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Journal articles on the topic 'Viral infection'

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Author: Grafiati

Published: 4 June 2021

Last updated: 18 May 2024

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1

Kumar, Rajiv, and Fatemeh Mohammadipanah. "Nanomedicine, Viral Infection and Cytokine Stor." International Journal of Clinical Case Reports and Reviews 8, no. 4 (September 30, 2021): 01–03. http://dx.doi.org/10.31579/2690-4861/156.

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Recently, emerged outbreaks of various viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), MERS-CoV, and ZIKA infections, are fatal for human life. These life-threatening infections to public health pointed out as a major cause responsible for initiating severe diseases globally. These viral infections heightened the morbidity rates and thus, it is a deadly fear to human life. Researchers left no stone unturned for searching newer therapeutic targets and remedies to treat these viral infections and outbreaks. Simultaneously, some of the researchers have gained success in the discovery of an efficient treatment and development of an effective vaccine [1]. In view of that, numerous developments have been made for innovating nanotherapies, which can treat viral infection and few of them are written off as nanomedicine, have been become reality.

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2

Barroso-González, Jonathan, Laura García-Expósito, Isabel Puigdomènech, Laura de Armas-Rillo, José-David Machado, Julià Blanco, and Agustín Valenzuela-Fernández. "Viral infection." Communicative & Integrative Biology 4, no. 4 (July 2011): 398–408. http://dx.doi.org/10.4161/cib.16716.

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3

Bose, Avirup, Debabrata Saha, and Naba K. Gupta. "Viral Infection." Archives of Biochemistry and Biophysics 342, no. 2 (June 1997): 362–72. http://dx.doi.org/10.1006/abbi.1997.0138.

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4

Saha, Debabrata, Shiyong Wu, Avirup Bose, Nabendu Chatterjee, Arup Chakraborty, Madhumita Chatterjee, and Naba K. Gupta. "Viral Infection." Archives of Biochemistry and Biophysics 342, no. 2 (June 1997): 373–82. http://dx.doi.org/10.1006/abbi.1997.0139.

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5

Han, Mingyuan, Charu Rajput, Tomoko Ishikawa, Caitlin Jarman, Julie Lee, and Marc Hershenson. "Small Animal Models of Respiratory Viral Infection Related to Asthma." Viruses 10, no. 12 (December 1, 2018): 682. http://dx.doi.org/10.3390/v10120682.

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Respiratory viral infections are strongly associated with asthma exacerbations. Rhinovirus is most frequently-detected pathogen; followed by respiratory syncytial virus; metapneumovirus; parainfluenza virus; enterovirus and coronavirus. In addition; viral infection; in combination with genetics; allergen exposure; microbiome and other pathogens; may play a role in asthma development. In particular; asthma development has been linked to wheezing-associated respiratory viral infections in early life. To understand underlying mechanisms of viral-induced airways disease; investigators have studied respiratory viral infections in small animals. This report reviews animal models of human respiratory viral infection employing mice; rats; guinea pigs; hamsters and ferrets. Investigators have modeled asthma exacerbations by infecting mice with allergic airways disease. Asthma development has been modeled by administration of virus to immature animals. Small animal models of respiratory viral infection will identify cell and molecular targets for the treatment of asthma.

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6

Uluğ, Mehmet. "A viral infection of the hands: Orf." Journal of Microbiology and Infectious Diseases 03, no. 01 (March 1, 2013): 41–44. http://dx.doi.org/10.5799/ahinjs.02.2013.01.0078.

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7

Basmaci, Romain, Philippe Bidet, and Stéphane Bonacorsi. "Kingella kingae and Viral Infections." Microorganisms 10, no. 2 (January 21, 2022): 230. http://dx.doi.org/10.3390/microorganisms10020230.

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Kingella kingae (K. kingae) is an oropharyngeal commensal agent of toddlers and the primary cause of osteoarticular infections in 6–23-month-old children. Knowing that the oropharynx of young children is the reservoir and the portal of entry of K. kingae, these results suggested that a viral infection may promote K. kingae infection. In this narrative review, we report the current knowledge of the concomitance between K. kingae and viral infections. This hypothesis was first suggested because some authors described that symptoms of viral infections were frequently concomitant with K. kingae infection. Second, specific viral syndromes, such as hand, foot and mouth disease or stomatitis, have been described in children experiencing a K. kingae infection. Moreover, some clusters of K. kingae infection occurring in daycare centers were preceded by viral outbreaks. Third, the major viruses identified in patients during K. kingae infection were human rhinovirus or coxsackievirus, which both belong to the Picornaviridae family and are known to facilitate bacterial infections. Finally, a temporal association was observed between human rhinovirus circulation and K. kingae infection. Although highly probable, the role of viral infection in the K. kingae pathophysiology remains unclear and is based on case description or temporal association. Molecular studies are needed.

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8

Schabert, Vernon F., Essy Mozaffari, Yi-Chien Lee, and Roman Casciano. "Double-Stranded DNA (dsDNA) Viral Infections Among Allogeneic Hematopoietic Cell Transplant (HCT) Recipients in the First Year after Transplant." Blood 126, no. 23 (December 3, 2015): 3296. http://dx.doi.org/10.1182/blood.v126.23.3296.3296.

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Abstract Introduction: Double-stranded DNA (dsDNA) viral infections (including cytomegalovirus, adenoviruses, BK virus, and Epstein-Barr virus) can lead to significant morbidity and mortality among immunocompromised patients following allogeneic hematopoietic stem cell transplant (HCT). The lack of a broad-spectrum antiviral with the safety and tolerability to prevent viral infections poses management challenges for patients at risk of multiple dsDNA viral infections. Using a large US insurance claims database, this study describes the incidence of dsDNA viral infections and co-infections among allogeneic HCT recipients. Methods: The MarketScan Research Databases were used to identify commercial and Medicare enrollees with an ICD-9 or CPT procedure code for an allogeneic HCT between 7/1/2009 and 6/30/2014. Eligible patients were required to have 365 days of health plan enrollment prior to HCT, but no minimum enrollment was required post-HCT. Incidence of cytomegalovirus (CMV), adenovirus (AdV), BK virus, Epstein-Barr virus, herpes simplex, varicella zoster, and other dsDNA virus infection was measured from the date of the transplant until one year post-transplant. The rates of infection with two dsDNA viral infections or three or more dsDNA viral infections were assessed, and in-hospital mortality or transfer to hospice services within one year of transplant was reported by the number of observed dsDNA viral infection. Results: We identified 3,035 allogeneic HCT patients (mean age 47.3 years, 56.9% male), including 30.4% (n=924) with at least one dsDNA viral infection within the first year post-transplant. Of these, 69.2% had CMV infection (n=639), 5.4% had AdV infection (n=50), and 10.3% had BK virus infection (n=95). Among patients with a reported dsDNA viral infection, 17.6% (n=163) had more than one dsDNA viral infection, including 14.6% (n=135) with two dsDNA viral infections and 3.0% (n=28) with three or more viral infections. A statistically significant increase in the rate of in-hospital death or transfer to hospice within the first year post-transplant was observed for patients with reported dsDNA viral infection vs those without. Specifically, the rate of in-hospital mortality/transfer to hospice increased from 14.9% (315/2111) for patients without a reported dsDNA viral infection to 19.2% (146/761, p=0.0060) with one dsDNA viral infection, 23.0% (31/135, p=0.0121) for patients with two dsDNA viral infections, and 35.7% (10/28, p=0.0023) for patients with three or more dsDNA viral infections. Conclusions: A substantial proportion of allogeneic HCT recipients with a dsDNA viral infection have two or more dsDNA viral infections. Diagnoses on insurance claims may underestimate true incidence of dsDNA viral infection and co-infection. Mortality risk increases significantly with the number of dsDNA viral infections. Availability of a safe and well-tolerated broad spectrum antiviral for prevention of primary or reactivation infections could potentially reduce the morbidity and mortality associated with dsDNA viral infections and their significant sequelae. Disclosures Schabert: LASER Analytica: Employment. Mozaffari:Chimerix Inc.: Employment, Equity Ownership. Lee:LASER Analytica: Employment. Casciano:LASER Analytica: Employment.

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9

Cyr, Peggy R., and William Dexter. "Viral Skin Infection." Physician and Sportsmedicine 32, no. 7 (July 2004): 33–38. http://dx.doi.org/10.3810/psm.2004.07.444.

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10

Dykxhoorn, Derek M., and Judy Lieberman. "Silencing Viral Infection." PLoS Medicine 3, no. 7 (July 25, 2006): e242. http://dx.doi.org/10.1371/journal.pmed.0030242.

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11

CARROLL, D., P. KAMATH, and L. STEWART. "Congenital viral infection?" Lancet 365, no. 9464 (March 25, 2005): 1110. http://dx.doi.org/10.1016/s0140-6736(05)74237-9.

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12

Carroll, DN, P. Kamath, and L. Stewart. "Congenital viral infection?" Lancet 365, no. 9464 (March 2005): 1110. http://dx.doi.org/10.1016/s0140-6736(05)71149-1.

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13

Zeng, Wenwen, and Zhijian J. Chen. "MITAgating Viral Infection." Immunity 29, no. 4 (October 2008): 513–15. http://dx.doi.org/10.1016/j.immuni.2008.09.010.

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14

Ennis, Chris. "Preventing viral infection." Computer Fraud & Security Bulletin 11, no. 12 (October 1989): 11–13. http://dx.doi.org/10.1016/0142-0496(89)90145-8.

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15

Charles Povey, R. "Persistent Viral Infection." Veterinary Clinics of North America: Small Animal Practice 16, no. 6 (November 1986): 1075–95. http://dx.doi.org/10.1016/s0195-5616(86)50130-3.

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16

McIlwain, Benjamin. "Scrambling viral infection." Nature Chemical Biology 19, no. 10 (September 25, 2023): 1173. http://dx.doi.org/10.1038/s41589-023-01441-z.

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17

Mandelia, Yamini, Gary W. Procop, Sandra S. Richter, Sarah Worley, Wei Liu, and Frank Esper. "2627. Dynamics of Respiratory Viral Co-infections: Predisposition for and Clinical Impact of Viral Pairings in Children and Adults." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S916—S917. http://dx.doi.org/10.1093/ofid/ofz360.2305.

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Abstract Background The clinical relevance of respiratory viral co-infections is unclear. Few studies determine epidemiology and impact of specific co-infection pairings. Here we assess the dynamics of respiratory viral co-infections, determine any predisposition for specific pairings to occur and evaluate resulting clinical impact on hospitalization. Methods We reviewed respiratory viral panel results collected at The Cleveland Clinic between November 2013 to Jun 2018. Monthly prevalences, mono-infections and co-infections of 13 viral pathogens were tabulated. Employing a mathematical model which utilized each individual virus’ co-infection rate and prevalence patterns of concurrent circulating respiratory viruses, we calculated an expected number of occurrences for 132 viral pairing permutations. Expected vs observed co-infection occurrences were compared using binomial tests. For viral pairings occurring at significantly higher prevalence than expected, logistic regression models were used to compare hospitalization between patients with co-infection to ones with mono-infection. Results Of 30,535 respiratory samples, 9,843 (32.2%) samples were positive for at least 1 virus and 1,018 (10.82%) were co-infected. Co-infections occurred in 18% of pediatric samples and only 3% of adult samples (P < 0.001). Adenovirus C (ADVC had the highest co-infection rate (68.3%) while influenza B had the lowest (10.07%). Using our model, ADVC – rhinovirus (HRV), RSVA - HRV, and RSVB - HRV pairings occurred at significantly higher prevalence than expected (P < 0.05). In children, HRV-RSVB co-infection were significantly less likely to be hospitalized than patients with HRV mono-infections (ORmono/co = 2.3; 95% CI 1.1 to 4.7; P = 0.028). Additionally, HRV - ADVC co-infected children were less likely to be hospitalized than either HRV (ORmono/co = 3.3; 95% CI 1.6 to 6.8; P < 0.001) or ADVC (ORmono/co = 1.9; 95% CI 1.1 to 3.2; P = 0.024) mono-infected children. Regardless of the infecting virus, children were less likely to be hospitalized than similarly-infected adults. Conclusion Respiratory viral co-infections are largely a pediatric phenomenon. Select viral pairings occur more often than predicted by our model, many of which are associated with altered severity of resultant disease. Disclosures All authors: No reported disclosures.

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18

Cukuranovic, Jovana, Sladjana Ugrenovic, Ivan Jovanovic, Milan Visnjic, and Vladisav Stefanovic. "Viral Infection in Renal Transplant Recipients." Scientific World Journal 2012 (2012): 1–18. http://dx.doi.org/10.1100/2012/820621.

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Viruses are among the most common causes of opportunistic infection after transplantation. The risk for viral infection is a function of the specific virus encountered, the intensity of immune suppression used to prevent graft rejection, and other host factors governing susceptibility. Although cytomegalovirus is the most common opportunistic pathogen seen in transplant recipients, numerous other viruses have also affected outcomes. In some cases, preventive measures such as pretransplant screening, prophylactic antiviral therapy, or posttransplant viral monitoring may limit the impact of these infections. Recent advances in laboratory monitoring and antiviral therapy have improved outcomes. Studies of viral latency, reactivation, and the cellular effects of viral infection will provide clues for future strategies in prevention and treatment of viral infections. This paper will summarize the major viral infections seen following transplant and discuss strategies for prevention and management of these potential pathogens.

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19

Teng, Shaolei, and Qiyi Tang. "ACE2 enhance viral infection or viral infection aggravate the underlying diseases." Computational and Structural Biotechnology Journal 18 (2020): 2100–2106. http://dx.doi.org/10.1016/j.csbj.2020.08.002.

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20

Fournier, P. E., R. Charrel, and D. Raoult. "Viral Endocarditis or Simple Viral Disseminated Infection?" Clinical Infectious Diseases 53, no. 12 (October 25, 2011): 1298. http://dx.doi.org/10.1093/cid/cir681.

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21

Yamaya, Mutsuo. "Virus Infection-Induced Bronchial Asthma Exacerbation." Pulmonary Medicine 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/834826.

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Infection with respiratory viruses, including rhinoviruses, influenza virus, and respiratory syncytial virus, exacerbates asthma, which is associated with processes such as airway inflammation, airway hyperresponsiveness, and mucus hypersecretion. In patients with viral infections and with infection-induced asthma exacerbation, inflammatory mediators and substances, including interleukins (ILs), leukotrienes and histamine, have been identified in the airway secretions, serum, plasma, and urine. Viral infections induce an accumulation of inflammatory cells in the airway mucosa and submucosa, including neutrophils, lymphocytes and eosinophils. Viral infections also enhance the production of inflammatory mediators and substances in airway epithelial cells, mast cells, and other inflammatory cells, such as IL-1, IL-6, IL-8, GM-CSF, RANTES, histamine, and intercellular adhesion molecule-1. Viral infections affect the barrier function of the airway epithelial cells and vascular endothelial cells. Recent reports have demonstrated augmented viral production mediated by an impaired interferon response in the airway epithelial cells of asthma patients. Several drugs used for the treatment of bronchial asthma reduce viral and pro-inflammatory cytokine release from airway epithelial cells infected with viruses. Here, I review the literature on the pathogenesis of the viral infection-induced exacerbation of asthma and on the modulation of viral infection-induced airway inflammation.

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22

Tang, Qiyi, Nadia R. Roan, and Yasuhiro Yamamura. "Seminal Plasma and Semen Amyloids Enhance Cytomegalovirus Infection in Cell Culture." Journal of Virology 87, no. 23 (September 11, 2013): 12583–91. http://dx.doi.org/10.1128/jvi.02083-13.

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Among the modes of transmission available to the cytomegalovirus (CMV) is sexual transmission, primarily via semen. Both male-to-female (M-F) and male-to-male (M-M) sexual transmission significantly contribute toward the spread of CMV infections in the global population. Semen plays an important role in carrying the viral particle that invades the vaginal or rectal mucosa, thereby initiating viral replication. Both semen and seminal plasma (SP) can enhance HIV-1 infection in cell culture, and two amyloid fibrils, semen-derived enhancer of viral infection (SEVI) and amyloids derived from the semenogelins (SEM amyloids), have been identified as seminal factors sufficient to enhance HIV-1 infection (J. Munch et al., Cell131:1059–1071, 2007; N. R. Roan et al., Cell Host Microbe10:541–550, 2011; F. Arnold et al., J. Virol. 86:1244–1249, 2012). Whether SP, SEVI, or SEM amyloids can enhance other viral infections has not been extensively examined. In this study, we found that SP, SEVI, and SEM amyloids strongly enhance both human CMV (HCMV) and murine CMV infection in cell culture. SEVI and SEM amyloids increased infection rates by >10-fold, as determined by both flow cytometry and fluorescence microscopy. Viral replication was increased by 50- to 100-fold. Moreover, viral growth curve assays showed that SP, SEVI, and SEM amyloids sped up the kinetics of CMV replication such that the virus reached its replicative peak more quickly. Finally, we discovered that SEM amyloids and SEVI counteracted the effect of anti-gH in protecting against CMV infection. Collectively, the data suggest that semen enhances CMV infection through interactions between semen amyloid fibrils and viral particles, and these interactions may prevent HCMV from being neutralized by anti-gH antibody.

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Aksoy, S., H. Harputluoglu, S. Kilickap, D. Sener Dede, O. Dizdar, K. Altundag, and I. Barista. "Rituximab-induced viral infections in lymphoma patients." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 18509. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.18509.

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18509 Background: Recently, a chimeric mouse human monoclonal antibody, rituximab, has been used successfully to treat cases of B-cell non-Hodgkin’s lymphoma (NHL) and some autoimmune diseases. However, several viral infections related to rituximab have been reported in literature, but not well characterized. Methods: To further investigate this topic, relevant English language studies were identified through Medline. For our search we used the generic name rituximab, and the key phrases virus/virus infection. The references from the identified articles were reviewed for additional sources. Results: There were 64 previously reported cases (26 male, 23 female, and 15 gender not reported) that had experienced serious viral infection after rituximab treatment. The median age of the cases was 61 years (range; 21–79 years). The median time period from the start of rituximab treatment to viral infection diagnosis was 5.0 months (range, 1–20). Most frequently experienced viral infections were hepatitis B virus infection in 25 (39.1%) cases, Cytomegalovirus infection in 15 (23.4%) cases, varicella zoster infection in 6 (9.4%) cases, and other viral infections in 18 (28.1%) cases. Thirteen (52.0%) of the patients with hepatitis B virus infection died due to hepatic failure. Thirty-nine of the cases had viral infections other than HBV and 13 of them died due to these specific infections. Conclusions: Viral infections after the rituximab treatment in lymphoma patients are important to recognize and treat early because of their association with substantial morbidity and mortality. In these case series, about 40% of these viral infections resulted in death. Close monitoring for viral infections in patients receiving rituximab is necessary. [Table: see text] No significant financial relationships to disclose.

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24

Tong-Minh, Kirby, Katrijn Daenen, Henrik Endeman, Christian Ramakers, Diederik Gommers, Eric van Gorp, and Yuri van der Does. "Performance of the FebriDx Rapid Point-of-Care Test for Differentiating Bacterial and Viral Respiratory Tract Infections in Patients with a Suspected Respiratory Tract Infection in the Emergency Department." Journal of Clinical Medicine 13, no. 1 (December 27, 2023): 163. http://dx.doi.org/10.3390/jcm13010163.

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FebriDx is a rapid point-of-care test combining qualitative measurements of C-reactive protein (CRP) and Myxovirus Resistance Protein A (MxA) using a disposable test device to detect and differentiate acute bacterial from viral respiratory tract infections. The goal of this study was to investigate the diagnostic accuracy of FebriDx in patients with suspected respiratory tract infections in the emergency department (ED). This was an observational cohort study, performed in the ED of an academic hospital. Patients were included if they had a suspected infection. The primary outcome was the presence of a bacterial or viral infection, determined by clinical adjudication by an expert panel. The sensitivity, specificity, and positive and negative predictive value of FebriDx for the presence of bacterial versus non-bacterial infections, and viral versus non-viral infections were calculated. Between March 2019 and November 2020, 244 patients were included. A bacterial infection was present in 41%, viral infection was present in 24%, and 4% of the patients had both viral and bacterial pathogens. FebriDx demonstrated high sensitivity in the detection of bacterial infection (87%), high NPV (91%) to rule out bacterial infection, and high specificity (94%) for viral infection in patients with a suspected infection in the ED.

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Jones, Brent D., Eli J. Kaufman, and Alison J. Peel. "Viral Co-Infection in Bats: A Systematic Review." Viruses 15, no. 9 (August 31, 2023): 1860. http://dx.doi.org/10.3390/v15091860.

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Co-infection is an underappreciated phenomenon in contemporary disease ecology despite its ubiquity and importance in nature. Viruses, and other co-infecting agents, can interact in ways that shape host and agent communities, influence infection dynamics, and drive evolutionary selective pressures. Bats are host to many viruses of zoonotic potential and have drawn increasing attention in their role as wildlife reservoirs for human spillover. However, the role of co-infection in driving viral transmission dynamics within bats is unknown. Here, we systematically review peer-reviewed literature reporting viral co-infections in bats. We show that viral co-infection is common in bats but is often only reported as an incidental finding. Biases identified in our study database related to virus and host species were pre-existing in virus studies of bats generally. Studies largely speculated on the role co-infection plays in viral recombination and few investigated potential drivers or impacts of co-infection. Our results demonstrate that current knowledge of co-infection in bats is an ad hoc by-product of viral discovery efforts, and that future targeted co-infection studies will improve our understanding of the role it plays. Adding to the broader context of co-infection studies in other wildlife species, we anticipate our review will inform future co-infection study design and reporting in bats. Consideration of detection strategy, including potential viral targets, and appropriate analysis methodology will provide more robust results and facilitate further investigation of the role of viral co-infection in bat reservoirs.

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Tobagar, Mawladad, Saeed Khan Sadaqat, and Karimullah Tobagar. "Viral Hepatitis." Journal for Research in Applied Sciences and Biotechnology 2, no. 6 (January 22, 2024): 232–40. http://dx.doi.org/10.55544/jrasb.2.6.33.

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Background: The primary goals of conducting surveillance for viral hepatitis are to direct prevention and control activities for these diseases and to evaluate the impact of these activities. Any person with a hepatitis virus infection is a potential source of infection to others. Surveillance would help accomplish the goals by providing information on: Creating a network of laboratories for diagnosis of viral hepatitis. 2. Monitor trends in incidence of and risk factors for disease. Assess burden of disease 4. Identify infected persons requiring counseling and /or post exposure prophylaxis. 5. Identify and control outbreaks. Methodology: Laboratory based targeted sousveillance in sentinel geographical regions/population. Clinical Case Definition: An acute illness with discrete onset of symptoms (e.g., fatigue, abdominal pain, loss of appetite, intermittent nausea, vomiting), and jaundice. (sourcewww.cdc.gov.in) NCDC will be the nodal agency for implementation of the project. Results: HBV, HCV and HDV are transmitted through contaminated blood or blood components or through the use of contaminated needles and syringes. In several populations, a common route of transmission of HBV infection is from infected pregnant women to their infants around the time of delivery. In many people with HBV or HCV infection, no route of transmission can be identified. In addition, specific vaccines and/or passive immune prophylaxis (use of specific immunoglobulin products) are also useful in preventing transmission of some infections. and also HAV vaccine is the most effective method for specific pre-exposure prophylaxis. and two different vaccines based on inactivated cell culture are available. Both vaccines are highly antigenic, especially in adults, and induce protective antibody levels in more than 95% of recipients after the first dose of vaccine. Individuals at high risk of repeated exposure to HBV, such as personnel Health Care Anti-HBs titer should be evaluated one month after the third dose. An Anti-HBs titer of 10 IU/L (or 10 mIU/mL) is protective. After reaching this titer, there is no need for further booster doses. Conclusion: Viral hepatitis is a systemic infection affecting predominantly the liver and causing its inflammation. It may be acute (recent infection, relatively rapid onset) or chronic. Viral hepatitis is caused by infection with one of the five known hepatotropic viruses, which are named as hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV), respectively. These viruses are quite divergent in their structure, epidemiology, routes of transmission, incubation period, clinical presentations, natural history, diagnosis, and preventive and treatment options.

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27

Ghafouri-Fard, Soudeh, Bashdar Mahmud Hussen, Hazha Hadayat Jamal, Mohammad Taheri, and Guive Sharifi. "The Emerging Role of Non-Coding RNAs in the Regulation of Virus Replication and Resultant Cellular Pathologies." International Journal of Molecular Sciences 23, no. 2 (January 13, 2022): 815. http://dx.doi.org/10.3390/ijms23020815.

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Non-coding RNAs, particularly lncRNAs and miRNAs, have recently been shown to regulate different steps in viral infections and induction of immune responses against viruses. Expressions of several host and viral lncRNAs have been found to be altered during viral infection. These lncRNAs can exert antiviral function via inhibition of viral infection or stimulation of antiviral immune response. Some other lncRNAs can promote viral replication or suppress antiviral responses. The current review summarizes the interaction between ncRNAs and herpes simplex virus, cytomegalovirus, and Epstein–Barr infections. The data presented in this review helps identify viral-related regulators and proposes novel strategies for the prevention and treatment of viral infection.

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28

ICHINOHE, Takesh, and Akiko IWASAKI. "Inflammasomes in viral infection." Uirusu 59, no. 1 (2009): 13–22. http://dx.doi.org/10.2222/jsv.59.13.

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29

Heike, Toshio, and Haruki Mikawa. "Viral Infection and Interferon." Japanese Journal of Clinical Immunology 9, no. 3 (1986): 147–56. http://dx.doi.org/10.2177/jsci.9.147.

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30

Herengt, Angela, Jacob Thyrsted, and Christian K. Holm. "NRF2 in Viral Infection." Antioxidants 10, no. 9 (September 18, 2021): 1491. http://dx.doi.org/10.3390/antiox10091491.

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The transcription factor NRF2 is central to redox homeostasis in animal cells and is a well-known driver of chemoresistance in many types of cancer. Recently, new roles have been ascribed to NRF2 which include regulation of antiviral interferon responses and inflammation. In addition, NRF2 is emerging as an important factor in antiviral immunity through interferon-independent mechanisms. In the review, we give an overview of the scientific progress on the involvement and importance of NRF2 in the context of viral infection.

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31

Hashimoto, Shu, Ken Matsumoto, Yasuhiro Gon, Toshio Ichiwata, Noriaki Takahashi, and Tomoko Kobayashi. "Viral Infection in Asthma." Allergology International 57, no. 1 (2008): 21–31. http://dx.doi.org/10.2332/allergolint.r-07-156.

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32

Kvansakul, Marc. "Viral Infection and Apoptosis." Viruses 9, no. 12 (November 23, 2017): 356. http://dx.doi.org/10.3390/v9120356.

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Schneider-Schaulies, Jürgen, and Sibylle Schneider-Schaulies. "Sphingolipids in viral infection." Biological Chemistry 396, no. 6-7 (June 1, 2015): 585–95. http://dx.doi.org/10.1515/hsz-2014-0273.

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Abstract Viruses exploit membranes and their components such as sphingolipids in all steps of their life cycle including attachment and membrane fusion, intracellular transport, replication, protein sorting and budding. Examples for sphingolipid-dependent virus entry are found for: human immunodeficiency virus (HIV), which besides its protein receptors also interacts with glycosphingolipids (GSLs); rhinovirus, which promotes the formation of ceramide-enriched platforms and endocytosis; or measles virus (MV), which induces the surface expression of its own receptor CD150 via activation of sphingomyelinases (SMases). While SMase activation was implicated in Ebola virus (EBOV) attachment, the virus utilizes the cholesterol transporter Niemann-Pick C protein 1 (NPC1) as ‘intracellular’ entry receptor after uptake into endosomes. Differential activities of SMases also affect the intracellular milieu required for virus replication. Sindbis virus (SINV), for example, replicates better in cells lacking acid SMase (ASMase). Defined lipid compositions of viral assembly and budding sites influence virus release and infectivity, as found for hepatitis C virus (HCV) or HIV. And finally, viruses manipulate cellular signaling and the sphingolipid metabolism to their advantage, as for example influenza A virus (IAV), which activates sphingosine kinase 1 and the transcription factor NF-κB.

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Hope, Thomas J. "Bridging efficient viral infection." Nature Cell Biology 9, no. 3 (March 2007): 243–44. http://dx.doi.org/10.1038/ncb0307-243.

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Crow, T. J. "Maternal viral infection hypothesis." British Journal of Psychiatry 161, no. 4 (October 1992): 570–71. http://dx.doi.org/10.1192/s0007125000129915.

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Waterer, Grant. "Controlling epidemic viral infection." Current Opinion in Infectious Diseases 24, no. 2 (April 2011): 130–36. http://dx.doi.org/10.1097/qco.0b013e328343b720.

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Meckes, D. G., and N. Raab-Traub. "Microvesicles and Viral Infection." Journal of Virology 85, no. 24 (October 5, 2011): 12844–54. http://dx.doi.org/10.1128/jvi.05853-11.

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Luczkowiak, Joanna, Antonio Muñoz, Macarena Sánchez-Navarro, Renato Ribeiro-Viana, Anthony Ginieis, Beatriz M. Illescas, Nazario Martín, Rafael Delgado, and Javier Rojo. "Glycofullerenes Inhibit Viral Infection." Biomacromolecules 14, no. 2 (January 10, 2013): 431–37. http://dx.doi.org/10.1021/bm3016658.

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Tomecki, Kenneth J. "Viral infection and cancer." Journal of the American Academy of Dermatology 36, no. 5 (May 1997): 776. http://dx.doi.org/10.1016/s0190-9622(97)80338-6.

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Morris, J. D. H., A. L. W. F. Eddleston, and T. Crook. "Viral infection and cancer." Lancet 346, no. 8977 (September 1995): 754–58. http://dx.doi.org/10.1016/s0140-6736(95)91510-9.

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Malhotra, R., and R. B. Sim. "Collectins and viral infection." Trends in Microbiology 3, no. 6 (June 1995): 240–44. http://dx.doi.org/10.1016/s0966-842x(00)88932-5.

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Petty, Ross E., and Aubrey J. Tingle. "Arthritis and viral infection." Journal of Pediatrics 113, no. 5 (November 1988): 948–49. http://dx.doi.org/10.1016/s0022-3476(88)80037-4.

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Sullivan, Christopher S., and Don Ganem. "MicroRNAs and Viral Infection." Molecular Cell 20, no. 1 (October 2005): 3–7. http://dx.doi.org/10.1016/j.molcel.2005.09.012.

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Virgin, Herbert W., E. John Wherry, and Rafi Ahmed. "Redefining Chronic Viral Infection." Journal of End-to-End-testing 138, no. 1 (July 10, 2009): 30–50. http://dx.doi.org/10.1016/s9999-9994(09)20378-3.

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Naumenko, Victor, Madison Turk, Craig N. Jenne, and Seok-Joo Kim. "Neutrophils in viral infection." Cell and Tissue Research 371, no. 3 (January 11, 2018): 505–16. http://dx.doi.org/10.1007/s00441-017-2763-0.

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Goldman, Richard, William Lang, and David Lyman. "Acute aids viral infection." American Journal of Medicine 81, no. 6 (December 1986): 1122–23. http://dx.doi.org/10.1016/0002-9343(86)90434-1.

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Ramsay, Margaret. "Viral Infection in Pregnancy." Obstetrician & Gynaecologist 7, no. 2 (April 2005): 142. http://dx.doi.org/10.1576/toag.7.2.142.27087.

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Wang, Janet F. "Hepatitis B Viral Infection." AAOHN Journal 35, no. 10 (October 1987): 430–38. http://dx.doi.org/10.1177/216507998703501002.

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Marsland, Benjamin J., Manfred Kopf, and Graham Le Gros. "Viral infection and allergy." Nature Immunology 5, no. 9 (September 1, 2004): 865. http://dx.doi.org/10.1038/ni0904-865a.

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Saphire, Erica Ollmann, and Paul W. H. I. Parren. "Listening for viral infection." Nature Biotechnology 19, no. 9 (September 2001): 823–24. http://dx.doi.org/10.1038/nbt0901-823.

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