as tools to study JUNV biology and its close teamwork with the host. Elucidating relevant interactions of the virus with the host cell machinery is highly necessary to better understand the mechanistic basis beyond virus multiplication, disease pathogenesis and viral subversion of the immune response. Altogether, this knowledge becomes essential for identifying potential targets for the rational design of novel antiviral treatments to combat JUNV as well as other pathogenic arenaviruses.

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Sorin, Masha, and Ganjam Kalpana. "Dynamics of Virus-Host Interplay in HIV-1 Replication." Current HIV Research 4, no. 2 (April 1, 2006): 117–30. http://dx.doi.org/10.2174/157016206776055048.

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Chavez, Jerald, and Rong Hai. "Effects of Cigarette Smoking on Influenza Virus/Host Interplay." Pathogens 10, no. 12 (December 17, 2021): 1636. http://dx.doi.org/10.3390/pathogens10121636.

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Cigarette smoking has been shown to increase the risk of respiratory infection, resulting in the exacerbation of infectious disease outcomes. Influenza viruses are a major respiratory viral pathogen, which are responsible for yearly epidemics that result in between 20,000 and 50,000 deaths in the US alone. However, there are limited general summaries on the impact of cigarette smoking on influenza pathogenic outcomes. Here, we will provide a systematic summarization of the current understanding of the interplay of smoking and influenza viral infection with a focus on examining how cigarette smoking affects innate and adaptive immune responses, inflammation levels, tissues that contribute to systemic chronic inflammation, and how this affects influenza A virus (IAV) disease outcomes. This summarization will: (1) help to clarify the conflict in the reports on viral pathogenicity; (2) fill knowledge gaps regarding critical anti-viral defenses such as antibody responses to IAV; and (3) provide an updated understanding of the underlying mechanism behind how cigarette smoking influences IAV pathogenicity.

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Reid, Colleen, Adriana Airo, and Tom Hobman. "The Virus-Host Interplay: Biogenesis of +RNA Replication Complexes." Viruses 7, no. 8 (August 6, 2015): 4385–413. http://dx.doi.org/10.3390/v7082825.

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Marsh, Glenn A., and Hans J. Netter. "Henipavirus Infection: Natural History and the Virus-Host Interplay." Current Treatment Options in Infectious Diseases 10, no. 2 (April 30, 2018): 197–216. http://dx.doi.org/10.1007/s40506-018-0155-y.

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Hwang, Hye Suk, Mincheol Chang, and Yoong Ahm Kim. "Influenza–Host Interplay and Strategies for Universal Vaccine Development." Vaccines 8, no. 3 (September 20, 2020): 548. http://dx.doi.org/10.3390/vaccines8030548.

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Influenza is an annual epidemic and an occasional pandemic caused by pathogens that are responsible for infectious respiratory disease. Humans are highly susceptible to the infection mediated by influenza A viruses (IAV). The entry of the virus is mediated by the influenza virus hemagglutinin (HA) glycoprotein that binds to the cellular sialic acid receptors and facilitates the fusion of the viral membrane with the endosomal membrane. During IAV infection, virus-derived pathogen-associated molecular patterns (PAMPs) are recognized by host intracellular specific sensors including toll-like receptors (TLRs), C-type lectin receptors, retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) either on the cell surface or intracellularly in endosomes. Herein, we comprehensively review the current knowledge available on the entry of the influenza virus into host cells and the molecular details of the influenza virus–host interface. We also highlight certain strategies for the development of universal influenza vaccines.

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Brandt, Ludivine, Sara Cristinelli, and Angela Ciuffi. "Single-Cell Analysis Reveals Heterogeneity of Virus Infection, Pathogenicity, and Host Responses: HIV as a Pioneering Example." Annual Review of Virology 7, no. 1 (September 29, 2020): 333–50. http://dx.doi.org/10.1146/annurev-virology-021820-102458.

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While analyses of cell populations provide averaged information about viral infections, single-cell analyses offer individual consideration, thereby revealing a broad spectrum of diversity as well as identifying extreme phenotypes that can be exploited to further understand the complex virus-host interplay. Single-cell technologies applied in the context of human immunodeficiency virus (HIV) infection proved to be valuable tools to help uncover specific biomarkers as well as novel candidate players in virus-host interactions. This review aims at providing an updated overview of single-cell analyses in the field of HIV and acquired knowledge on HIV infection, latency, and host response. Although HIV is a pioneering example, similar single-cell approaches have proven to be valuable for elucidating the behavior and virus-host interplay in a range of other viruses.

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Damas, Nkerorema Djodji, Nicolas Fossat, and Troels K. H. Scheel. "Functional Interplay between RNA Viruses and Non-Coding RNA in Mammals." Non-Coding RNA 5, no. 1 (January 14, 2019): 7. http://dx.doi.org/10.3390/ncrna5010007.

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Exploring virus–host interactions is key to understand mechanisms regulating the viral replicative cycle and any pathological outcomes associated with infection. Whereas interactions at the protein level are well explored, RNA interactions are less so. Novel sequencing methodologies have helped uncover the importance of RNA–protein and RNA–RNA interactions during infection. In addition to messenger RNAs (mRNAs), mammalian cells express a great number of regulatory non-coding RNAs, some of which are crucial for regulation of the immune system whereas others are utilized by viruses. It is thus becoming increasingly clear that RNA interactions play important roles for both sides in the arms race between virus and host. With the emerging field of RNA therapeutics, such interactions are promising antiviral targets. In this review, we discuss direct and indirect RNA interactions occurring between RNA viruses or retroviruses and host non-coding transcripts upon infection. In addition, we review RNA virus derived non-coding RNAs affecting immunological and metabolic pathways of the host cell typically to provide an advantage to the virus. The relatively few known examples of virus–host RNA interactions suggest that many more await discovery.

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Marques, Mariana, Marisa Pereira, Maria João Amorim, Ana Raquel Soares, and Daniela Ribeiro. "Influenza A Virus Disturbs the Host Cell Protein Homeostasis by Inducing the Accumulation of Insoluble Proteins." Proceedings 50, no. 1 (June 16, 2020): 69. http://dx.doi.org/10.3390/proceedings2020050069.

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Influenza A virus (IAV) is the causative agent for most of the annual respiratory epidemics in humans and the major influenza pandemics in the last century, and is associated with high morbidity and mortality, especially in the elderly. In order to efficiently replicate, this virus hijacks the host cellular machinery and requires precise interactions with host components. However, cells have evolved specific defense mechanisms to counteract the effects induced by the virus. In fact, upon IAV infection, several processes within the cytosol and the endoplasmic reticulum, related to protein synthesis and processing, have shown to contribute either as part of an effective replication cycle or as part of an effective cellular antiviral response. Recent reports show contradictory findings regarding the control of the cellular proteostasis mechanisms by both the virus and the host cell. With this study, we aimed to further unravel the interplay between IAV and the host cell proteostasis-related mechanisms at early time-points post-infection. Our results suggest that the virus disturbs host cell protein homeostasis by inducing the accumulation of insoluble proteins in a process that seems to be related to viral RNA processing. We further analyzed the interplay between IAV infection and the endoplasmic reticulum unfolded protein response. Our results may lead to a better understanding of the interplay between IAV and the host cell and, furthermore, contribute to the development of novel antiviral strategies.

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Li, Yang, Changbo Qu, Peifa Yu, Xumin Ou, Qiuwei Pan, and Wenshi Wang. "The Interplay between Host Innate Immunity and Hepatitis E Virus." Viruses 11, no. 6 (June 11, 2019): 541. http://dx.doi.org/10.3390/v11060541.

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Hepatitis E virus (HEV) infection represents an emerging global health issue, whereas the clinical outcomes vary dramatically among different populations. The host innate immune system provides a first-line defense against the infection, but dysregulation may partially contribute to severe pathogenesis. A growing body of evidence has indicated the active response of the host innate immunity to HEV infection both in experimental models and in patients. In turn, HEV has developed sophisticated strategies to counteract the host immune system. In this review, we aim to comprehensively decipher the processes of pathogen recognition, interferon, and inflammatory responses, and the involvement of innate immune cells in HEV infection. We further discuss their implications in understanding the pathogenic mechanisms and developing antiviral therapies.

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Levraud, Jean-Pierre, Nuno Palha, Christelle Langevin, and Pierre Boudinot. "Through the looking glass: witnessing host–virus interplay in zebrafish." Trends in Microbiology 22, no. 9 (September 2014): 490–97. http://dx.doi.org/10.1016/j.tim.2014.04.014.

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De Rijck, Jan, Linos Vandekerckhove, Frauke Christ, and Zeger Debyser. "Lentiviral nuclear import: a complex interplay between virus and host." BioEssays 29, no. 5 (2007): 441–51. http://dx.doi.org/10.1002/bies.20561.

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Zhang, Jinwei. "Interplay between Host tRNAs and HIV-1: A Structural Perspective." Viruses 13, no. 9 (September 13, 2021): 1819. http://dx.doi.org/10.3390/v13091819.

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The cellular metabolism of host tRNAs and life cycle of HIV-1 cross paths at several key virus–host interfaces. Emerging data suggest a multi-faceted interplay between host tRNAs and HIV-1 that plays essential roles, both structural and regulatory, in viral genome replication, genome packaging, and virion biogenesis. HIV-1 not only hijacks host tRNAs and transforms them into obligatory reverse transcription primers but further commandeers tRNAs to regulate the localization of its major structural protein, Gag, via a specific interface. This review highlights recent advances in understanding tRNA–HIV-1 interactions, primarily from a structural perspective, which start to elucidate their underlying molecular mechanisms, intrinsic specificities, and biological significances. Such understanding may provide new avenues toward developing HIV/AIDS treatments and therapeutics including small molecules and RNA biologics that target these host–virus interfaces.

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Hussain, Khairunnisa’ Mohamed, and Justin Jang Hann Chu. "Insights into the interplay between chikungunya virus and its human host." Future Virology 6, no. 10 (October 2011): 1211–23. http://dx.doi.org/10.2217/fvl.11.101.

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Devhare, Pradip, Mridula Madiyal, Chiranjay Mukhopadhyay, Shiran Shetty, and Shamee Shastry. "Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors." International Journal of Molecular Sciences 22, no. 17 (August 26, 2021): 9259. http://dx.doi.org/10.3390/ijms22179259.

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Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can become chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.

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Terasaki, Kaori, and Shinji Makino. "Interplay between the Virus and Host in Rift Valley Fever Pathogenesis." Journal of Innate Immunity 7, no. 5 (2015): 450–58. http://dx.doi.org/10.1159/000373924.

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Rift Valley fever virus (RVFV) belongs to the genus Phlebovirus, family Bunyaviridae, and carries single-stranded tripartite RNA segments. The virus is transmitted by mosquitoes and has caused large outbreaks among ruminants and humans in sub-Saharan African and Middle East countries. The disease is characterized by a sudden onset of fever, headache, muscle pain, joint pain, photophobia, and weakness. In most cases, patients recover from the disease after a period of weeks, but some also develop retinal or macular changes, which result in vision impairment that lasts for an undefined period of time, and severe disease, characterized by hemorrhagic fever or encephalitis. The virus also causes febrile illness resulting in a high rate of spontaneous abortions in ruminants. The handling of wild-type RVFV requires high-containment facilities, including biosafety level 4 or enhanced biosafety level 3 laboratories. Nonetheless, studies clarifying the mechanisms of the RVFV-induced diseases and preventing them are areas of active research throughout the world. By primarily referring to recent studies using several animal model systems, protein expression systems, and specific mutant viruses, this review describes the current knowledge about the mechanisms of pathogenesis of RVF and biological functions of various viral proteins that affect RVFV pathogenicity.

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Desai, Dipen Vijay, and Smita Shrikant Kulkarni. "Herpes Simplex Virus: The Interplay Between HSV, Host, and HIV-1." Viral Immunology 28, no. 10 (December 2015): 546–55. http://dx.doi.org/10.1089/vim.2015.0012.

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Pardy, Ryan D., Stefanie F. Valbon, and Martin J. Richer. "Running interference: Interplay between Zika virus and the host interferon response." Cytokine 119 (July 2019): 7–15. http://dx.doi.org/10.1016/j.cyto.2019.02.009.

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Elgretli, Wesal, Tianyan Chen, Nadine Kronfli, and Giada Sebastiani. "Hepatitis C Virus-Lipid Interplay: Pathogenesis and Clinical Impact." Biomedicines 11, no. 2 (January 19, 2023): 271. http://dx.doi.org/10.3390/biomedicines11020271.

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Hepatitis C virus (HCV) infection represents the major cause of chronic liver disease, leading to a wide range of hepatic diseases, including cirrhosis and hepatocellular carcinoma. It is the leading indication for liver transplantation worldwide. In addition, there is a growing body of evidence concerning the role of HCV in extrahepatic manifestations, including immune-related disorders and metabolic abnormalities, such as insulin resistance and steatosis. HCV depends on its host cells to propagate successfully, and every aspect of the HCV life cycle is closely related to human lipid metabolism. The virus circulates as a lipid-rich particle, entering the hepatocyte via lipoprotein cell receptors. It has also been shown to upregulate lipid biosynthesis and impair lipid degradation, resulting in significant intracellular lipid accumulation (steatosis) and circulating hypocholesterolemia. Patients with chronic HCV are at increased risk for hepatic steatosis, dyslipidemia, and cardiovascular disease, including accelerated atherosclerosis. This review aims to describe different aspects of the HCV viral life cycle as it impacts host lipoproteins and lipid metabolism. It then discusses the mechanisms of HCV-related hepatic steatosis, hypocholesterolemia, and accelerated atherosclerosis.

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Ferreira, Ana Rita, Bruno Ramos, Alexandre Nunes, and Daniela Ribeiro. "Hepatitis C Virus: Evading the Intracellular Innate Immunity." Journal of Clinical Medicine 9, no. 3 (March 13, 2020): 790. http://dx.doi.org/10.3390/jcm9030790.

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Hepatitis C virus (HCV) infections constitute a major public health problem and are the main cause of chronic hepatitis and liver disease worldwide. The existing drugs, while effective, are expensive and associated with undesirable secondary effects. There is, hence, an urgent need to develop novel therapeutics, as well as an effective vaccine to prevent HCV infection. Understanding the interplay between HCV and the host cells will certainly contribute to better comprehend disease progression and may unravel possible new cellular targets for the development of novel antiviral therapeutics. Here, we review and discuss the interplay between HCV and the host cell innate immunity. We focus on the different cellular pathways that respond to, and counteract, HCV infection and highlight the evasion strategies developed by the virus to escape this intracellular response.

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Nersisyan, Stepan, Narek Engibaryan, Aleksandra Gorbonos, Ksenia Kirdey, Alexey Makhonin, and Alexander Tonevitsky. "Potential role of cellular miRNAs in coronavirus-host interplay." PeerJ 8 (September 14, 2020): e9994. http://dx.doi.org/10.7717/peerj.9994.

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Host miRNAs are known as important regulators of virus replication and pathogenesis. They can interact with various viruses through several possible mechanisms including direct binding of viral RNA. Identification of human miRNAs involved in coronavirus-host interplay becomes important due to the ongoing COVID-19 pandemic. In this article we performed computational prediction of high-confidence direct interactions between miRNAs and seven human coronavirus RNAs. As a result, we identified six miRNAs (miR-21-3p, miR-195-5p, miR-16-5p, miR-3065-5p, miR-424-5p and miR-421) with high binding probability across all analyzed viruses. Further bioinformatic analysis of binding sites revealed high conservativity of miRNA binding regions within RNAs of human coronaviruses and their strains. In order to discover the entire miRNA-virus interplay we further analyzed lungs miRNome of SARS-CoV infected mice using publicly available miRNA sequencing data. We found that miRNA miR-21-3p has the largest probability of binding the human coronavirus RNAs and being dramatically up-regulated in mouse lungs during infection induced by SARS-CoV.

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Becker, Sara, Annette Fink, Jürgen Podlech, Matthias J. Reddehase, and Niels A. Lemmermann. "Host-Adapted Gene Families Involved in Murine Cytomegalovirus Immune Evasion." Viruses 14, no. 1 (January 11, 2022): 128. http://dx.doi.org/10.3390/v14010128.

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Cytomegaloviruses (CMVs) are host species-specific and have adapted to their respective mammalian hosts during co-evolution. Host-adaptation is reflected by “private genes” that have specialized in mediating virus-host interplay and have no sequence homologs in other CMV species, although biological convergence has led to analogous protein functions. They are mostly organized in gene families evolved by gene duplications and subsequent mutations. The host immune response to infection, both the innate and the adaptive immune response, is a driver of viral evolution, resulting in the acquisition of viral immune evasion proteins encoded by private gene families. As the analysis of the medically relevant human cytomegalovirus by clinical investigation in the infected human host cannot make use of designed virus and host mutagenesis, the mouse model based on murine cytomegalovirus (mCMV) has become a versatile animal model to study basic principles of in vivo virus-host interplay. Focusing on the immune evasion of the adaptive immune response by CD8+ T cells, we review here what is known about proteins of two private gene families of mCMV, the m02 and the m145 families, specifically the role of m04, m06, and m152 in viral antigen presentation during acute and latent infection.

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Weis, Sabrina, and Aartjan J. W. te Velthuis. "Influenza Virus RNA Synthesis and the Innate Immune Response." Viruses 13, no. 5 (April 28, 2021): 780. http://dx.doi.org/10.3390/v13050780.

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Infection with influenza A and B viruses results in a mild to severe respiratory tract infection. It is widely accepted that many factors affect the severity of influenza disease, including viral replication, host adaptation, innate immune signalling, pre-existing immunity, and secondary infections. In this review, we will focus on the interplay between influenza virus RNA synthesis and the detection of influenza virus RNA by our innate immune system. Specifically, we will discuss the generation of various RNA species, host pathogen receptors, and host shut-off. In addition, we will also address outstanding questions that currently limit our knowledge of influenza virus replication and host adaption. Understanding the molecular mechanisms underlying these factors is essential for assessing the pandemic potential of future influenza virus outbreaks.

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Cokarić Brdovčak, Maja, Andreja Zubković, and Igor Jurak. "Herpes Simplex Virus 1 Deregulation of Host MicroRNAs." Non-Coding RNA 4, no. 4 (November 23, 2018): 36. http://dx.doi.org/10.3390/ncrna4040036.

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Viruses utilize microRNAs (miRNAs) in a vast variety of possible interactions and mechanisms, apparently far beyond the classical understanding of gene repression in humans. Likewise, herpes simplex virus 1 (HSV-1) expresses numerous miRNAs and deregulates the expression of host miRNAs. Several HSV-1 miRNAs are abundantly expressed in latency, some of which are encoded antisense to transcripts of important productive infection genes, indicating their roles in repressing the productive cycle and/or in maintenance/reactivation from latency. In addition, HSV-1 also exploits host miRNAs to advance its replication or repress its genes to facilitate latency. Here, we discuss what is known about the functional interplay between HSV-1 and the host miRNA machinery, potential targets, and the molecular mechanisms leading to an efficient virus replication and spread.

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Wakabayashi, Rei, Yusuke Nakahama, Viet Nguyen, and J. Luis Espinoza. "The Host-Microbe Interplay in Human Papillomavirus-Induced Carcinogenesis." Microorganisms 7, no. 7 (July 13, 2019): 199. http://dx.doi.org/10.3390/microorganisms7070199.

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Every year nearly half a million new cases of cervix cancer are diagnosed worldwide, making this malignancy the fourth commonest cancer in women. In 2018, more than 270,000 women died of cervix cancer globally with 85% of them being from developing countries. The majority of these cancers are caused by the infection with carcinogenic strains of human papillomavirus (HPV), which is also causally implicated in the development of other malignancies, including cancer of the anus, penis cancer and head and neck cancer. HPV is by far the most common sexually transmitted infection worldwide, however, most infected people do not develop cancer and do not even have a persistent infection. The development of highly effective HPV vaccines against most common high-risk HPV strains is a great medical achievement of the 21st century that could prevent up to 90% of cervix cancers. In this article, we review the current understanding of the balanced virus-host interaction that can lead to either virus elimination or the establishment of persistent infection and ultimately malignant transformation. We also highlight the influence of certain factors inherent to the host, including the immune status, genetic variants and the coexistence of other microbe infections and microbiome composition in the dynamic of HPV infection induced carcinogenesis.

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Byrd-Leotis, Lauren, Richard D. Cummings, and David A. Steinhauer. "The Interplay between the Host Receptor and Influenza Virus Hemagglutinin and Neuraminidase." International Journal of Molecular Sciences 18, no. 7 (July 17, 2017): 1541. http://dx.doi.org/10.3390/ijms18071541.

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Xiaofeng, Li, Qin Chengfeng, Zhao Hui, Ji Xue, and Huang Xingyao. "Interplay between Zika virus and host type I interferon mediated immune response." Chinese Science Bulletin 63, no. 5-6 (January 23, 2018): 495–501. http://dx.doi.org/10.1360/n972017-01129.

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Walker, Alexander P., and Ervin Fodor. "Interplay between Influenza Virus and the Host RNA Polymerase II Transcriptional Machinery." Trends in Microbiology 27, no. 5 (May 2019): 398–407. http://dx.doi.org/10.1016/j.tim.2018.12.013.

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Tripathi, Shashank, Jyoti Batra, and Sunil K. Lal. "Interplay between influenza A virus and host factors: targets for antiviral intervention." Archives of Virology 160, no. 8 (May 29, 2015): 1877–91. http://dx.doi.org/10.1007/s00705-015-2452-9.

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Varga, Steven M., and Thomas J. Braciale. "RSV-Induced Immunopathology: Dynamic Interplay between the Virus and Host Immune Response." Virology 295, no. 2 (April 2002): 203–7. http://dx.doi.org/10.1006/viro.2002.1382.

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Wang, Linya, and Jing-hsiung James Ou. "Hepatitis C virus and autophagy." Biological Chemistry 396, no. 11 (November 1, 2015): 1215–22. http://dx.doi.org/10.1515/hsz-2015-0172.

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Abstract Autophagy is a catabolic process by which cells remove protein aggregates and damaged organelles for recycling. It can also be used by cells to remove intracellular microbial pathogens, including viruses, in a process known as xenophagy. However, many viruses have developed mechanisms to subvert this intracellular antiviral response and even use this pathway to support their own replications. Hepatitis C virus (HCV) is one such virus and is an important human pathogen that can cause severe liver diseases. Recent studies indicated that HCV could activate the autophagic pathway to support its replication. This review summarizes the current knowledge on the interplay between HCV and autophagy and how this interplay affects HCV replication and host innate immune responses.

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Rodríguez-Martín, Daniel, Andrés Louloudes-Lázaro, Miguel Avia, Verónica Martín, José M. Rojas, and Noemí Sevilla. "The Interplay between Bluetongue Virus Infections and Adaptive Immunity." Viruses 13, no. 8 (July 31, 2021): 1511. http://dx.doi.org/10.3390/v13081511.

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Viral infections have long provided a platform to understand the workings of immunity. For instance, great strides towards defining basic immunology concepts, such as MHC restriction of antigen presentation or T-cell memory development and maintenance, have been achieved thanks to the study of lymphocytic choriomeningitis virus (LCMV) infections. These studies have also shaped our understanding of antiviral immunity, and in particular T-cell responses. In the present review, we discuss how bluetongue virus (BTV), an economically important arbovirus from the Reoviridae family that affects ruminants, affects adaptive immunity in the natural hosts. During the initial stages of infection, BTV triggers leucopenia in the hosts. The host then mounts an adaptive immune response that controls the disease. In this work, we discuss how BTV triggers CD8+ T-cell expansion and neutralizing antibody responses, yet in some individuals viremia remains detectable after these adaptive immune mechanisms are active. We present some unpublished data showing that BTV infection also affects other T cell populations such as CD4+ T-cells or γδ T-cells, as well as B-cell numbers in the periphery. This review also discusses how BTV evades these adaptive immune mechanisms so that it can be transmitted back to the arthropod host. Understanding the interaction of BTV with immunity could ultimately define the correlates of protection with immune mechanisms that would improve our knowledge of ruminant immunology.

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Francis, Magen, Morgan King, and Alyson Kelvin. "Back to the Future for Influenza Preimmunity—Looking Back at Influenza Virus History to Infer the Outcome of Future Infections." Viruses 11, no. 2 (January 30, 2019): 122. http://dx.doi.org/10.3390/v11020122.

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The influenza virus-host interaction is a classic arms race. The recurrent and evolving nature of the influenza virus family allows a single host to be infected several times. Locked in co-evolution, recurrent influenza virus infection elicits continual refinement of the host immune system. Here we give historical context of circulating influenza viruses to understand how the individual immune history is mirrored by the history of influenza virus circulation. Original Antigenic Sin was first proposed as the negative influence of the host’s first influenza virus infection on the next and Imprinting modernizes Antigenic Sin incorporating both positive and negative outcomes. Building on imprinting, we refer to preimmunity as the continual refinement of the host immune system with each influenza virus infection. We discuss imprinting and the interplay of influenza virus homology, vaccination, and host age establishing preimmunity. We outline host signatures and outcomes of tandem infection according to the sequence of virus and classify these relationships as monosubtypic homologous, monosubtypic heterologous, heterosubtypic, or heterotypic sequential infections. Finally, the preimmunity knowledge gaps are highlighted for future investigation. Understanding the effects of antigenic variable recurrent influenza virus infection on immune refinement will advance vaccination strategies, as well as pandemic preparedness.

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Marques, Mariana, Bruno Ramos, Ana Soares, and Daniela Ribeiro. "Cellular Proteostasis During Influenza A Virus Infection—Friend or Foe?" Cells 8, no. 3 (March 9, 2019): 228. http://dx.doi.org/10.3390/cells8030228.

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In order to efficiently replicate, viruses require precise interactions with host components and often hijack the host cellular machinery for their own benefit. Several mechanisms involved in protein synthesis and processing are strongly affected and manipulated by viral infections. A better understanding of the interplay between viruses and their host-cell machinery will likely contribute to the development of novel antiviral strategies. Here, we discuss the current knowledge on the interactions between influenza A virus (IAV), the causative agent for most of the annual respiratory epidemics in humans, and the host cellular proteostasis machinery during infection. We focus on the manipulative capacity of this virus to usurp the cellular protein processing mechanisms and further review the protein quality control mechanisms in the cytosol and in the endoplasmic reticulum that are affected by this virus.

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Begum, Feroza, Sandeepan Das, Debica Mukherjee, and Upasana Ray. "Hijacking the Host Immune Cells by Dengue Virus: Molecular Interplay of Receptors and Dengue Virus Envelope." Microorganisms 7, no. 9 (September 6, 2019): 323. http://dx.doi.org/10.3390/microorganisms7090323.

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Dengue virus (DENV) is one of the lethal pathogens in the hot climatic regions of the world and has been extensively studied to decipher its mechanism of pathogenesis and the missing links of its life cycle. With respect to the entry of DENV, multiple receptors have been recognized in different cells of the human body. However, scientists still argue whether these identified receptors are the exclusive entry mediators for the virus. Adding to the complexity, DENV has been reported to be infecting multiple organ types in its human host. Also, more than one receptor in a particular cell has been discerned to take part in mediating the ingress of DENV. In this review, we aim to discuss the different cells of the human immune system that support DENV infection and their corresponding receptors that DENV deploy to gain access to the cells.

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Pohl, Marie O., Caroline Lanz, and Silke Stertz. "Late stages of the influenza A virus replication cycle—a tight interplay between virus and host." Journal of General Virology 97, no. 9 (September 1, 2016): 2058–72. http://dx.doi.org/10.1099/jgv.0.000562.

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Braciale, T. J. "Respiratory Syncytial Virus and T Cells: Interplay between the Virus and the Host Adaptive Immune System." Proceedings of the American Thoracic Society 2, no. 2 (August 1, 2005): 141–46. http://dx.doi.org/10.1513/pats.200503-022aw.

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Ng, Wy Ching, Michelle D. Tate, Andrew G. Brooks, and Patrick C. Reading. "Soluble Host Defense Lectins in Innate Immunity to Influenza Virus." Journal of Biomedicine and Biotechnology 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/732191.

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Host defenses against viral infections depend on a complex interplay of innate (nonspecific) and adaptive (specific) components. In the early stages of infection, innate mechanisms represent the main line of host defense, acting to limit the spread of virus in host tissues prior to the induction of the adaptive immune response. Serum and lung fluids contain a range of lectins capable of recognizing and destroying influenza A viruses (IAV). Herein, we review the mechanisms by which soluble endogenous lectins mediate anti-IAV activity, including their role in modulating IAV-induced inflammation and disease and their potential as prophylactic and/or therapeutic treatments during severe IAV-induced disease.

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Ke, Po-Yuan. "The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions." International Journal of Molecular Sciences 19, no. 12 (December 7, 2018): 3940. http://dx.doi.org/10.3390/ijms19123940.

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Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis. Flavivirus infections underlie multiple human diseases and thus exert an immense burden on public health worldwide. Mounting evidence indicates that host autophagy is subverted to modulate the life cycles of flaviviruses, such as hepatitis C virus, dengue virus, Japanese encephalitis virus, West Nile virus and Zika virus. The diverse interplay between autophagy and flavivirus infection not only regulates viral growth in host cells but also counteracts host stress responses induced by viral infection. In this review, we summarize the current knowledge on the role of autophagy in the flavivirus life cycle. We also discuss the impacts of virus-induced autophagy on the pathogeneses of flavivirus-associated diseases and the potential use of autophagy as a therapeutic target for curing flavivirus infections and related human diseases.

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Chitrika Subhadarsanee, Prasad V Dhadse, Vidya Baliga, and Komal Bhombe. "Coronavirus disease and diabetes – Interplay of two pandemics." International Journal of Research in Pharmaceutical Sciences 11, SPL1 (October 19, 2020): 1048–53. http://dx.doi.org/10.26452/ijrps.v11ispl1.3443.

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“Coronavirus disease (COVID-19)” is induced by a novel enveloped virus having single-stranded RNA which was originated in Wuhan city of Hubei, province, China. The coronavirus has a protein envelope. On the outer surface, the virus has spike-like glycoprotein, which is responsible for the attachment and entrance inside host cells. It transmits rapidly affecting more than 160 countries globally, so, the World Health Organization (WHO) announced it as a pandemic. It is considered as a relative of severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS), COVID-19 is caused by a beta coronavirus named SARS-CoV-2 that affects the lower respiratory tract and manifests as pneumonia in humans. It is an airborne disease as announced by WHO and the incubation period ranges from 2 to 14 days. The clinical spectrum of COVID-19 is heterogeneous, ranging from mild flu-like symptoms to acute respiratory distress syndrome, multiple organ failure and death. Till now, so specific treatment is invented so, prevention plays a significant role. The current situation is only limiting the spread of disease. Coronavirus infection leads to the activation of adaptive and innate immune responses, resulting in massive inflammation (to so-called cytokine storm), which in turn can lead to damage to various tissues, septic shock and multiple organ failure. According to WHO, older individuals and people having associated co-morbidities like diabetes, hypertension, cardiovascular disease, obesity, etc., are at higher risk of getting infected by the coronavirus. This review explains the renewed correlation between diabetes and COVID-19. It also highlights the potential mechanisms by which diabetes regulates the host immune response and host-viral interactions.

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Slingenbergh, Jan. "Animal Virus Ecology and Evolution Are Shaped by the Virus Host-Body Infiltration and Colonization Pattern." Pathogens 8, no. 2 (May 25, 2019): 72. http://dx.doi.org/10.3390/pathogens8020072.

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The current classification of animal viruses is largely based on the virus molecular world. Less attention is given to why and how virus fitness results from the success of virus transmission. Virus transmission reflects the infection-shedding-transmission dynamics, and with it, the organ system involvement and other, macroscopic dimensions of the host environment. This study describes the transmission ecology of the world main livestock viruses, 36 in total, a mix of RNA, DNA and retroviruses. Following an iterative process, the viruses are virtually ranked in an outer- to inner-body fashion, by organ system, on ecological grounds. Also portrayed are the shifts in virus host tropism and virus genome. The synthesis of the findings reveals a predictive virus evolution framework, based on the outer- to inner-body changes in the interplay of host environment-transmission modes-organ system involvement-host cell infection cycle-virus genome. Outer-body viruses opportunistically respond to the variation in the external environment. For example, respiratory and enteric viruses tend to be associated with poultry and pig mass rearing. Ruminant and equine viruses tend to be more deep-rooted and host-specific, and also establish themselves in the vital inner-body systems. It is concluded that the framework may assist the study of new emerging viruses and pandemic risks.

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Park, Eun-Sook, Mehrangiz Dezhbord, Ah Ram Lee, and Kyun-Hwan Kim. "The Roles of Ubiquitination in Pathogenesis of Influenza Virus Infection." International Journal of Molecular Sciences 23, no. 9 (April 21, 2022): 4593. http://dx.doi.org/10.3390/ijms23094593.

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The ubiquitin system denotes a potent post-translational modification machinery that is capable of activation or deactivation of target proteins through reversible linkage of a single ubiquitin or ubiquitin chains. Ubiquitination regulates major cellular functions such as protein degradation, trafficking and signaling pathways, innate immune response, antiviral defense, and virus replication. The RNA sensor RIG-I ubiquitination is specifically induced by influenza A virus (IAV) to activate type I IFN production. Influenza virus modulates the activity of major antiviral proteins in the host cell to complete its full life cycle. Its structural and non-structural proteins, matrix proteins and the polymerase complex can regulate host immunity and antiviral response. The polymerase PB1-F2 of mutated 1918 IAV, adapts a novel IFN antagonist function by sending the DDX3 into proteasomal degradation. Ultimately the fate of virus is determined by the outcome of interplay between viral components and host antiviral proteins and ubiquitination has a central role in the encounter of virus and its host cell.

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Wichit, Sineewanlaya, Nuttamonpat Gumpangseth, Rodolphe Hamel, Sakda Yainoy, Siwaret Arikit, Chuchard Punsawad, and Dorothée Missé. "Chikungunya and Zika Viruses: Co-Circulation and the Interplay between Viral Proteins and Host Factors." Pathogens 10, no. 4 (April 9, 2021): 448. http://dx.doi.org/10.3390/pathogens10040448.

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Chikungunya and Zika viruses, both transmitted by mosquito vectors, have globally re-emerged over for the last 60 years and resulted in crucial social and economic concerns. Presently, there is no specific antiviral agent or vaccine against these debilitating viruses. Understanding viral–host interactions is needed to develop targeted therapeutics. However, there is presently limited information in this area. In this review, we start with the updated virology and replication cycle of each virus. Transmission by similar mosquito vectors, frequent co-circulation, and occurrence of co-infection are summarized. Finally, the targeted host proteins/factors used by the viruses are discussed. There is an urgent need to better understand the virus–host interactions that will facilitate antiviral drug development and thus reduce the global burden of infections caused by arboviruses.

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Tam, Patricia E. "Coxsackievirus Myocarditis: Interplay between Virus and Host in the Pathogenesis of Heart Disease." Viral Immunology 19, no. 2 (June 2006): 133–46. http://dx.doi.org/10.1089/vim.2006.19.133.

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Shen, Yong, Suzhan Zhang, Ren Sun, Tingting Wu, and Jing Qian. "Understanding the interplay between host immunity and Epstein-Barr virus in NPC patients." Emerging Microbes & Infections 4, no. 1 (January 1, 2015): 1–9. http://dx.doi.org/10.1038/emi.2015.20.

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Herbein, Georges. "Tumors and Cytomegalovirus: An Intimate Interplay." Viruses 14, no. 4 (April 14, 2022): 812. http://dx.doi.org/10.3390/v14040812.

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Human cytomegalovirus (HCMV) is a herpesvirus that alternates lytic and latent infection, infecting between 40 and 95% of the population worldwide, usually without symptoms. During its lytic cycle, HCMV can result in fever, asthenia, and, in some cases, can lead to severe symptoms such as hepatitis, pneumonitis, meningitis, retinitis, and severe cytomegalovirus disease, especially in immunocompromised individuals. Usually, the host immune response keeps the virus in a latent stage, although HCMV can reactivate in an inflammatory context, which could result in sequential lytic/latent viral cycles during the lifetime and thereby participate in the HCMV genomic diversity in humans and the high level of HCMV intrahost genomic variability. The oncomodulatory role of HCMV has been reported, where the virus will favor the development and spread of cancerous cells. Recently, an oncogenic role of HCMV has been highlighted in which the virus will directly transform primary cells and might therefore be defined as the eighth human oncovirus. In light of these new findings, it is critical to understand the role of the immune landscape, including the tumor microenvironment present in HCMV-harboring tumors. Finally, the oncomodulatory/oncogenic potential of HCMV could lead to the development of novel adapted therapeutic approaches against HCMV, especially since immunotherapy has revolutionized cancer therapeutic strategies and new therapeutic approaches are actively needed, particularly to fight tumors of poor prognosis.

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Journal articles on the topic 'Host-virus interplay'

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