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Journal articles on the topic 'Virus induced diseases'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Ludewig, Burkhard, Rolf M. Zinkernagel, and Hans Hengartner. "Transgenic Animal Models for Virus-Induced Autoimmune Diseases." Experimental Physiology 85, no. 6 (November 2000): 653–59. http://dx.doi.org/10.1111/j.1469-445x.2000.02093.x.

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2

Mori, Isamu, Takayuki Komatsu, Kenji Takeuchi, Kazuya Nakakuki, Masakatsu Sudo, and Yoshinobu Kimura. "Viremia induced by influenza virus." Microbial Pathogenesis 19, no. 4 (October 1995): 237–44. http://dx.doi.org/10.1016/s0882-4010(95)90290-2.

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3

M.G.M. Verjans, Georges, and Arnd Heiligenhaus. "Herpes Simplex Virus-Induced Ocular Diseases: Detrimental Interaction Between Virus and Host." Current Immunology Reviews 7, no. 3 (August 1, 2011): 310–27. http://dx.doi.org/10.2174/157339511796196557.

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4

Petrishcheva, Olga. "HIV-induced diseases in adults." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 5 (May 1, 2020): 12–19. http://dx.doi.org/10.33920/med-10-2005-02.

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Now, when the coronavirus pandemic has swept the whole world, few people recall that AIDS was called the plague of XX century. Manifestations of acquired immunodeficiency syndrome are the terminal stage of infection of the body with the human immunodeficiency virus, which belongs to retroviruses and leads to the development of secondary immunodeficiency. The first case of HIV infection in an adult was described in 1981 in America. A young homosexual sought help for a fungal infection resistant to treatment in one of the hospitals of San Francisco. Some time after the treatment, pneumonia developed in the young man, from the complications of which he soon died. Human immunodeficiency virus got its name only in 1982, and the disease caused by it began to be called acquired immunodeficiency syndrome. Today there are more than 40 million infected people in the world, 2/3 of whom live in Africa. Nearly 100 million people have been infected with HIV since the beginning of the epidemic, and the number of victims is twice as much as the number of people killed in the World War I. Despite the fact that this infection is not transmitted by airborne droplets, in the household and via contact, the growth rate of this disease continues to shock. So, every day about 5 thousand people in the world become infected with HIV, about 1 million die every year from the complications of this disease. It should be noted that only 71% of infected people know about their status, while all the rest continue to be a potential source of the spread of this terrible infection.

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5

Rose, John W. "Virus-Induced Demyelination: From Animal Models to Human Diseases." Mayo Clinic Proceedings 67, no. 9 (September 1992): 903–6. http://dx.doi.org/10.1016/s0025-6196(12)60833-7.

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6

Brault, Charlène, Pierre Levy, and Birke Bartosch. "Hepatitis C Virus-Induced Mitochondrial Dysfunctions." Viruses 5, no. 3 (March 21, 2013): 954–80. http://dx.doi.org/10.3390/v5030954.

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7

Akkina, Ramesh K., and Kevin P. Raisch. "Intracellular virus-induced polypeptides of pestivirus border disease virus." Virus Research 16, no. 1 (April 1990): 95–105. http://dx.doi.org/10.1016/0168-1702(90)90046-e.

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8

ABRAMSON, JON S., and J. GARY WHEELER. "Virus-induced neutrophil dysfunction." Pediatric Infectious Disease Journal 13, no. 7 (July 1994): 643–52. http://dx.doi.org/10.1097/00006454-199407000-00012.

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9

Dakhama, Azzeddine, Young Mok Lee, and Erwin W. Gelfand. "Virus-Induced Airway Dysfunction." Pediatric Infectious Disease Journal 24, Supplement (November 2005): S159—S169. http://dx.doi.org/10.1097/01.inf.0000188155.46381.15.

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10

Bondada, Megha, Yongxiu Yao, and Venugopal Nair. "Multifunctional miR-155 Pathway in Avian Oncogenic Virus-Induced Neoplastic Diseases." Non-Coding RNA 5, no. 1 (March 13, 2019): 24. http://dx.doi.org/10.3390/ncrna5010024.

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MicroRNAs (miRNAs) are small noncoding RNAs that fine-tune the responses of the cell by modulating the cell transcriptome and gene expression. MicroRNA 155 (miR-155) is a conserved multifunctional miRNA involved in multiple roles including the modulation of the immune responses. When deregulated, miR-155 can also contribute to cancer as has been demonstrated in several human malignancies such as diffuse large B cell lymphoma, chronic lymphocytic leukemia, as well as in Epstein–Barr virus (EBV)-induced B cell transformation. Avian oncogenic viruses such as Marek’s disease virus (MDV), avian leukosis virus (ALV), and reticuloendotheliosis virus (REV) that account for more than 90% of cancers in avian species, also make use of the miR-155 pathway during oncogenesis. While oncogenic retroviruses, such as ALV, activate miR-155 by insertional activation, acutely transforming retroviruses use transduced oncogenes such as v-rel to upregulate miR-155 expression. MDV on the other hand, encodes a functional miR-155 ortholog mdv1-miR-M4, similar to the miR-155 ortholog kshv-miR-K11 present in Kaposi’s sarcoma-associated herpesvirus (KSHV). We have shown that mdv1-miR-M4 is critical for the induction of MDV-induced lymphomas further demonstrating the oncogenic potential of miR-155 pathway in cancers irrespective of the diverse etiology. In this review, we discuss on our current understanding of miR-155 function in virus-induced lymphomas focusing primarily on avian oncogenic viruses.

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11

Gerhauser, Ingo, Florian Hansmann, Malgorzata Ciurkiewicz, Wolfgang Löscher, and Andreas Beineke. "Facets of Theiler’s Murine Encephalomyelitis Virus-Induced Diseases: An Update." International Journal of Molecular Sciences 20, no. 2 (January 21, 2019): 448. http://dx.doi.org/10.3390/ijms20020448.

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Theiler’s murine encephalomyelitis virus (TMEV), a naturally occurring, enteric pathogen of mice is a Cardiovirus of the Picornaviridae family. Low neurovirulent TMEV strains such as BeAn cause a severe demyelinating disease in susceptible SJL mice following intracerebral infection. Furthermore, TMEV infections of C57BL/6 mice cause acute polioencephalitis initiating a process of epileptogenesis that results in spontaneous recurrent epileptic seizures in approximately 50% of affected mice. Moreover, C3H mice develop cardiac lesions after an intraperitoneal high-dose application of TMEV. Consequently, TMEV-induced diseases are widely used as animal models for multiple sclerosis, epilepsy, and myocarditis. The present review summarizes morphological lesions and pathogenic mechanisms triggered by TMEV with a special focus on the development of hippocampal degeneration and seizures in C57BL/6 mice as well as demyelination in the spinal cord in SJL mice. Furthermore, a detailed description of innate and adaptive immune responses is given. TMEV studies provide novel insights into the complexity of organ- and mouse strain-specific immunopathology and help to identify factors critical for virus persistence.

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12

Okano, Motohiko, Masanori Nakanishi, Yuichi Taguchi, Yukio Sakiyama, and Shuzo Matsumoto. "Primary Immunodeficiency Diseases and Epstein-Barr Virus-induced Lymphoproliferative Disorders." Pediatrics International 34, no. 4 (August 1992): 385–92. http://dx.doi.org/10.1111/j.1442-200x.1992.tb00976.x.

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13

Kiss, K., A. Csepregi, L. Varga, E. Nemesánszky, M. Horányi, and G. Füst. "Complement parameters in alcoholic and virus induced chronic liver diseases." Journal of Hepatology 32 (2000): 218. http://dx.doi.org/10.1016/s0168-8278(00)81163-0.

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14

Doyle, Nicole, Philippa C. Hawes, Jennifer Simpson, Lorin H. Adams, and Helena J. Maier. "The Porcine Deltacoronavirus Replication Organelle Comprises Double-Membrane Vesicles and Zippered Endoplasmic Reticulum with Double-Membrane Spherules." Viruses 11, no. 11 (November 5, 2019): 1030. http://dx.doi.org/10.3390/v11111030.

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Porcine deltacoronavirus (PDCoV) was first identified in Hong Kong in 2012 from samples taken from pigs in 2009. PDCoV was subsequently identified in the USA in 2014 in pigs with a history of severe diarrhea. The virus has now been detected in pigs in several countries around the world. Following the development of tissue culture adapted strains of PDCoV, it is now possible to address questions regarding virus–host cell interactions for this genera of coronavirus. Here, we presented a detailed study of PDCoV-induced replication organelles. All positive-strand RNA viruses induce the rearrangement of cellular membranes during virus replication to support viral RNA synthesis, forming the replication organelle. Replication organelles for the Alpha-, Beta-, and Gammacoronavirus genera have been characterized. All coronavirus genera induced the formation of double-membrane vesicles (DMVs). In addition, Alpha- and Betacoronaviruses induce the formation of convoluted membranes, while Gammacoronaviruses induce the formation of zippered endoplasmic reticulum (ER) with tethered double-membrane spherules. However, the structures induced by Deltacoronaviruses, particularly the presence of convoluted membranes or double-membrane spherules, are unknown. Initially, the dynamics of PDCoV strain OH-FD22 replication were assessed with the onset of viral RNA synthesis, protein synthesis, and progeny particle release determined. Subsequently, virus-induced membrane rearrangements were identified in infected cells by electron microscopy. As has been observed for all other coronaviruses studied to date, PDCoV replication was found to induce the formation of double-membrane vesicles. Significantly, however, PDCoV replication was also found to induce the formation of regions of zippered endoplasmic reticulum, small associated tethered vesicles, and double-membrane spherules. These structures strongly resemble the replication organelle induced by avian Gammacoronavirus infectious bronchitis virus.

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15

Wang, Yimeng, Jianhong Zhou, Samuel G. Mackintosh, and Yuchun Du. "RuvB-Like Protein 2 Interacts with the NS1 Protein of Influenza A Virus and Affects Apoptosis That Is Counterbalanced by Type I Interferons." Viruses 13, no. 6 (May 31, 2021): 1038. http://dx.doi.org/10.3390/v13061038.

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The NS1 protein of influenza A virus (IAV) plays important roles in viral pathogenesis and host immune response. Through a proteomic approach, we have identified RuvB-like proteins 1 and 2 (RuvBL1 and RuvBL2) as interacting partners of the NS1 protein of IAVs. Infection of human lung A549 cells with A/PR/8/34 (PR8) virus resulted in reductions in the protein levels of RuvBL2 but not RuvBL1. Further studies with RuvBL2 demonstrated that the NS1-RuvBL2 interaction is RNA-independent, and RuvBL2 binds the RNA-binding domain of the NS1. Infection of interferon (IFN)-deficient Vero cells with wild-type or delNS1 PR8 virus reduced RuvBL2 protein levels and induced apoptosis; delNS1 virus caused more reductions in RuvBL2 protein levels and induced more apoptosis than did wild-type virus. Knockdown of RuvBL2 by siRNAs induced apoptosis and overexpression of RuvBL2 resulted in increased resistance to infection-induced apoptosis in Vero cells. These results suggest that a non-NS1 viral element or elements induce apoptosis by suppressing RuvBL2 protein levels, and the NS1 inhibits the non-NS1 viral element-induced apoptosis by maintaining RuvBL2 abundance in infected cells in the absence of IFN influence. In contrast to Vero cells, infection of IFN-competent A549 cells with PR8 virus caused reductions in RuvBL2 protein levels but did not induce apoptosis. Concomitantly, pretreatment of Vero cells with a recombinant IFN resulted in resistance to infection-induced apoptosis. These results demonstrate that the infection-induced, RuvBL2-regulated apoptosis in infected cells is counterbalanced by IFN survival signals. Our results reveal a novel mechanism underlying the infection-induced apoptosis that can be modulated by the NS1 and type I IFN signaling in IAV-infected cells.

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16

Sreekanth, Gopinathan Pillai, Aporn Chuncharunee, Pa-thai Yenchitsomanus, and Thawornchai Limjindaporn. "Crocetin Improves Dengue Virus-Induced Liver Injury." Viruses 12, no. 8 (July 30, 2020): 825. http://dx.doi.org/10.3390/v12080825.

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Dengue virus (DENV) infection is one of the most widespread mosquito-borne viral infections. Liver injury is commonly observed in severe DENV infection, and the present study aimed to examine the efficacy of crocetin treatment in an immunocompetent mouse model of DENV infection exhibiting liver injury. The efficacy of crocetin treatment in DENV-induced liver injury was assessed via both transaminase levels and histopathology analysis. A real-time polymerase chain reaction array was then used to describe the expression of 84 apoptosis-related genes. Using real-time RT-PCR and Western blot analysis, the gene expressions of host factors were investigated. Additionally, the effect of crocetin in NF-kB signaling during DENV infection was studied. We did not observe any significant reduction in virus production when DENV-infected mice were treated with crocetin. However, DENV-infected mice treated with crocetin showed reduced DENV-induced apoptosis. The real-time polymerase chain reaction array revealed pro-inflammatory cytokine expressions to be significantly reduced in the crocetin-treated DENV-infected mice. We also found that crocetin could effectively modulate antioxidant status in DENV-infected mice. Moreover, crocetin demonstrated the ability to reduce the nuclear translocation of NF-kB in DENV-infected mice. Our results suggest that crocetin treatment does not inhibit DENV replication in the liver of DENV-infected mice; however, we did find that crocetin improves host responses that reduce liver injury.

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17

Xu, Shan-Shan, Liang-Guo Xu, Cailei Yuan, Sheng-Na Li, Tian Chen, Weiying Wang, Changsheng Li, Lingzhen Cao, and Hua Rao. "FKBP8 inhibits virus-induced RLR-VISA signaling." Journal of Medical Virology 91, no. 3 (November 21, 2018): 482–92. http://dx.doi.org/10.1002/jmv.25327.

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18

Chiu, Yi-Shu, Yuh Tzean, Yi-Hui Chen, Chi-Wei Tsai, and Hsin-Hung Yeh. "Fungal F8-Culture Filtrate Induces Tomato Resistance against Tomato Yellow Leaf Curl Thailand Virus." Viruses 13, no. 8 (July 23, 2021): 1434. http://dx.doi.org/10.3390/v13081434.

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Tomato (Solanum lycopersicum) is an important economic crop worldwide. However, tomato production is jeopardized by the devastating tomato yellow leaf curl disease (TYLCD) caused by whitefly-transmitted begomoviruses (WTBs). In this study, we evaluated the efficacy of our previously developed plant antiviral immunity inducer, fungal F8-culture filtrate, on tomato to combat tomato yellow leaf curl Thailand virus (TYLCTHV), the predominant WTB in Taiwan. Our results indicated that F8-culture filtrate treatment induced strong resistance, did not reduce the growth of tomato, and induced prominent resistance against TYLCTHV both in the greenhouse and in the field. Among TYLCTHV-inoculated Yu-Nu tomato grown in the greenhouse, a greater percentage of plants treated with F8-culture filtrate (43–100%) were healthy-looking compared to the H2O control (0–14%). We found that TYLCTHV cannot move systemically only on the F8-culture filtrate pretreated healthy-looking plants. Tracking the expression of phytohormone-mediated immune maker genes revealed that F8-culture filtrate mainly induced salicylic acid-mediated plant immunity. Furthermore, callose depositions and the expression of the pathogen-induced callose synthase gene, POWDERY MILDEW RESISTANT 4 were only strongly induced by TYLCTHV on tomato pretreated with F8-culture filtrate. This study provides an effective way to induce tomato resistance against TYLCTHV.

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19

Fukumoto, F., Y. Masuda, and K. Hanada. "Pea Tissue Necrosis Induced by Cucumber mosaic virus Alone or Together with Watermelon mosaic virus." Plant Disease 87, no. 4 (April 2003): 324–28. http://dx.doi.org/10.1094/pdis.2003.87.4.324.

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Necrotic diseases of the stems, petioles, and leaves of pea plants (Pisum sativumL.), leading to wilting and death, occur in the Wakayama and Mie Prefectures of Japan. Based on host range, symptomatology, electron microscopy, and serological relationships, Watermelon mosaic virus (WMV) and three Cucumber mosaic virus (CMV) isolates (PE2, PE3A, and PB1) were isolated from diseased plants in the Wakayama Prefecture. In the Mie Prefecture, CMV (PEAN) also was isolated from pea plants with similar symptoms. Single infection with CMV (PB1 or PEAN) caused stem necrosis and eventual death of pea plants. Similar symptoms developed after double infection with WMV and PE2 or PE3A, whereas single infection with PE2 and PE3A induced symptomless infection in pea plants. We concluded either CMV alone or synergistic effects of mixed infection with CMV and WMV induced pea plant stem necrosis.

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20

Lau, Johnson Yiu-Nam. "IV. Pathogenetic mechanisms involved in hepatitis C virus-induced liver diseases." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 6 (December 1, 1998): G1217—G1220. http://dx.doi.org/10.1152/ajpgi.1998.275.6.g1217.

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The pathogenetic mechanisms for liver damage in acute hepatitis C are not clear, but a host immune cellular response may be involved. In chronic hepatitis C, there is strong evidence that host cellular immune response is involved in the control of viral replication and contributes to hepatocellular damage. As hepatitis C virus infection persists, continuous liver damage and regeneration, together with enhanced fibrogenesis, may eventually lead to cirrhosis in a proportion of patients. Transplant patients on high-dose immunosuppression may have high-level intrahepatic hepatitis C viral expression, and, in this setting, the virus may induce direct cytopathic liver damage.

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21

Martin, Robert R., Stuart MacFarlane, Sead Sabanadzovic, Diego Quito, Bindu Poudel, and Ioannis E. Tzanetakis. "Viruses and Virus Diseases of Rubus." Plant Disease 97, no. 2 (February 2013): 168–82. http://dx.doi.org/10.1094/pdis-04-12-0362-fe.

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Blackberry and raspberry are members of the family Rosaceae. They are classified in the genus Rubus, which comprises hundreds of species and has a center of origin in the Far East. Rubus is divided into 15 subgenera with blackberries classified in the Rubus (formerly Eubatus) and raspberries in the Idaeobatus subgenera. Rubus species are propagated vegetatively and are subject to infection by viruses during development, propagation, and fruit production stages. Reports of initial detection and symptoms of more than 30 viruses, virus-like diseases, and phytoplasmas affecting Rubus spp. were reviewed more than 20 years ago. Since the last review on Rubus viruses, significant progress has been made in the molecular characterization of many of the viruses that infect Rubus spp. Currently, reverse transcription–polymerase chain reaction detection methods are available for most of the viruses known to infect Rubus. The goals of this article are to update the knowledge on previously characterized viruses of Rubus, highlight recently described viruses, review the virus-induced symptoms, describe the advances made in their detection, and discuss our knowledge about several virus complexes that cause serious diseases in Rubus. Virus complexes have been identified recently as the major cause of diseases in blackberries and raspberries.

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22

Li, Chunfu, Hongliang Zhang, Lina Ji, Xiao Wang, Yongjun Wen, Guangpeng Li, Zhen Fu, and Yang Yang. "Deficient Incorporation of Rabies Virus Glycoprotein into Virions Enhances Virus-Induced Immune Evasion and Viral Pathogenicity." Viruses 11, no. 3 (March 4, 2019): 218. http://dx.doi.org/10.3390/v11030218.

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Previous studies have shown that wild-type (wt) rabies virus (RABV) evades the host immune response by restricting expression of glycoprotein (G), which blocks activation of dendritic cells (DCs) and induces production of virus-neutralizing antibodies (VNAs). In the present study, wt RABVs not only restricted G expression but also reduced incorporation of G into mature virions compared with laboratory-adapted viruses. A recombinant RABV expressing triple G was used to further determine whether G expression relates to incorporation. The recombinant virus showed higher expression and incorporation of G and activated more DCs than the virus that expressed a single copy of G. Removal of G from viruses using subtilisin or Dithiothreitol (DTT)/ Nonidet P-40 (NP40) almost completely abolishes DC activation and VNA production. Consequently, these G-depleted viruses cause lethal infection in mice. Thus, wt RABVs can subvert DC-induced antiviral immune response and maintain pathogenicity by decreasing G expression in infected cells and G incorporation into virions.

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23

Brown, Julia A., Gursewak Singh, Joshua A. Acklin, Silviana Lee, James E. Duehr, Anupa N. Chokola, Justin J. Frere, et al. "Dengue Virus Immunity Increases Zika Virus-Induced Damage during Pregnancy." Immunity 50, no. 3 (March 2019): 751–62. http://dx.doi.org/10.1016/j.immuni.2019.01.005.

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24

Wang, Hsiuying. "Anti-NMDA Receptor Encephalitis, Vaccination and Virus." Current Pharmaceutical Design 25, no. 43 (January 9, 2020): 4579–88. http://dx.doi.org/10.2174/1381612825666191210155059.

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Anti-N-methyl-d-aspartate (Anti-NMDA) receptor encephalitis is an acute autoimmune disorder. The symptoms range from psychiatric symptoms, movement disorders, cognitive impairment, and autonomic dysfunction. Previous studies revealed that vaccination might induce this disease. A few cases were reported to be related to H1N1 vaccine, tetanus/diphtheria/pertussis and polio vaccine, and Japanese encephalitis vaccine. Although vaccination is a useful strategy to prevent infectious diseases, in a low risk, it may trigger serious neurological symptoms. In addition to anti-NMDA receptor encephalitis, other neurological diseases were reported to be associated with a number of vaccines. In this paper, the anti-NMDA receptor encephalitis cases related to a number of vaccines and other neurological symptoms that might be induced by these vaccines were reviewed. In addition, anti-NMDA receptor encephalitis cases that were induced by virus infection were also reviewed.

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Buber, Jonathan, Noam Fink, Hanna Bin, and Meir Mouallem. "West Nile virus-induced pancreatitis." Travel Medicine and Infectious Disease 6, no. 6 (November 2008): 373–75. http://dx.doi.org/10.1016/j.tmaid.2008.08.001.

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26

Zhu, Liqian, Xiaotian Fu, Chen Yuan, Xinyi Jiang, and Gaiping Zhang. "Induction of Oxidative DNA Damage in Bovine Herpesvirus 1 Infected Bovine Kidney Cells (MDBK Cells) and Human Tumor Cells (A549 Cells and U2OS Cells)." Viruses 10, no. 8 (July 26, 2018): 393. http://dx.doi.org/10.3390/v10080393.

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Bovine herpesvirus 1 (BoHV-1) is an important pathogen of cattle that causes lesions in mucosal surfaces, genital tracts and nervous systems. As a novel oncolytic virus, BoHV-1 infects and kills numerous human tumor cells. However, the mechanisms underlying the virus-induced cell damages are not fully understood. In this study, we demonstrated that virus infection of MDBK cells induced high levels of DNA damage, because the percentage of comet tail DNA (tailDNA%) determined by comet assay, a direct indicator of DNA damage, and the levels of 8-hydroxyguanine (8-oxoG) production, an oxidative DNA damage marker, consistently increased following the virus infection. The expression of 8-oxoguanine DNA glycosylase (OGG-1), an enzyme responsible for the excision of 8-oxoG, was significantly decreased due to the virus infection, which corroborated with the finding that BoHV-1 infection stimulated 8-oxoG production. Furthermore, the virus replication in human tumor cells such as in A549 cells and U2OS cells also induced DNA damage. Chemical inhibition of reactive oxidative species (ROS) production by either ROS scavenger N-Acetyl-l-cysteine or NOX inhibitor diphenylene iodonium (DPI) significantly decreased the levels of tailDNA%, suggesting the involvement of ROS in the virus induced DNA lesions. Collectively, these results indicated that BoHV-1 infection of these cells elicits oxidative DNA damages, providing a perspective in understanding the mechanisms by which the virus induces cell death in both native host cells and human tumor cells.

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Flier, Jeffrey S., Lisa H. Underhill, Per Hollsberg, and David A. Hafler. "Pathogenesis of Diseases Induced by Human Lymphotropic Virus Type I Infection." New England Journal of Medicine 328, no. 16 (April 22, 1993): 1173–82. http://dx.doi.org/10.1056/nejm199304223281608.

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Emilia, Giovanni, Mario Luppi, M. Grazia Ferrari, Patrizia Barozzi, Roberto Marasca, and Giuseppe Torelli. "Hepatitis C virus-induced leuko-thrombocytopenia and haemolysis." Journal of Medical Virology 53, no. 2 (October 1997): 182–84. http://dx.doi.org/10.1002/(sici)1096-9071(19971003)53:2<182::aid-jmv12>3.0.co;2-l.

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Yoon, Ji-Won. "Pathogenic mechanisms of virus-induced type 1 diabetes." Microbial Pathogenesis 5, no. 2 (August 1988): 77–86. http://dx.doi.org/10.1016/0882-4010(88)90010-1.

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30

Padalko, Elizaveta, Dieter Nuyens, Armando De Palma, Erik Verbeken, Joeri L. Aerts, Erik De Clercq, Peter Carmeliet, and Johan Neyts. "The Interferon Inducer Ampligen [Poly(I)-Poly(C12U)] Markedly Protects Mice against Coxsackie B3 Virus-Induced Myocarditis." Antimicrobial Agents and Chemotherapy 48, no. 1 (January 2004): 267–74. http://dx.doi.org/10.1128/aac.48.1.267-274.2004.

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ABSTRACT Viral replication, as well as an immunopathological component, is assumed to be involved in coxsackie B virus-induced myocarditis. We evaluated the efficacy of the interferon inducer Ampligen on coxsackie B3 virus-induced myocarditis in C3H/HeNHsd mice. The efficacy of Ampligen was compared with that of the interferon inducer poly(inosinic acid)-poly(cytidylic acid) [poly(IC)], alpha interferon 2b (INTRON A), and pegylated alpha interferon 2b (PEG-INTRON-α-2b). Ampligen at 20 mg/kg of body weight/day was able to reduce the severity of virus-induced myocarditis, as assessed by morphometric analysis, by 98% (P = 3.0 × 10−8). When poly(IC) was administered at 15 mg/kg/day, it reduced the severity of virus-induced myocarditis by 93% (P = 5.6 × 10−5). Alpha interferon 2b (1 × 105 U/day) and pegylated alpha interferon 2b (5 × 105 U/day) were less effective and reduced the severity of virus-induced myocarditis by 66% (P = 0.0009) and 78% (P = 0.0002), respectively. The observed efficacies of Ampligen and poly(IC) were corroborated by the observation that the drugs also markedly reduced the virus titers in the heart, as detected by (i) quantitative real-time reverse transcription-PCR and (ii) titration for infectious virus content. Whereas the electrocardiograms for untreated mice with myocarditis were severely disturbed, the electrocardiographic parameters were normalized in Ampligen- and poly(IC)-treated mice. Even when start of treatment with Ampligen was delayed until day 2 postinfection, a time at which lesions had already appeared in untreated control animals, a marked protective effect on the development of viral myocarditis (as assessed at day 6 postinfection) was still noted.

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31

Poole, Brian D., Yuory V. Karetnyi, and Stanley J. Naides. "Parvovirus B19-Induced Apoptosis of Hepatocytes." Journal of Virology 78, no. 14 (July 15, 2004): 7775–83. http://dx.doi.org/10.1128/jvi.78.14.7775-7783.2004.

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ABSTRACT Parvovirus B19 (B19 virus) can persist in multiple tissues and has been implicated in a variety of diseases, including acute fulminant liver failure. The mechanism by which B19 virus induces liver failure remains unknown. Hepatocytes are nonpermissive for B19 virus replication. We previously reported that acute fulminant liver failure associated with B19 virus infection was characterized by hepatocellular dropout. We inoculated both primary hepatocytes and the hepatocellular carcinoma cell line Hep G2 with B19 virus and assayed for apoptosis by using annexin V staining. Reverse transcriptase PCR analysis and immunofluorescence demonstrated that B19 virus was able to infect the cells and produce its nonstructural protein but little or no structural capsid protein. Infection with B19 virus induced means of 28% of Hep G2 cells and 10% of primary hepatocytes to undergo apoptosis, which were four- and threefold increases, respectively, over background levels. Analysis of caspase involvement showed that B19 virus-inoculated cultures had a significant increase in the number of cells with active caspase 3. Inhibition studies demonstrated that caspases 3 and 9, but not caspase 8, are required for B19 virus-induced apoptosis.

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Morgan, A. J., M. Mackett, S. Finerty, J. R. Arrand, F. T. Scullion, and M. A. Epstein. "Recombinant vaccinia virus expressing epstein-barr virus glycoprotein gp340 protects cottontop tamarins against EB virus-induced malignant lymphomas." Journal of Medical Virology 25, no. 2 (June 1988): 189–95. http://dx.doi.org/10.1002/jmv.1890250209.

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Kolpikova, Elena P., Ana R. Tronco, Andreas B. Den Hartigh, Konner J. Jackson, Takao Iwawaki, and Susan L. Fink. "IRE1α Promotes Zika Virus Infection via XBP1." Viruses 12, no. 3 (March 3, 2020): 278. http://dx.doi.org/10.3390/v12030278.

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Zika virus (ZIKV) is an emergent member of the Flaviviridae family which causes severe congenital defects and other major sequelae, but the cellular processes that support ZIKV replication are incompletely understood. Related flaviviruses use the endoplasmic reticulum (ER) as a membranous platform for viral replication and induce ER stress during infection. Our data suggest that ZIKV activates IRE1α, a component of the cellular response to ER stress. IRE1α is an ER-resident transmembrane protein that possesses a cytosolic RNase domain. Upon activation, IRE1α initiates nonconventional cytoplasmic splicing of XBP1 mRNA. Spliced XBP1 encodes a transcription factor, which upregulates ER-related targets. We find that ZIKV infection induces XBP1 mRNA splicing and induction of XBP1 target genes. Small molecule inhibitors of IRE1α, including those specific for the nuclease function, prevent ZIKV-induced cytotoxicity, as does genetic disruption of IRE1α. Optimal ZIKV RNA replication requires both IRE1α and XBP1. Spliced XBP1 has been described to cause ER expansion and remodeling and we find that ER redistribution during ZIKV infection requires IRE1α nuclease activity. Finally, we demonstrate that inducible genetic disruption of IRE1α and XBP1 impairs ZIKV replication in a mouse model of infection. Together, our data indicate that the ER stress response component IRE1α promotes ZIKV infection via XBP1 and may represent a potential therapeutic target.

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Das Sarma, Jayasri. "A Mechanism of Virus-Induced Demyelination." Interdisciplinary Perspectives on Infectious Diseases 2010 (2010): 1–28. http://dx.doi.org/10.1155/2010/109239.

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Myelin forms an insulating sheath surrounding axons in the central and peripheral nervous systems and is essential for rapid propagation of neuronal action potentials. Demyelination is an acquired disorder in which normally formed myelin degenerates, exposing axons to the extracellular environment. The result is dysfunction of normal neuron-to-neuron communication and in many cases, varying degrees of axonal degeneration. Numerous central nervous system demyelinating disorders exist, including multiple sclerosis. Although demyelination is the major manifestation of most of the demyelinating diseases, recent studies have clearly documented concomitant axonal loss to varying degrees resulting in long-term disability. Axonal injury may occur secondary to myelin damage (outside-in model) or myelin damage may occur secondary to axonal injury (inside-out model). Viral induced demyelination models, has provided unique imminent into the cellular mechanisms of myelin destruction. They illustrate mechanisms of viral persistence, including latent infections, virus reactivation and viral-induced tissue damage. These studies have also provided excellent paradigms to study the interactions between the immune system and the central nervous system (CNS). In this review we will discuss potential cellular and molecular mechanism of central nervous system axonal loss and demyelination in a viral induced mouse model of multiple sclerosis.

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Raut, S. D., K. K. Rajak, R. Kumar, V. K. Singh, A. Saxena, D. Chaudhary, D. Muthuchelvan, and A. B. Pandey. "Characterization of cytopathogenicity of classical swine fever virus isolate induced by Newcastle disease virus." VirusDisease 26, no. 1-2 (May 23, 2015): 70–76. http://dx.doi.org/10.1007/s13337-015-0253-0.

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Assunção-Miranda, Iranaia, Christine Cruz-Oliveira, and Andrea T. Da Poian. "Molecular Mechanisms Involved in the Pathogenesis of Alphavirus-Induced Arthritis." BioMed Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/973516.

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Arthritogenic alphaviruses, including Ross River virus (RRV), Chikungunya virus (CHIKV), Sindbis virus (SINV), Mayaro virus (MAYV), O'nyong-nyong virus (ONNV), and Barmah Forest virus (BFV), cause incapacitating and long lasting articular disease/myalgia. Outbreaks of viral arthritis and the global distribution of these diseases point to the emergence of arthritogenic alphaviruses as an important public health problem. This review discusses the molecular mechanisms involved in alphavirus-induced arthritis, exploring the recent data obtained within vitrosystems andin vivostudies using animal models and samples from patients. The factors associated to the extension and persistence of symptoms are highlighted, focusing on (a) virus replication in target cells, and tissues, including macrophages and muscle cells; (b) the inflammatory and immune responses with recruitment and activation of macrophage, NK cells and T lymphocytes to the lesion focus and the increase of inflammatory mediators levels; and (c) the persistence of virus or viral products in joint and muscle tissues. We also discuss the importance of the establishment of novel animal models to test new molecular targets and to develop more efficient and selective drugs to treat these diseases.

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Doyle, Nicole, Benjamin Neuman, Jennifer Simpson, Philippa Hawes, Judith Mantell, Paul Verkade, Hasan Alrashedi, and Helena Maier. "Infectious Bronchitis Virus Nonstructural Protein 4 Alone Induces Membrane Pairing." Viruses 10, no. 9 (September 6, 2018): 477. http://dx.doi.org/10.3390/v10090477.

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Positive-strand RNA viruses, such as coronaviruses, induce cellular membrane rearrangements during replication to form replication organelles allowing for efficient viral RNA synthesis. Infectious bronchitis virus (IBV), a pathogenic avian Gammacoronavirus of significant importance to the global poultry industry, has been shown to induce the formation of double membrane vesicles (DMVs), zippered endoplasmic reticulum (zER) and tethered vesicles, known as spherules. These membrane rearrangements are virally induced; however, it remains unclear which viral proteins are responsible. In this study, membrane rearrangements induced when expressing viral non-structural proteins (nsps) from two different strains of IBV were compared. Three non-structural transmembrane proteins, nsp3, nsp4, and nsp6, were expressed in cells singularly or in combination and the effects on cellular membranes investigated using electron microscopy and electron tomography. In contrast to previously studied coronaviruses, IBV nsp4 alone is necessary and sufficient to induce membrane pairing; however, expression of the transmembrane proteins together was not sufficient to fully recapitulate DMVs. This indicates that although nsp4 is able to singularly induce membrane pairing, further viral or host factors are required in order to fully assemble IBV replicative structures. This study highlights further differences in the mechanism of membrane rearrangements between members of the coronavirus family.

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Othumpangat, Sreekumar, Donald H. Beezhold, Christina M. Umbright, and John D. Noti. "Influenza Virus-Induced Novel miRNAs Regulate the STAT Pathway." Viruses 13, no. 6 (May 23, 2021): 967. http://dx.doi.org/10.3390/v13060967.

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MicroRNAs (miRNAs) are essential regulators of gene expression in humans and can control pathogenesis and host–virus interactions. Notably, the role of specific host miRNAs during influenza virus infections are still ill-defined. The central goal of this study was to identify novel miRNAs and their target genes in response to influenza virus infections in airway epithelium. Human airway epithelial cells exposed to influenza A virus (IAV) induced several novel miRNAs that were identified using next-generation sequencing (NGS) and their target genes by biochemical methods. NGS analysis predicted forty-two RNA sequences as possible miRNAs based on computational algorithms. The expression patterns of these putative miRNAs were further confirmed using RT-PCR in human bronchial epithelial cells exposed to H1N1, H9N1(1P10), and H9N1 (1WF10) strains of influenza virus. A time-course study showed significant downregulation of put-miR-34 in H1N1 and put-miR-35 in H9N1(1P10)-infected cells, which is consistent with the NGS data. Additionally, put-miR-34 and put-miR-35 showed a high fold enrichment in an argonaute-immunoprecipitation assay compared to the controls, indicating their ability to form a complex with argonaute protein and RNA-induced silencing complex (RISC), which is a typical mode of action found with miRNAs. Our earlier studies have shown that the replication and survival of influenza virus is modulated by certain transcription factors such as NF-ĸB. To identify the target(s) of these putative miRNAs, we screened 84 transcription factors that have a role in viral pathogenesis. Cells transfected with mimic of the put-miR-34 showed a significant decrease in the expression of Signal Transducers and Activators of Transcription 3 (STAT3), whereas the inhibitor of put-miR-34 showed a significant increase in STAT3 expression and its phosphorylation. In addition, put-miR-34 had 76% homology to the untranslated region of STAT3. NGS and PCR array data submitted to the Gene Ontology project also predicted the role of transcription factors modulated by put-miR-34. Our data suggest that put-miR-34 may be a good target for antiviral therapy.

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Banning, A. P., M. G. Brook, and B. A. Bannister. "Detection of antihepatitis C virus antibody in severe Epstein-Barr virus-induced hepatitis." Journal of Infection 22, no. 3 (May 1991): 298–99. http://dx.doi.org/10.1016/s0163-4453(05)80018-0.

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SRINIVAS, RANGA V., HELENE BERNSTEIN, CHERIE OLIVER, and RICHARD W. COMPANS. "Calmodulin Antagonists Inhibit Human Immunodeficiency Virus-Induced Cell Fusion but Not Virus Replication." AIDS Research and Human Retroviruses 10, no. 11 (November 1994): 1489–96. http://dx.doi.org/10.1089/aid.1994.10.1489.

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Riccetti, Silvia, Alessandro Sinigaglia, Giovanna Desole, Norbert Nowotny, Marta Trevisan, and Luisa Barzon. "Modelling West Nile Virus and Usutu Virus Pathogenicity in Human Neural Stem Cells." Viruses 12, no. 8 (August 12, 2020): 882. http://dx.doi.org/10.3390/v12080882.

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West Nile virus (WNV) and Usutu virus (USUV) are genetically related neurotropic mosquito-borne flaviviruses, which frequently co-circulate in nature. Despite USUV seeming to be less pathogenic for humans than WNV, the clinical manifestations induced by these two viruses often overlap and may evolve to produce severe neurological complications. The aim of this study was to investigate the effects of WNV and USUV infection on human induced pluripotent stem cell-derived neural stem cells (hNSCs), as a model of the neural progenitor cells in the developing fetal brain and in adult brain. Zika virus (ZIKV), a flavivirus with known tropism for NSCs, was used as the positive control. Infection of hNSCs and viral production, effects on cell viability, apoptosis, and innate antiviral responses were compared among viruses. WNV displayed the highest replication efficiency and cytopathic effects in hNSCs, followed by USUV and then ZIKV. In these cells, both WNV and USUV induced the overexpression of innate antiviral response genes at significantly higher levels than ZIKV. Expression of interferon type I, interleukin-1β and caspase-3 was significantly more elevated in WNV- than USUV-infected hNSCs, in agreement with the higher neuropathogenicity of WNV and the ability to inhibit the interferon response pathway.

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Pascual-Iglesias, Sanchez, Penzes, Sola, Enjuanes, and Zuñiga. "Recombinant Chimeric Transmissible Gastroenteritis Virus (TGEV) - Porcine Epidemic Diarrhea Virus (PEDV) Virus Provides Protection against Virulent PEDV." Viruses 11, no. 8 (July 25, 2019): 682. http://dx.doi.org/10.3390/v11080682.

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Porcine epidemic diarrhea virus (PEDV) is an enteric coronavirus causing high morbidity and mortality in porcine herds worldwide. Although both inactivated and live attenuated vaccines have been extensively used, the emergence of highly virulent strains and the recurrent outbreaks even in vaccinated farms highlight the need of effective vaccines. Engineering of genetically defined live attenuated vaccines is a rational approach for novel vaccine development. In this line, we engineered an attenuated virus based on the transmissible gastroenteritis virus (TGEV) genome, expressing a chimeric spike protein from a virulent United States (US) PEDV strain. This virus (rTGEV-RS-SPEDV) was attenuated in highly-sensitive five-day-old piglets, as infected animals did not lose weight and none of them died. In addition, the virus caused very minor tissue damage compared with a virulent virus. The rTGEV-RS-SPEDV vaccine candidate was also attenuated in three-week-old animals that were used to evaluate the protection conferred by this virus, compared with the protection induced by infection with a virulent PEDV US strain (PEDV-NVSL). The rTGEV-RS-SPEDV virus protected against challenge with a virulent PEDV strain, reducing challenge virus titers in jejunum and leading to undetectable challenge virus RNA levels in feces. The rTGEV-RS-SPEDV virus induced a humoral immune response specific for PEDV, including neutralizing antibodies. Altogether, the data indicated that rTGEV-RS-SPEDV is a promising vaccine candidate against virulent PEDV infection.

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Nishio, Akira, and Barbara Rehermann. "Virus-Induced Interferon Regulates the Urea Cycle." Immunity 51, no. 6 (December 2019): 975–77. http://dx.doi.org/10.1016/j.immuni.2019.11.012.

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Oleszak, Emilia L., J. Robert Chang, Herman Friedman, Christos D. Katsetos, and Chris D. Platsoucas. "Theiler's Virus Infection: a Model for Multiple Sclerosis." Clinical Microbiology Reviews 17, no. 1 (January 2004): 174–207. http://dx.doi.org/10.1128/cmr.17.1.174-207.2004.

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SUMMARY Both genetic background and environmental factors, very probably viruses, appear to play a role in the etiology of multiple sclerosis (MS). Lessons from viral experimental models suggest that many different viruses may trigger inflammatory demyelinating diseases resembling MS. Theiler's virus, a picornavirus, induces in susceptible strains of mice early acute disease resembling encephalomyelitis followed by late chronic demyelinating disease, which is one of the best, if not the best, animal model for MS. During early acute disease the virus replicates in gray matter of the central nervous system but is eliminated to very low titers 2 weeks postinfection. Late chronic demyelinating disease becomes clinically apparent approximately 2 weeks later and is characterized by extensive demyelinating lesions and mononuclear cell infiltrates, progressive spinal cord atrophy, and axonal loss. Myelin damage is immunologically mediated, but it is not clear whether it is due to molecular mimicry or epitope spreading. Cytokines, nitric oxide/reactive nitrogen species, and costimulatory molecules are involved in the pathogenesis of both diseases. Close similarities between Theiler's virus-induced demyelinating disease in mice and MS in humans, include the following: major histocompatibility complex-dependent susceptibility; substantial similarities in neuropathology, including axonal damage and remyelination; and paucity of T-cell apoptosis in demyelinating disease. Both diseases are immunologically mediated. These common features emphasize the close similarities of Theiler's virus-induced demyelinating disease in mice and MS in humans.

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Gómez, Ricardo M., Alejandra Yep, Mirta Schattner, and María I. Berría. "Junin virus-induced astrocytosis is impaired by iNOS inhibition." Journal of Medical Virology 69, no. 1 (November 14, 2002): 145–49. http://dx.doi.org/10.1002/jmv.10254.

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Imagawa, Akihisa. "Fulminant type 1 diabetes-is it virus-induced diabetes?" Journal of Medical Virology 83, no. 9 (July 7, 2011): 1675. http://dx.doi.org/10.1002/jmv.22060.

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Coughlin, Melissa M., William J. Bellini, and Paul A. Rota. "Contribution of dendritic cells to measles virus induced immunosuppression." Reviews in Medical Virology 23, no. 2 (December 20, 2012): 126–38. http://dx.doi.org/10.1002/rmv.1735.

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Dulout, Fernando N., Horacio E. Panisse, Guadalupe Carballal, Huberto N. von Guradze, Julio C. DeLuca, José R. Oubiña, and Cristina Videla°. "Junin Virus-Induced Chromosomal Aberrations in the Guinea Pig." Intervirology 24, no. 4 (1985): 193–98. http://dx.doi.org/10.1159/000149643.

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Guo, Fang, Yanxing Han, Xuesen Zhao, Jianghua Wang, Fei Liu, Chunxiao Xu, Lai Wei, et al. "STING Agonists Induce an Innate Antiviral Immune Response against Hepatitis B Virus." Antimicrobial Agents and Chemotherapy 59, no. 2 (December 15, 2014): 1273–81. http://dx.doi.org/10.1128/aac.04321-14.

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ABSTRACTChronicity of hepatitis B virus (HBV) infection is due to the failure of a host to mount a sufficient immune response to clear the virus. The aim of this study was to identify small-molecular agonists of the pattern recognition receptor (PRR)-mediated innate immune response to control HBV infection. To achieve this goal, a coupled mouse macrophage and hepatocyte culture system mimicking the intrahepatic environment was established and used to screen small-molecular compounds that activate macrophages to produce cytokines, which in turn suppress HBV replication in a hepatocyte-derived stable cell line supporting HBV replication in a tetracycline-inducible manner. An agonist of the mouse stimulator of interferon (IFN) genes (STING), 5,6-dimethylxanthenone-4-acetic acid (DMXAA), was found to induce a robust cytokine response in macrophages that efficiently suppressed HBV replication in mouse hepatocytes by reducing the amount of cytoplasmic viral nucleocapsids. Profiling of cytokines induced by DMXAA and agonists of representative Toll-like receptors (TLRs) in mouse macrophages revealed that, unlike TLR agonists that induced a predominant inflammatory cytokine/chemokine response, the STING agonist induced a cytokine response dominated by type I IFNs. Moreover, as demonstrated in an HBV hydrodynamic mouse model, intraperitoneal administration of DMXAA significantly induced the expression of IFN-stimulated genes and reduced HBV DNA replication intermediates in the livers of mice. This study thus proves the concept that activation of the STING pathway induces an antiviral cytokine response against HBV and that the development of small-molecular human STING agonists as immunotherapeutic agents for treatment of chronic hepatitis B is warranted.

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Smatti, Maria K., Farhan S. Cyprian, Gheyath K. Nasrallah, Asmaa A. Al Thani, Ruba O. Almishal, and Hadi M. Yassine. "Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms." Viruses 11, no. 8 (August 19, 2019): 762. http://dx.doi.org/10.3390/v11080762.

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For a long time, viruses have been shown to modify the clinical picture of several autoimmune diseases, including type 1 diabetes (T1D), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome (SS), herpetic stromal keratitis (HSK), celiac disease (CD), and multiple sclerosis (MS). Best examples of viral infections that have been proposed to modulate the induction and development of autoimmune diseases are the infections with enteric viruses such as Coxsackie B virus (CVB) and rotavirus, as well as influenza A viruses (IAV), and herpesviruses. Other viruses that have been studied in this context include, measles, mumps, and rubella. Epidemiological studies in humans and experimental studies in animal have shown that viral infections can induce or protect from autoimmunopathologies depending on several factors including genetic background, host-elicited immune responses, type of virus strain, viral load, and the onset time of infection. Still, data delineating the clear mechanistic interaction between the virus and the immune system to induce autoreactivity are scarce. Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena. Therefore, a better understanding of the immune-related molecular processes in virus-induced autoimmunity is warranted. Here we provide an overview of the current understanding of viral-induced autoimmunity and the mechanisms that are associated with this phenomenon.

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