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BAR, Hassan. "Hematological Cancer and Viral Infection." Virology & Immunology Journal 8, no. 4 (October 23, 2024): 1–5. http://dx.doi.org/10.23880/vij-16000353.
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Hematological cancer patients are particularly vulnerable to the morbidity and death caused by viral infections. But, it is not well known how common viral infections are or what effects they have on patients undergoing traditional nontransplant treatment. How severe and how long T-cell-mediated immune suppression is determines the variation in viral infection incidence and prognosis between patient groups. Topics covered in this mini-review article include late CMV infection, new viral pathogens (human herpesvirus-6, BK virus, adenovirus, and human metapneumovirus), advancements in molecular diagnostics, and the possibility of novel agents for viral prophylaxis (maribavir) or preemptive therapy (valganciclovir). The infections caused by these viruses have been extensively studied. If we want to understand the range of these viral diseases and come up with effective ways to prevent and cure them, we need well-designed prospective trials. Patients undergoing nontransplant treatment for hematological malignancies are at greater risk for viral infections; this is especially important given the rising use of drugs like alemtuzumab, which cause significant T-cell depletion.
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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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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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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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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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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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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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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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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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Karathanasi, Vassiliki, Malamatenia Bourazani, Christina Orfanou, Savvas Titsinidis, Konstantinos Tosios, Nikolaos Spanakis, and Georgia Vrioni. "Common oral viral infections." ACTA MICROBIOLOGICA HELLENICA 59, no. 1 (March 22, 2014): 29–37. https://doi.org/10.5281/zenodo.10012687.
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Oral cavity as being an "open gate" of the human body comprises an appropriate field for the establishment of varying infections. Oral viral infections can be either primary and localized or secondary to systematic infection. The most common oral viral infections are caused by herpes viruses, enteroviruses and human papilloma viruses. Among herpes viruses, herpes simplex virus 1(HSV-1), vericella-zoster virus (VZV) and Epstein-Barr virus (EBV) affect the oral cavity more frequently. HSV-1 and VZV appear in the form of vesicles that break leaving secondary painful ulcerations. EBV within the development of infectious mononucleosis can cause pharyngo-amygdaligitis, periamygdalic apostemas, ulcerative necrotizing gingivitis and atypical ulcerations and petechiae of the palate. Additionally, EBV is the causing factor of oral hairy leukoplakia, a painless whitish lesion of the lateral tongue borders that comprises a pathognomonic feature of HIV infection. Coxsackie viruses are the main enteroviruses that affect oral mucosa and might develop herpetic angina or mouth-hand-foot disease that is characterized by the simultaneous development of the maculopapular exanthema in mouth, hands and feet. Finally, HPV oral infection is primarily sexually transmitted and leads to the development of either benign tumors such as papillomas and condylomata or oral squamous cell carcinoma depending on the virus type involved in the infection. Diagnosis of oral viral infection is accomplished by the combination of a thorough medical and dental history, clinical examination and the application of adequate laboratory tests. The knowledge of the common oral viral infections is necessary as they can be the first clinical manifestation of an underlying systematic disease. Thus, the correct and immediate diagnosis of the oral viral infection might contribute to the treatment success and improve the prognosis and the quality of life of the patient.
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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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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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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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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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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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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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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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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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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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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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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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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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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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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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Jones, Brent D., Eli J. Kaufman, and Alison J. Peel. "Viral Co-Infection in Bats: A Systematic Review." Viruses 15, no. 9 (June 7, 2023): 1860. https://doi.org/10.5281/zenodo.13446073.
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(Uploaded by Plazi for the Bat Literature Project) 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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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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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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Khajuria, Atul, Parmila Malik, Jyotsana Khattri, Lalit Singh, and Veeresh VG. "Prevalence of thrombocytopenia in patients with viral infection across different cities in India." Panacea Journal of Medical Sciences 14, no. 3 (December 15, 2024): 771–74. https://doi.org/10.18231/j.pjms.2024.137.
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Thrombocytopenia, which signifies a low platelet count usually below 150 × 109/L, is a common finding following or during many viral infections. Viral infection innate and adapt immune response where platelets play a passive role in antiviral activity. The patients with viral infection are at risk of developing decreased platelet count and develop the chance of bleeding. The present study designed to find the prevalence of thrombocytopenia in patients with viral infection. : A descriptive cross section survey design used to identify the prevalence rate of thrombocytopenia in patients with viral infection in India the cities studied are Lakhimpur 960 patients, Panipat 1345 patients, Sonipat 1357 patients, Gohana 758 patients, Delhi 1165 patients, a total 5585 patients diagnosed with viral infection samples were selected of which 395 patients developed thrombocytopenia, the samples were analyzed at various selected diagnostic centers.: The present study found that in Lakhimpur for 960 patients with viral infection 48 patients samples developed thrombocytopenia, Panipat for 1345 patients with viral infection 118 patients samples developed thrombocytopenia, Sonipat for 1357 patients with viral infection 85 patients samples developed thrombocytopenia, Gohana for 758 patients with viral infection 49 patients samples developed thrombocytopenia and in Delhi for 1165 patients with viral infection 95 patients samples developed thrombocytopenia respectively. The overall prevalence of thrombocytopenia among patients with viral infection is 7.07%. Viral infection caused due to any virus triggers the immune response where in platelets act as passive bystanders during viral infection, the knowledge of viral infection and better management of infection bring down the thrombolytes and cause thrombocytopenia. The present study identified the prevalence of the thrombocytopenia among patients with viral infection.
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Wilson, Elizabeth, and David Brooks. "Blockade of chronic type I interferon signaling to control persistent virus infection (P6048)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 49.7. http://dx.doi.org/10.4049/jimmunol.190.supp.49.7.
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Abstract While both immunostimulatory and inhibitory signals are triggered by acute viral infections, persistent infections are characterized by sustained expression of an immunosuppressive program that inhibits antiviral immunity, interferes with viral clearance, and poses a barrier to effective antiviral therapeutics. However, the signals that govern the immunosuppressive program are not understood. Viral infections elicit type I interferons (IFN-I) and these proteins have potent direct antiviral effects. However, IFN-I expression has also been associated with hyper immune activation and increased disease severity in persistent viral infections. We demonstrate that antibody blockade of IFN-I signaling diminished chronic immune activation, and the immunosuppressive program, while increasing multiple immune parameters associated with control of virus replication, ultimately allowing for clearance of the persistent infection. These data highlight the duality of the IFN-I response during viral infection-serving both as a direct extinguisher of viral replication and as a central rheostat and regulator of the immunosuppressive program, dampening T cell responses and preventing viral clearance. Thus, we identify IFN-I as a key factor in immuno-surveillance during viral infection and demonstrate that therapeutic ablation of chronic IFN-I signaling can enable control of persistent viral infection.
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Kwok, Chun Shing, Kirellos Said Abbas, Adnan I. Qureshi, Duwarakan Satchithananda, and Josip Andelo Borovac. "The Impact of Concomitant Diagnosis of Viral Infections on in-Hospital Mortality in Patients Hospitalized with a Diagnosis of Heart Failure in the United States: Insights from the National Inpatient Sample." Viruses 14, no. 11 (October 31, 2022): 2418. http://dx.doi.org/10.3390/v14112418.
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The impact of viral infections on patients admitted with a diagnosis of heart failure is not well understood. We conducted a retrospective cohort study using data from the National Inpatient Sample in the United States to evaluate the proportion of admissions with a diagnosis of heart failure and viral infections, and we explored how viral infections had impact on in-hospital mortality and length of stay. There were a total of 20,713,539 admission records with a diagnosis of heart failure included in the analysis and 3.8% had a concomitant diagnosis of viral infection. The mean length of stay was 20.1 ± 26.9 days, 12.9 ± 13.6 days, 12.1 ± 13.8 days, and 5.1 ± 6.5 days for records with a diagnosis of cytomegalovirus, viral meningitis/encephalitis, herpes simplex infection, and no viral infection, respectively. The most common diagnoses of viral infections were influenza (n = 240,260) and chronic viral hepatitis (n = 194,400), and the highest rates of mortality were observed for records with a diagnosis of cytomegalovirus (13.2%), acute viral hepatitis (12.5%), and viral meningitis/encephalitis (11.1%). The viral infections significantly associated with increased odds of mortality were cytomegalovirus infection (OR 1.84 95% CI 1.57–2.16), acute hepatitis (OR 1.29 95% CI 1.15–1.45), and HIV (OR 1.22 95% CI 1.11–1.34). In conclusion, viral infections are co-diagnosis in 3.8% of patient records with heart failure and detection of some viruses may be important as they increase mortality and may prolong length of stay in hospital.
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Baz, Rachid, Sagar Lonial, Mohamad Hussein, Arlene S. Swern, and Meletios A. Dimopoulos. "Lenalidomide (LEN) Therapy In Combination with Dexamethasone (DEX) Is Associated with a Low Incidence of Viral Infections." Blood 116, no. 21 (November 19, 2010): 1950. http://dx.doi.org/10.1182/blood.v116.21.1950.1950.
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Abstract Abstract 1950 Background: Multiple myeloma (MM) is associated with compromised immune function, involving both humoral and cellular mechanisms, and infections are a common problem. The risk of opportunistic infection is higher in relapsed/refractory (RR) MM due to the cumulative immunosuppression associated with prior therapies. Opportunistic viral infections, such as herpes zoster, occur in 5–13% of MM patients (pts) versus < 1% in the general population. LEN improves immune function by enhancing antigen-specific CD8+ T-cell proliferation, cytokine production and cytotoxicity, and natural killer cell activity. LEN+DEX has shown a predictable safety profile in pts with RRMM, but is associated with higher rates of grade (G) 3/4 neutropenia versus DEX alone. Although G3/4 neutropenia is 30–41%, the rate of G3/4 febrile neutropenia is low (3.4%; Dimopoulos M, et al. N Eng J Med 2007;357:2123-32; Weber D, et al. N Eng J Med 2007;357:2133-42). The occurrence of viral infections in this setting has not been formally evaluated. Methods: This subanalysis is based on pooled data for pts treated with LEN+DEX from two pivotal, large, phase 3 registration studies (MM-009 and MM-010). The median duration of follow-up in all surviving pts as of data cutoff on July 2008 for MM009 and March 2008 for MM010 was 48 months. In these two studies, pts were randomized to receive either LEN 25 mg or placebo (PBO) on days 1–21 and oral DEX 40 mg on days 1–4, 9–12, and 17–20 for the first 4 cycles, after which DEX was administered on days 1–4 only of each 28-day cycle. Neutropenia was managed with dose adjustments and G-CSF per protocol. Protocol did not specify antiviral prophylaxis during the study. Pts diagnosed with relevant viral infection were included in this analysis and categorized as follows: herpes simplex infections (viral conjunctivitis not otherwise specified [NOS], herpes simplex, herpes viral infection NOS, herpes stomatitis), herpes zoster infections (herpes zoster, herpes zoster ophthalmic), and other viral infections (viral infection NOS). The same adverse events (AEs) but within a different time period or with a change in severity were counted as separate events. Viral infection events include the categories of herpes simplex, herpes zoster, and other viral infections. Results: Of 351 pts treated with PBO+DEX, 37 pts (11%) had 45 viral infection events; 4/45 (9%) were G3/4. Of 353 pts treated with LEN+DEX, 42 pts (12%) had viral infection events with 26 (7.4%) having herpes simplex, 20 (5.7%) herpes zoster, and 6 (1.7%) other viral infections. Among these 42 pts, 77 viral infection events were reported; 7/77 (9%) were G3/4. When events were adjusted for pt-months, overall incidence of viral infection was significantly lower with LEN+DEX versus PBO+DEX (0.9 vs 2.0 events per 100 pt-months; P < 0.01). The median time to both first viral infection event and first G3/4 viral infection event was 5 months. The median duration of G3/4 infection was 14 days. Four pts (1%) experienced 5 serious AEs with a median duration of 11 days. The occurrence of viral infection events remained constant over time with LEN+DEX, and did not increase during the duration of therapy. Conclusions: LEN+DEX therapy is associated with a low incidence of viral infection and the incidence remained constant over the duration of therapy. The incidence of viral infections on LEN+DEX is significantly lower, despite a large number of pts who crossed over from PBO+DEX to the LEN+DEX arm. These data support the predictable safety profile of LEN+DEX, thereby supporting lenalidomide continuous therapy in pts with RRMM. Disclosures: Baz: Celgene Corporation: Membership on an entity's Board of Directors or advisory committees, Research Funding. Lonial:Novartis: Consultancy; BMS: Consultancy; Millennium Pharmaceuticals: Consultancy, Research Funding; Celgene Corporation: Consultancy. Hussein:Celgene Corporation: Employment. Swern:Celgene Corporation: Employment. Dimopoulos:Celgene Corporation: Honoraria.
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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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Brooks, David G., Dorian B. McGavern, and Michael B. Oldstone. "IL-10 blockade resurrects T cell activity and eliminates a persistent viral infection (46.3)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S61. http://dx.doi.org/10.4049/jimmunol.178.supp.46.3.
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Abstract By definition persistent viral infections are accompanied by immune evasion, and most notably the failure to sustain robust T cell responses, responses that are essential to control of these infections. Identifying and understanding the immunoregulatory mechanisms that direct productive versus abortive T cell responses to viral infections is critical, but currently unclear. Using the model of persistent lymphocytic choriomeningitis virus (LCMV) infection, we found that upregulation of interleukin (IL)-10 early during infection induces T cell exhaustion and directly leads to viral persistence. Blockade of IL-10 activity induced sustained T cell function, the rapid elimination of an otherwise persistent virus infection and development of functional memory T cells capable of preventing re-infection. Antibody blockade of the IL-10 receptor during the chronic phase of infection restored T cell activity and eliminated an established persistent viral infection. Further, by manipulating this immunoregulatory molecule we significantly enhance immune responses to vaccination, indicating a potential “adjuvant” role to anti-IL10 immunotherapy. Thus, we propose a novel therapy to treat persistent viral infection by targeting host immunoregulatory molecules and reactivating antiviral T cells.
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Imanbayeva, Lira. "A CLINICAL CASE OF A LETHAL OUTCOME OF VIRAL HEPATITIS A AGAINST THE BACKGRAUND OF SEVERE FORM OF HERPES INFECTION." Alatoo Academic Studies 21, no. 3 (September 30, 2021): 354–59. http://dx.doi.org/10.17015/aas.2021.213.038.
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To date, among viral infections, herpes infections in terms of morbidity occupy a leading position in both children and adults. According to the WHO, this infection is the second most common viral infection after influenza. Herpes viruses are capable of infecting almost all organs and systems of the human body, causing acute, chronic and latent forms of infection. Herpes viruses are hepatotropic and can cause severe fatal hepatitis. In recent decades, not only an increase in morbidity has been observed everywhere, but, unfortunately, there has been an increase in the number of mortalities, which is explained by their widespread distribution and difficulties in diagnosis.
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Kane, Melissa, and Tatyana Golovkina. "Common Threads in Persistent Viral Infections." Journal of Virology 84, no. 9 (December 2, 2009): 4116–23. http://dx.doi.org/10.1128/jvi.01905-09.
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ABSTRACT Most viral infections are self-limiting, resulting in either clearance of the pathogen or death of the host. However, a subset of viruses can establish permanent infection and persist indefinitely within the host. Even though persisting viruses are derived from various viral families with distinct replication strategies, they all utilize common mechanisms for establishment of long-lasting infections. Here, we discuss the commonalities between persistent infections with herpes-, retro-, flavi-, arena-, and polyomaviruses that distinguish them from acutely infecting viral pathogens. These shared strategies include selection of cell subsets ideal for long-term maintenance of the viral genome, modulation of viral gene expression, viral subversion of apoptotic pathways, and avoidance of clearance by the immune system.
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Steele, Harrison, Andrew J. Tague, and Danielle Skropeta. "The Role of Sialylation in Respiratory Viral Infection and Treatment." Current Medicinal Chemistry 28, no. 26 (September 8, 2021): 5251–67. http://dx.doi.org/10.2174/0929867328666210201153901.
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Respiratory infections caused by viruses such as influenza and coronavirus are a serious global problem due to their high infection rates and potential to spark pandemics, such as the current COVID-19 pandemic. Although preventing these infections by using vaccines has been the most successful strategy to date, effective vaccines are not always available. Therefore, developing broad-spectrum anti-viral drugs to treat such infections is essential, especially in the case of immunocompromised patients or for outbreaks of novel virus strains. Sialic acids have been highlighted as a key molecule in the viral infection cycle, with terminally sialylated glycans acting as a target for several viral proteins involved in infection, particularly respiratory infection. Inhibitors of one such protein, neuraminidase, are the only anti-influenza drugs currently on the market. Problems with neuraminidase inhibitors, including the development of resistance and a relatively narrow spectrum of activity, drive the need for an improved understanding of the viral infection cycle and the development of more resilient, broader-spectrum anti-viral treatments. Hence, this review outlines the various roles played by sialic acids in respiratory viral infection and provides examples of drugs that exploit sialic acids to inhibit viral infections. It has been concluded that drugs targeting host cell expression of sialic acid could be especially well suited to inhibiting a broad spectrum of respiratory infections. This warrants the continued design and improvement of such drugs in an attempt to lessen the burden of respiratory infections.
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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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Ephraim, Richard K. D. "Prevalence of Hepatitis B, C and HIV infections among haemodialysis patients at the Cape Coast Teaching Hospital, Ghana; A retrospective study." Annals of Medical Laboratory Science 2, no. 1 (March 30, 2022): 42–51. http://dx.doi.org/10.51374/annalsmls.2022.2.1.0057.
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Background: End stage renal disease (ESRD) patients undergoing hemodialysis could be at a higher risk of acquiring viral infections such as hepatitis B, C (HBV, HCV) and human immunodeficiency virus (HIV). The study investigated the prevalence of HBV, HCV, HIV and identified the determinants of these viral infections among end stage renal disease (ESRD) patients undergoing hemodialysis at the Cape Coast Teaching Hospital (CCTH). Methods: This retrospective hospital-based record review was conducted at the CCTH among 89 patients who underwent hemodialysis in at the renal unit of the hospital. The viral infection histories of all the recruited patients were collected as well as clinical and demographic data to identify the determinants of viral infections. Results: Of the 89 patients comprising of 59 (66.3%) males and 30 (33.7%) females, 11(12.4%) were found to be positive for HbsAg, and 6 (6.7%) were found to be positive for HCV infection. Five (5.6%) patients were positive for HIV and 5 (5.6%) participants had co-infection of HBV and HCV. No co-infection of the three viral infections was reported among the participants. Of the various parameters assessed, only average monthly dialysis sessions varied significantly by gender. Univariate logistics regression analysis indicated that HCV [OR=64.17; 95% CI (6.42-641.41) p<0.001] and HBV [OR=35.45; 95% CI (3.78-332.35) p=0.002] infection was a significant independent risk factor of acquiring HBV and HCV infection respectively. The commonest causes of ESRD among participants were hypertension (54.5%) and chronic glomerulonephritis (27.3%). Conclusion: Prevalence rates of the three viral infections studied were high. The likelihood of getting infected with one viral agent as a result of an already existing viral agent was significant. There is therefore an urgent need for the intensification of health education on the occurrence so as to help curb a possible escalation of the viral infection in the general population.
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Buonsenso, Danilo, Rosa Morello, Francesco Mariani, Bianca Mazzoli, Cristina De Rose, Ilaria Lazzareschi, Francesca Raffaelli, Rita Blandino, Maurizio Sanguinetti, and Piero Valentini. "Utility of Rapid Nasopharyngeal Swab for Respiratory Pathogens in the Diagnosis of Viral Infections in Children Hospitalized with Fever: A Prospective Validation Study to Improve Antibiotic Use." Children 11, no. 2 (February 9, 2024): 225. http://dx.doi.org/10.3390/children11020225.
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Introduction: Fever is among the most common reason for medical assessment and antibiotic prescription in practice. The aim of this study was to evaluate positive and negative predictive values of rapid nasopharyngeal swabs for respiratory pathogens to discriminate viral from bacterial infections. Methods: We prospectively tested children with signs and/or symptoms of infections (e.g., fever, cough, wheezing, suspected urinary tract infection) admitted to a paediatric department. Following discharge, clinical phenotypes were assigned defining a cohort of children having probable/certain viral infection, probable/certain bacterial infection, other inflammatory conditions or healthy controls. Results: In this study, 190 children were enrolled (50.5% females, median age 30.5 (8–86) months). In total, 102 patients (53.7%) were affected by respiratory viral infections, 16 (8.4%) by bacterial infections, 29 (15.3%) were healthy controls and 43 (22.6%) were affected by another pathological condition manifested with fever. In total, 84.3% of patients classified as viral infection tested positive for viruses, compared with 18.8% of patients with bacterial infection (p < 0.001), 18.6% of patients with other condition (p < 0.001) and 17.2% of control patients (p < 0.001). The positive predictive value of NPSs in the diagnosis of viral infection was 88.6% and the negative predictive value was 75.0%. Conclusion: Our findings suggest that rapid NPS tests for respiratory viruses are a useful tool to confirm viral infections in children with fever and improve antibiotic use.
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A. P., Krithika, and Ramya R. "Acute Pancreatitis: a late complication of dengue fever." International Journal of Contemporary Pediatrics 5, no. 2 (February 22, 2018): 676. http://dx.doi.org/10.18203/2349-3291.ijcp20180581.
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Acute pancreatitis following viral infection is rare in children. Acute pancreatitis complicating viral infections has been described in the form of isolated case reports and small series. The commonly implicated viral infections have been coxsackie virus, hepatitis viruses, mumps, varicella, herpes simplex and cytomegalovirus. However, the etio- pathogenesis of pancreatitis in viral infections remains unclear. Also, the natural history of such pancreatitis has not been adequately studied. Here we present a case of acute pancreatitis following dengue infection.
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Liang, Zhuoxin, Wenqiang Zhang, Yongjiang Jiang, Ping Wu, Senxiong Zhang, Shaolin Xu, Jinjian Fu, and Eric McGrath. "Clinical Impact of Combined Viral and Bacterial Infection in Pediatric Mycoplasmal Community-Acquired Pneumonia in Western China." Nanoscience and Nanotechnology Letters 12, no. 11 (November 1, 2020): 1315–22. http://dx.doi.org/10.1166/nnl.2020.3237.
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Community-acquired pneumonia (CAP) refers to an infection contracted outside the hospital that leads to lung parenchyma inflammation. The clinical characteristics of Mycoplasma pneumoniae (M. pneumoniae) infection in CAP patients were rarely reported. The aim of this study was to describe the clinical characteristic and the impact of co-infections of M. pneumoniae with viral and bacterial pathogens in hospitalized children with CAP in Liuzhou, China. This study retrospects children diagnosed with CAP due to M. pneumoniae infection at a tertiary maternal and child health care hospital. Data related to co-infection pathogens, demographics, clinical characteristics, and hospitalization cost were collected from the electronic medical system in this hospital. A total of 983 children were diagnosed with mycoplasmal CAP in 2017. Among them, 18.2% had a bacterial-M. pneumoniae co-infection and 11.3% had a viral-M. pneumoniae co-infection. The highest infection rate of M. pneumoniae was 19.1% in February and March, while the highest rates of bacterial-M. pneumoniae and viral-M. pneumoniae co-infections were 3.6% in December and 2.3% in January, respectively. The prevalence of coughing and wheezing had significant differences between the bacterial- or viral-M. pneumoniae co-infections and the mono-infection groups. Furthermore, the chest X-ray progression, pleural effusions, respiratory failure, and ventilation rates were higher in the respiratory viral- and bacterial-M. pneumoniae co-infection groups than in the mono-infection group. Children with a bacterial or respiratory viral co-infection had a longer hospitalization and spent more on treatment fees than those with a M. pneumoniae mono-infection (P value <0.001). We conclude that children with mycoplasmal CAP, either with a bacterial or viral co-infection, who show signs of coughing and wheezing and have a radiographic progression, will have a severe disease progression and should be specifically treated and managed.
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Czuppon, Peter, Florence Débarre, Antonio Gonçalves, Olivier Tenaillon, Alan S. Perelson, Jérémie Guedj, and François Blanquart. "Success of prophylactic antiviral therapy for SARS-CoV-2: Predicted critical efficacies and impact of different drug-specific mechanisms of action." PLOS Computational Biology 17, no. 3 (March 1, 2021): e1008752. http://dx.doi.org/10.1371/journal.pcbi.1008752.
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Repurposed drugs that are safe and immediately available constitute a first line of defense against new viral infections. Despite limited antiviral activity against SARS-CoV-2, several drugs are being tested as medication or as prophylaxis to prevent infection. Using a stochastic model of early phase infection, we evaluate the success of prophylactic treatment with different drug types to prevent viral infection. We find that there exists a critical efficacy that a treatment must reach in order to block viral establishment. Treatment by a combination of drugs reduces the critical efficacy, most effectively by the combination of a drug blocking viral entry into cells and a drug increasing viral clearance. Below the critical efficacy, the risk of infection can nonetheless be reduced. Drugs blocking viral entry into cells or enhancing viral clearance reduce the risk of infection more than drugs that reduce viral production in infected cells. The larger the initial inoculum of infectious virus, the less likely is prevention of an infection. In our model, we find that as long as the viral inoculum is smaller than 10 infectious virus particles, viral infection can be prevented almost certainly with drugs of 90% efficacy (or more). Even when a viral infection cannot be prevented, antivirals delay the time to detectable viral loads. The largest delay of viral infection is achieved by drugs reducing viral production in infected cells. A delay of virus infection flattens the within-host viral dynamic curve, possibly reducing transmission and symptom severity. Thus, antiviral prophylaxis, even with reduced efficacy, could be efficiently used to prevent or alleviate infection in people at high risk.
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Zawitkowska, Joanna, Katarzyna Drabko, Krzysztof Czyżewski, Magdalena Dziedzic, Kamila Jaremek, Patrycja Zalas-Więcek, Anna Szmydki-Baran, et al. "Viral Infection Profile in Children Treated for Acute Lymphoblastic Leukemia—Results of Nationwide Study." Pathogens 11, no. 10 (September 24, 2022): 1091. http://dx.doi.org/10.3390/pathogens11101091.
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Viral infections can be a serious complication of therapy in children with acute lymphoblastic leukemia (ALL). In this study, we focused on the incidence and the profile of viral infection in children with ALL treated in 17 pediatric oncology centers in Poland in the two-year periods of 2018–2019 and 2020–2021. We also compared the frequency of viral infections in 2018–2019 to that in 2020–2021. In 2020–2021, a total of 192 children with ALL had a viral infection during intensive chemotherapy. A total number of 312 episodes of viral infections were diagnosed. The most common infections detected in the samples were: COVID-19 (23%), rhinovirus (18%), and respiratory syncytial virus (14%). COVID-19 and BK virus infections were the reason for the death 1% of all patients. In 2018–2019, a total of 53 ALL patients who had a viral infection were reported and 72 viral events were observed, mainly adenovirus (48.6%), rotavirus (31.9%), and herpes zoster (8.3%). No deaths were reported during this period. The cumulative incidence of viral infections in 2018–2019 was 10.4%, while for 2020–2021, it was 36.7%. In conclusion, a high incidence of COVID-19 infection was observed among pediatric patients with ALL in Poland. The mortality rate in our material was low. The viral profile in ALL children undergoing chemotherapy can be useful for clinicians to improve prophylactic and therapeutic strategies.
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Yao, W., L. Hertel, and L. M. Wahl. "Dynamics of recurrent viral infection." Proceedings of the Royal Society B: Biological Sciences 273, no. 1598 (May 23, 2006): 2193–99. http://dx.doi.org/10.1098/rspb.2006.3563.
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In chronic viral infection, low levels of viral replication and infectious particle production are maintained over long periods, punctuated by brief bursts of high viral production and release. We apply well-established principles of modelling virus dynamics to the study of chronic viral infection, demonstrating that a model which incorporates the distinct contributions of cytotoxic T lymphocytes (CTLs) and antibodies exhibits long periods of quiescence followed by brief bursts of viral production. This suggests that for recurrent viral infections, no special mechanism or exogenous trigger is necessary to provoke an episode of reactivation; rather, the system may naturally cycle through recurrent episodes at intervals which can be many years long. We also find that exogenous factors which cause small fluctuations in the natural course of the infection can trigger a recurrent episode. Our model predicts that longer periods between recurrences are associated with more severe viral episodes. Four factors move the system towards less frequent, more severe episodes: decreased viral infectivity, decreased CTL efficacy, decreased memory T cell response and increased antibody efficacy.
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Diniz, Edna Maria de Albuquerque, Renata Amato Vieira, Maria Esther Jurfest Ceccon, Maria Akiko Ishida, and Flávio Adolfo Costa Vaz. "Incidence of respiratory viruses in preterm infants submitted to mechanical ventilation." Revista do Instituto de Medicina Tropical de São Paulo 47, no. 1 (February 2005): 37–44. http://dx.doi.org/10.1590/s0036-46652005000100007.
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The objectives of this study were to determine the incidence of infection by respiratory viruses in preterm infants submitted to mechanical ventilation, and to evaluate the clinical, laboratory and radiological patterns of viral infections among hospitalized infants in the neonatal intensive care unit (NICU) with any kind of acute respiratory failure. Seventy-eight preterm infants were studied from November 2000 to September 2002. The newborns were classified into two groups: with viral infection (Group I) and without viral infection (Group II). Respiratory viruses were diagnosed in 23 preterm infants (29.5%); the most frequent was respiratory syncytial virus (RSV) (14.1%), followed by influenza A virus (10.2%). Rhinorrhea, wheezing, vomiting and diarrhea, pneumonia, atelectasis, and interstitial infiltrate were significantly more frequent in newborns with nosocomial viral infection. There was a correlation between nosocomial viral infection and low values of C-reactive protein. Two patients with mixed infection from Group I died during the hospital stay. In conclusion, RSV was the most frequent virus in these patients. It was observed that, although the majority of viral lower respiratory tract infections had a favorable course, some patients presented a serious and prolonged clinical manifestation, especially when there was concomitant bacterial or fungal infection.
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Miller, Sara E. "Aids-Associated Viral Infections." Microscopy and Microanalysis 5, S2 (August 1999): 1098–99. http://dx.doi.org/10.1017/s143192760001881x.
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Infection with human immunodeficiency virus (HIV) eventually causes a profound decrease in the body's ability to eradicate or control infections with microorganisms, including viruses. Some infections in AIDS patients are due to common organisms which are of little significance in immunocompetent individuals. Other organisms can be harbored continuously, occasionally causing disease, but normally being suppressed after a heightened immune defense; in AIDS patients, these infections can be life-threatening. Further, practices that predispose to HIV infection also permit entry of other organisms, such as hepatitis and herpesviruses. Electron microscopy is beneficial as an adjunct to other modalities for viral detection. Methods for identifying viruses, both in fluids by negative staining and in tissues by thin sectioning, have been published. Some viral pathogens, including HIV itself, are best documented by other means.HIV has been demonstrated by EM in infected individuals, but because it destroys and makes scarce the cells for which it has an affinity, it is difficult to find them.
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Swaminath, Sharmada, and Alistair B. Russell. "The use of single-cell RNA-seq to study heterogeneity at varying levels of virus–host interactions." PLOS Pathogens 20, no. 1 (January 18, 2024): e1011898. http://dx.doi.org/10.1371/journal.ppat.1011898.
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The outcome of viral infection depends on the diversity of the infecting viral population and the heterogeneity of the cell population that is infected. Until almost a decade ago, the study of these dynamic processes during viral infection was challenging and limited to certain targeted measurements. Presently, with the use of single-cell sequencing technology, the complex interface defined by the interactions of cells with infecting virus can now be studied across the breadth of the transcriptome in thousands of individual cells simultaneously. In this review, we will describe the use of single-cell RNA sequencing (scRNA-seq) to study the heterogeneity of viral infections, ranging from individual virions to the immune response between infected individuals. In addition, we highlight certain key experimental limitations and methodological decisions that are critical to analyzing scRNA-seq data at each scale.
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Deng, Xufang, Monika Evdokimova, Amornrat O’Brien, Cynthia L. Rowe, Nina M. Clark, Amanda Harrington, Gail E. Reid, Susan L. Uprichard, and Susan C. Baker. "Breakthrough Infections with Multiple Lineages of SARS-CoV-2 Variants Reveals Continued Risk of Severe Disease in Immunosuppressed Patients." Viruses 13, no. 9 (September 1, 2021): 1743. http://dx.doi.org/10.3390/v13091743.
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The pandemic of COVID-19 caused by SARS-CoV-2 infection continues to spread around the world. Vaccines that elicit protective immunity have reduced infection and mortality, however new viral variants are arising that may evade vaccine-induced immunity or cause disease in individuals who are unable to develop robust vaccine-induced responses. Investigating the role of viral variants in causing severe disease, evading vaccine-elicited immunity, and infecting vulnerable individuals is important for developing strategies to control the pandemic. Here, we report fourteen breakthrough infections of SARS-CoV-2 in vaccinated individuals with symptoms ranging from asymptomatic/mild (6/14) to severe disease (8/14). High viral loads with a median Ct value of 19.6 were detected in the nasopharyngeal specimens from subjects regardless of disease severity. Sequence analysis revealed four distinct virus lineages, including alpha and gamma variants of concern. Immunosuppressed individuals were more likely to be hospitalized after infection (p = 0.047), however no specific variant was associated with severe disease. Our results highlight the high viral load that can occur in asymptomatic breakthrough infections and the vulnerability of immunosuppressed individuals to post-vaccination infections by diverse variants of SARS-CoV-2.
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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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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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