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Статті в журналах з теми "Flavivirus Infection"
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Fontoura, Marina Alves, Rebeca Fróes Rocha, and Rafael Elias Marques. "Neutrophil Recruitment and Participation in Severe Diseases Caused by Flavivirus Infection." Life 11, no. 7 (July 20, 2021): 717. http://dx.doi.org/10.3390/life11070717.
Повний текст джерелаАнотація:
Neutrophils are first-line responders to infections and are recruited to target tissues through the action of chemoattractant molecules, such as chemokines. Neutrophils are crucial for the control of bacterial and fungal infections, but their role in the context of viral infections has been understudied. Flaviviruses are important human viral pathogens transmitted by arthropods. Infection with a flavivirus may result in a variety of complex disease manifestations, including hemorrhagic fever, encephalitis or congenital malformations. Our understanding of flaviviral diseases is incomplete, and so is the role of neutrophils in such diseases. Here we present a comprehensive overview on the participation of neutrophils in severe disease forms evolving from flavivirus infection, focusing on the role of chemokines and their receptors as main drivers of neutrophil function. Neutrophil activation during viral infection was shown to interfere in viral replication through effector functions, but the resulting inflammation is significant and may be detrimental to the host. For congenital infections in humans, neutrophil recruitment mediated by CXCL8 would be catastrophic. Evidence suggests that control of neutrophil recruitment to flavivirus-infected tissues may reduce immunopathology in experimental models and patients, with minimal loss to viral clearance. Further investigation on the roles of neutrophils in flaviviral infections may reveal unappreciated functions of this leukocyte population while increasing our understanding of flaviviral disease pathogenesis in its multiple forms.
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Musso, Didier, and Philippe Desprès. "Serological Diagnosis of Flavivirus-Associated Human Infections." Diagnostics 10, no. 5 (May 14, 2020): 302. http://dx.doi.org/10.3390/diagnostics10050302.
Повний текст джерелаАнотація:
Arthropod-borne viruses (arboviruses) belonging to the Flavivirus genus of the Flaviviridae family, are a major public health threat in tropical and subtropical regions, and have recently become a medical concern in temperate zones. Most flaviviruses are classified as zoonotic viruses. Human flavivirus infections can be asymptomatic, responsible for unspecific symptoms in the first few days following infection, or responsible for severe complications potentially resulting in death. During the first days following symptom onset, laboratory diagnosis of acute human flavivirus infection is mainly based on molecular detection of the viral genome by RT-PCR methods, followed by the capture of specific antibodies using serological tests after the first week of infection. The detection of antibodies that have virus neutralizing activity can be used to confirm flavivirus infection. However, human flavivirus infections induce the production of cross-reactive antibodies, often making serology inconclusive. Indeed, serological diagnosis of flavivirus infection can be hampered by a patient’s history of flavivirus exposure, particularly in regions where multiple antigenically related flaviviruses co-circulate. We focus our mini review on conventional immunoassays that allow the diagnosis of major flavivirus-associated human infections in basic, routine and high-profile central health centers; and the interpretation of diagnostic serology tests for patients living within different epidemiological situations.
3
Wu, Bingan, Zhongtian Qi, and Xijing Qian. "Recent Advancements in Mosquito-Borne Flavivirus Vaccine Development." Viruses 15, no. 4 (March 23, 2023): 813. http://dx.doi.org/10.3390/v15040813.
Повний текст джерелаАнотація:
Lately, the global incidence of flavivirus infection has been increasing dramatically and presents formidable challenges for public health systems around the world. Most clinically significant flaviviruses are mosquito-borne, such as the four serotypes of dengue virus, Zika virus, West Nile virus, Japanese encephalitis virus and yellow fever virus. Until now, no effective antiflaviviral drugs are available to fight flaviviral infection; thus, a highly immunogenic vaccine would be the most effective weapon to control the diseases. In recent years, flavivirus vaccine research has made major breakthroughs with several vaccine candidates showing encouraging results in preclinical and clinical trials. This review summarizes the current advancement, safety, efficacy, advantages and disadvantages of vaccines against mosquito-borne flaviviruses posing significant threats to human health.
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Qiu, Yang, Yan-Peng Xu, Miao Wang, Meng Miao, Hui Zhou, Jiuyue Xu, Jing Kong, et al. "Flavivirus induces and antagonizes antiviral RNA interference in both mammals and mosquitoes." Science Advances 6, no. 6 (February 2020): eaax7989. http://dx.doi.org/10.1126/sciadv.aax7989.
Повний текст джерелаАнотація:
Mosquito-borne flaviviruses infect both mammals and mosquitoes. RNA interference (RNAi) has been demonstrated as an anti-flavivirus mechanism in mosquitoes; however, whether and how flaviviruses induce and antagonize RNAi-mediated antiviral immunity in mammals remains unknown. We show that the nonstructural protein NS2A of dengue virus-2 (DENV2) act as a viral suppressor of RNAi (VSR). When NS2A-mediated RNAi suppression was disabled, the resulting mutant DENV2 induced Dicer-dependent production of abundant DENV2-derived siRNAs in differentiated mammalian cells. VSR-disabled DENV2 showed severe replication defects in mosquito and mammalian cells and in mice that were rescued by RNAi deficiency. Moreover, NS2As of multiple flaviviruses act as VSRs in vitro and during viral infection in both organisms. Overall, our findings demonstrate that antiviral RNAi can be induced by flavivirus, while flavivirus uses NS2A as a bona fide VSR to evade RNAi in mammals and mosquitoes, highlighting the importance of RNAi in flaviviral vector-host life cycles.
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Ke, Po-Yuan. "The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions." International Journal of Molecular Sciences 19, no. 12 (December 7, 2018): 3940. http://dx.doi.org/10.3390/ijms19123940.
Повний текст джерелаАнотація:
Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis. Flavivirus infections underlie multiple human diseases and thus exert an immense burden on public health worldwide. Mounting evidence indicates that host autophagy is subverted to modulate the life cycles of flaviviruses, such as hepatitis C virus, dengue virus, Japanese encephalitis virus, West Nile virus and Zika virus. The diverse interplay between autophagy and flavivirus infection not only regulates viral growth in host cells but also counteracts host stress responses induced by viral infection. In this review, we summarize the current knowledge on the role of autophagy in the flavivirus life cycle. We also discuss the impacts of virus-induced autophagy on the pathogeneses of flavivirus-associated diseases and the potential use of autophagy as a therapeutic target for curing flavivirus infections and related human diseases.
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Zhao, Rong, Meiyue Wang, Jing Cao, Jing Shen, Xin Zhou, Deping Wang, and Jimin Cao. "Flavivirus: From Structure to Therapeutics Development." Life 11, no. 7 (June 25, 2021): 615. http://dx.doi.org/10.3390/life11070615.
Повний текст джерелаАнотація:
Flaviviruses are still a hidden threat to global human safety, as we are reminded by recent reports of dengue virus infections in Singapore and African-lineage-like Zika virus infections in Brazil. Therapeutic drugs or vaccines for flavivirus infections are in urgent need but are not well developed. The Flaviviridae family comprises a large group of enveloped viruses with a single-strand RNA genome of positive polarity. The genome of flavivirus encodes ten proteins, and each of them plays a different and important role in viral infection. In this review, we briefly summarized the major information of flavivirus and further introduced some strategies for the design and development of vaccines and anti-flavivirus compound drugs based on the structure of the viral proteins. There is no doubt that in the past few years, studies of antiviral drugs have achieved solid progress based on better understanding of the flavivirus biology. However, currently, there are no fully effective antiviral drugs or vaccines for most flaviviruses. We hope that this review may provide useful information for future development of anti-flavivirus drugs and vaccines.
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Ledermann, Jeremy P., Maria A. Lorono-Pino, Christine Ellis, Kali D. Saxton-Shaw, Bradley J. Blitvich, Barry J. Beaty, Richard A. Bowen, and Ann M. Powers. "Evaluation of Widely Used Diagnostic Tests To Detect West Nile Virus Infections in Horses Previously Infected with St. Louis Encephalitis Virus or Dengue Virus Type 2." Clinical and Vaccine Immunology 18, no. 4 (February 23, 2011): 580–87. http://dx.doi.org/10.1128/cvi.00201-10.
Повний текст джерелаАнотація:
ABSTRACTPrimary West Nile virus (WNV) infections can be diagnosed using a number of tests that detect infectious particles, nucleic acid, and specific IgM and/or IgG antibodies. However, serological identification of the infecting agent in secondary or subsequent flavivirus infections is problematic due to the extensive cross-reactivity of flavivirus antibodies. This is particularly difficult in the tropical Americas where multiple flaviviruses cocirculate. A study of sequential flavivirus infection in horses was undertaken using three medically important flaviviruses and five widely utilized diagnostic assays to determine if WNV infection in horses that had a previous St. Louis encephalitis virus (SLEV) or dengue virus type 2 (DENV-2) infection could be diagnosed. Following the primary inoculation, 25% (3/12) and 75% (3/4) of the horses mounted antibody responses against SLEV and DENV-2, respectively. Eighty-eight percent of horses subsequently inoculated with WNV had a WNV-specific antibody response that could be detected with one of these assays. The plaque reduction neutralization test (PRNT) was sensitive in detection but lacked specificity, especially following repeated flavivirus exposure. The WNV-specific IgM enzyme-linked immunosorbent assay (IgM ELISA) was able to detect an IgM antibody response and was not cross-reactive in a primary SLEV or DENV response. The WNV-specific blocking ELISA was specific, showing positives only following a WNV injection. Of great importance, we demonstrated that timing of sample collection and the need for multiple samples are important, as the infecting etiology could be misdiagnosed if only a single sample is tested.
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Liao, Ching-Len, Yi-Ling Lin, Bi-Ching Wu, Chang-Huei Tsao, Mei-Chuan Wang, Chiu-I. Liu, Yue-Ling Huang, Jui-Hui Chen, Jia-Pey Wang, and Li-Kuang Chen. "Salicylates Inhibit Flavivirus Replication Independently of Blocking Nuclear Factor Kappa B Activation." Journal of Virology 75, no. 17 (September 1, 2001): 7828–39. http://dx.doi.org/10.1128/jvi.75.17.7828-7839.2001.
Повний текст джерелаАнотація:
ABSTRACT Flaviviruses comprise a positive-sense RNA genome that replicates exclusively in the cytoplasm of infected cells. Whether flaviviruses require an activated nuclear factor(s) to complete their life cycle and trigger apoptosis in infected cells remains elusive. Flavivirus infections quickly activate nuclear factor kappa B (NF-κB), and salicylates have been shown to inhibit NF-κB activation. In this study, we investigated whether salicylates suppress flavivirus replication and virus-induced apoptosis in cultured cells. In a dose-dependent inhibition, we found salicylates within a range of 1 to 5 mM not only restricted flavivirus replication but also abrogated flavivirus-triggered apoptosis. However, flavivirus replication was not affected by a specific NF-κB peptide inhibitor, SN50, and a proteosome inhibitor, lactacystin. Flaviviruses also replicated and triggered apoptosis in cells stably expressing IκBα-ΔN, a dominant-negative mutant that antagonizes NF-κB activation, as readily as in wild-type BHK-21 cells, suggesting that NF-κB activation is not essential for either flavivirus replication or flavivirus-induced apoptosis. Salicylates still diminished flavivirus replication and blocked apoptosis in the same IκBα-ΔN cells. This inhibition of flaviviruses by salicylates could be partially reversed by a specific p38 mitogen-activated protein (MAP) kinase inhibitor, SB203580. Together, these results show that the mechanism by which salicylates suppress flavivirus infection may involve p38 MAP kinase activity but is independent of blocking the NF-κB pathway.
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Wahaab, Abdul, Bahar E. Mustafa, Muddassar Hameed, Nigel J. Stevenson, Muhammad Naveed Anwar, Ke Liu, Jianchao Wei, Yafeng Qiu, and Zhiyong Ma. "Potential Role of Flavivirus NS2B-NS3 Proteases in Viral Pathogenesis and Anti-flavivirus Drug Discovery Employing Animal Cells and Models: A Review." Viruses 14, no. 1 (December 28, 2021): 44. http://dx.doi.org/10.3390/v14010044.
Повний текст джерелаАнотація:
Flaviviruses are known to cause a variety of diseases in humans in different parts of the world. There are very limited numbers of antivirals to combat flavivirus infection, and therefore new drug targets must be explored. The flavivirus NS2B-NS3 proteases are responsible for the cleavage of the flavivirus polyprotein, which is necessary for productive viral infection and for causing clinical infections; therefore, they are a promising drug target for devising novel drugs against different flaviviruses. This review highlights the structural details of the NS2B-NS3 proteases of different flaviviruses, and also describes potential antiviral drugs that can interfere with the viral protease activity, as determined by various studies. Moreover, optimized in vitro reaction conditions for studying the NS2B-NS3 proteases of different flaviviruses may vary and have been incorporated in this review. The increasing availability of the in silico and crystallographic/structural details of flavivirus NS2B-NS3 proteases in free and drug-bound states can pave the path for the development of promising antiflavivirus drugs to be used in clinics. However, there is a paucity of information available on using animal cells and models for studying flavivirus NS2B-NS3 proteases, as well as on the testing of the antiviral drug efficacy against NS2B-NS3 proteases. Therefore, on the basis of recent studies, an effort has also been made to propose potential cellular and animal models for the study of flavivirus NS2B-NS3 proteases for the purposes of exploring flavivirus pathogenesis and for testing the efficacy of possible drugs targets, in vitro and in vivo.
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Habarugira, Gervais, Jasmin Moran, Jessica J. Harrison, Sally R. Isberg, Jody Hobson-Peters, Roy A. Hall, and Helle Bielefeldt-Ohmann. "Evidence of Infection with Zoonotic Mosquito-Borne Flaviviruses in Saltwater Crocodiles (Crocodylus porosus) in Northern Australia." Viruses 14, no. 5 (May 21, 2022): 1106. http://dx.doi.org/10.3390/v14051106.
Повний текст джерелаАнотація:
The risk of flavivirus infections among the crocodilian species was not recognised until West Nile virus (WNV) was introduced into the Americas. The first outbreaks caused death and substantial economic losses in the alligator farming industry. Several other WNV disease episodes have been reported in crocodilians in other parts of the world, including Australia and Africa. Considering that WNV shares vectors with other flaviviruses, crocodilians are highly likely to also be exposed to flaviviruses other than WNV. A serological survey for flaviviral infections was conducted on saltwater crocodiles (Crocodylus porosus) at farms in the Northern Territory, Australia. Five hundred serum samples, collected from three crocodile farms, were screened using a pan-flavivirus-specific blocking ELISA. The screening revealed that 26% (n = 130/500) of the animals had antibodies to flaviviruses. Of these, 31.5% had neutralising antibodies to WNVKUN (Kunjin strain), while 1.5% had neutralising antibodies to another important flavivirus pathogen, Murray Valley encephalitis virus (MVEV). Of the other flaviviruses tested for, Fitzroy River virus (FRV) was the most frequent (58.5%) in which virus neutralising antibodies were detected. Our data indicate that farmed crocodiles in the Northern Territory are exposed to a range of potentially zoonotic flaviviruses, in addition to WNVKUN. While these flaviviruses do not cause any known diseases in crocodiles, there is a need to investigate whether infected saltwater crocodiles can develop a viremia to sustain the transmission cycle or farmed crocodilians can be used as sentinels to monitor the dynamics of arboviral infections in tropical areas.
Дисертації з теми "Flavivirus Infection"
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Gollins, S. W. "Mechanisms of flavivirus neutralization and cellular infection." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355752.
Повний текст джерела
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Dejarnac, Ophélie. "Molecular and cellular basis of phosphatidylserine receptors mediated flavivirus infection." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC297/document.
Повний текст джерелаАнотація:
Le virus de la dengue (DENV) et le virus Zika (ZIKV) sont deux virus transmis par le moustique et responsables de maladies importantes chez l’Homme. En absence de vaccin et de traitements antiviraux efficaces, ces pathogènes représentent des problèmes de santé publique majeurs. Les bases moléculaires des interactions qu’établissent le DENV et ZIKV et la cellule hôte lors de l’entrée virale sont peu connues. Notre laboratoire a récemment identifié, les protéines TIM (TIM-1 et TIM-4) et TAM (Tyro3 et Axl), deux familles de récepteurs à la phosphatidylsérine (PtdSer) impliqués dans la reconnaissance et l’élimination des cellules apoptotiques par phagocytose, comme de nouveaux facteurs d’entrée du DENV. Les récepteurs TIM et TAM permettent l’infection par le DENV en interagissant avec la PtdSer associée aux virions selon un mécanisme similaire à la reconnaissance des cellules apoptotiques (mimétisme apoptotique). L’objectif général de mon travail de thèse a été d’explorer les mécanismes moléculaires et cellulaires par lesquels TIM-1 et Axl médient l’entrée des flavivirus. A l’aide de techniques d’imagerie en temps réel nous avons montré que TIM-1 et DENV sont co-internalisés et que TIM-1 joue un rôle actif dans l’entrée du DENV. Notamment, nous avons montré que deux résidus lysine présentes dans le domaine cytoplasmique de TIM-1 sont importantes pour l’ubiquitination du récepteur et pour l’endocytose du virus. La recherche de partenaires de TIM-1 par des études de spectrométrie de masse a permis d’identifier STAM, un membre du complexe ESCRT-0 impliqué dans le trafic des récepteurs ubiquitinés, comme facteur important pour l’infection. Collectivement, nos résultats suggèrent très fortement que TIM-1 est le premier récepteur bona fide caractérisé pour le DENV.Identifier les facteurs d’entrée du ZIKV représente un enjeu majeur dans la compréhension du tropisme et de la pathogénèse associée à ce virus. Nous avons montré que le récepteur Axl est essentiel pour l’entrée du ZIKV dans les cellules microgliales, les astrocytes du cerveau humain en développement ainsi que dans les fibroblastes de la peau. Nos études ont démontré un double rôle du récepteur Axl dans l’infection par ZIKV. Axl lie et permet l’internalisation des particules virales, mais aussi, contribue à l’établissement d’un environnement favorable à la réplication virale en inhibant la réponse immunitaire innée. En conclusion, ce travail a contribué à améliorer notre compréhension des mécanismes d’entrée des virus DENV et ZIKV. Nos résultats indiquent que ces deux virus exploitent plusieurs récepteurs aux phospholipides pour initier leur cycle infectieux, ce qui pourrait contribuer à l’élargissement de leur tropismeDengue virus (DENV) and ZIKA virus (ZIKV) are two mosquito-borne viruses responsible for important diseases in humans. Since there is currently no vaccine neither antiviral treatment available against these human pathogens, they are two major health concerns. The molecular basis of DENV and ZIKV host cell interactions leading to virus entry are poorly understood, hampering the discovery of new targets for antiviral intervention. Our laboratory recently discovered that TIM (TIM-1 and TIM-4) and TAM (Tyro3 and Axl) proteins, two receptor families that contribute to the phosphatidylserine (PtdSer)-dependent phagocytic removal of apoptotic cells, are DENV entry factors. TIM and TAM receptors mediate DENV infection by interacting with virion-associated PtdSer through a mechanism similar to the recognition and engulfment of apoptotic cells by phagocytes (viral apoptotic mimicry). The general objective of my PhD was to establish a detailed understanding of the molecular mechanisms by which TIM-1 and Axl mediated infection. Using live imaging, we demonstrated that TIM-1 and DENV are co-internalised and TIM-1 play an active role during DENV endocytosis. We showed that TIM-1 cytoplasmic domain is essential for DENV internalization, especially, we identified two lysine residues that are essential for TIM-1 ubiquitination and DENV endocytosis. Proteomic analysis of TIM-1 interacting partners identified STAM, a member of the ESCRT-0 complex involved in intracellular sorting of ubiquitinated cargos, as an essential host factor for DENV infection. Collectively our results establish TIM-1 as the first identified DENV bona fide receptor.Identifying ZIKV entry factors represents a major challenge in the understanding of ZIKV tropism and pathogenesis. We showed that Axl is responsible for ZIKV infection of microglial cells and astrocytes in the human developing brain and primary fibroblasts in human skin, suggesting an important role of this receptor during ZIKV life cycle. We also highlighted the dual role of the Axl receptor in ZIKV infection, which simultaneously promotes viral entry and dampens the innate immune response to facilitate a post entry step of the ZIKV life cycle. In conclusion, this work provided new insights in our understanding of the DENV and ZIKV entry program. Both viruses engage phospholipid receptors for their infectious entry, providing a rational to ascertain therapeutic strategies targeting virion-associated phospholipids
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Nguyen, Jennifer B. "Molecular Mechanisms of Host-Pathogen Interactions in Flavivirus and Hookworm Infection." Thesis, Yale University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3580786.
Повний текст джерелаАнотація:
Microbial pathogens and their hosts have evolved complex adaptations to ensure their individual survival, resulting in a so-called "molecular arms race." While hosts may have acquired diverse mechanisms to protect themselves from the microbial invader, pathogens have developed elaborate strategies to evade and subvert these defenses. Viruses and hookworms are important pathogens which have evolved to successfully invade and infect their human hosts. Although structural biology has provided significant mechanistic insight into these processes of invasion, many specific host-pathogen interactions and their dynamics have not been well studied or characterized.
The work presented in this dissertation clarifies the mechanisms of cellular entry of one particular family of viruses, the flaviviruses, and discusses strategies for viral clearance by host cells. Additional insight into the role of a cytoplasmic DNA sensor, LRRFIP1, in mediating an innate immune response to non-flavivirus microbial infection is presented. Finally, strategies for the development of small-molecule or peptide inhibitors of virus entry and hookworm infection are proposed.
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Ottendorfer, Christy L. "Impact of West Nile virus on the natural history of St. Louis encephalitis virus in Florida." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002452.
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Desole, Giovanna. "Comparative analysis of Zika virus and other Flavivirus infection in human neural cells." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3424985.
Повний текст джерелаАнотація:
Background: Zika virus (ZIKV), West Nile virus (WNV) and dengue virus (DENV) are mosquito-borne flaviviruses that generally cause mild or asymptomatic disease in humans. However, ZIKV infection has been associated with fetal microcephaly and Guillain-Barrè syndrome in adults; WNV infection may evolve to severe neuroinvasive disease in the elderly and immunocompromised subjects; DENV may rarely cause neurological complications in infected individuals. In addition, another emerging mosquito-borne flavivirus, Usutu virus (USUV), which may cause fatal neuroinvasive disease in different bird species, has been recently shown to infect humans but its pathogenicity is unknown.
Aim of the study: In the context of the recent outbreak of ZIKV in the Americas and the increasing evidences of an association between ZIKV infection and the occurrence of fetal microcephaly, aim of this study was to investigate the effect of ZIKV infection in human neural cells in comparison with other flavivirus infections. To this aim, ZIKV infectivity, replication kinetics, cytopathic effect (CPE), and induction of innate antiviral responses were investigated in human induced pluripotent stem cells (hiPSCs), hiPSCs-derived neural stem cells (NSCs) and neurons and compared with other flaviviruses, i.e., WNV, DENV and USUV.
Methods: NSCs and neurons were differentiated from hiPSCs. hiPSCs, NSCs, and neurons were infected with isolates of ZIKV Asian lineage (KU853013), WNV lineage 2 (KF179640), DENV serotype 2, and USUV Europe lineage 1 (AY453411). Time course experiments were performed to evaluate viral load by qRT-PCR and TCID50, expression of host genes involved in antiviral innate immunity by qRT-PCR, expression of cell differentiation markers by IF and qRT-PCR, cell viability and cell death by flow cytometry. The impact of ZIKV on embryogenesis and neurogenesis was evaluated by infection of hiPSCs and NSCs during neural differentiation and embryo body formation.
Results: ZIKV infected and replicated efficiently in NSCs, neurons and hiPSCs. Infection led to typical CPE and cell death by apoptosis. ZIKV infection of hiPSCs, NSCs, and neurons induced the expression of innate immune response genes, especially the cellular pattern recognition receptor (PRR) IFH1 gene (MDA5), IFN-induced protein with tetratricopeptide repeats 1 (IFIT1) and 2 (IFIT2). Infected embryoid bodies were massively destroyed by ZIKV infection and infected hiPSCs and NSCs died before ending the neural differentiation process. ZIKV replication efficiency in NSCs was significantly higher than that of DENV-2 and USUV, but lower than that of WNV. In particular, WNV replicated more efficiently, induced more cell death and higher levels of antiviral gene expression than ZIKV in NSCs, neurons and hiPSCs. The induction of innate immune response genes in NSCs after infection with ZIKV and DENV-2 infection was milder than after infection with WNV and USUV, in agreement with the adaptation of these viruses to the human host and their ability to shut down the antiviral response.
Conclusion: ZIKV infects and replicates efficiently in NSCs and induces cell death abrogating neural development, although less efficiently than WNV. Because of the similarities between flaviviruses in their interactions with host neural cells, it is conceivable that infection of other human cells, such as those involved in the extablishment of the blood-placenta barrier, are crucial for ZIKV-induced damage of the fetal brain.Presupposti dello studio: Zika virus (ZIKV), West Nile virus (WNV), dengue virus (DENV) e Usutu virus (USUV) sono trasmessi da zanzare ed appartengono al genere Flavivirus della famiglia Flaviviridae. L’infezione da ZIKV è associata a microcefalia fetale e sindrome di Guillan-Barrè; WNV può causare una grave sindrome neuroinvasiva nell’anziano e nei soggetti immunocompromessi; l’infezione da DENV raramente si associa a complicazioni neurologiche; USUV può causare una sindrome neuroinvasiva fatale in diverse specie di uccelli, è stato dimostrato che può infettare pure l’uomo, ma la sua patogenicità resta ancora da chiarire. Scopo: Alla luce della recente epidemia di ZIKV in America e di una probabile associazione tra l’infezione da ZIKV e lo sviluppo di microcefalia fetale, lo scopo di questo studio è stato confrontare l’infezione da ZIKV sulle cellule neurali umane con l’infezione da WNV, DENV e USUV. A tal fine, la cinetica di replicazione, l’effetto citopatico e l’immunità innata indotta dall’infezione virale sono state analizzate in cellule staminali pluripotenti indotte (hiPSCs), cellule staminali neurali derivate da iPSCs e neuroni. Materiali e metodi: Le NSCs ed i neuroni sono stati differenziati da hiPSCs. I diversi tipi cellulari sono stati infettati con l’isolato di ZIKV lignaggio asiatico (KU853013), WNV lignaggio 2 (KF179640), DENV sierotipo 2 e USUV lignaggio 1 europeo (AY453411). La carica virale è stata valutata a diversi tempi dall’infezione mediante qRT-PCR e TCID50, il livello di espressione dei geni coinvolti nell’immunità innata è stato analizzato mediante qRT-PCR e l’espressione dei markers di differenziamento cellulare mediante IF e qRT-PCR, la sopravvivenza cellulare e l’apoptosi mediante il saggio MTT e analisi dell’attivazione di caspasi-3. L’impatto dell’infezione da ZIKV sull’embriogenesi e la neurogenesi è stato valutato infettando le hiPSCs e le NSCs durante il differenziamento neurale e durante la formazione dei corpi embrioidi. Risultati: ZIKV era in grado di infettare e replicare efficientemente nelle NSCs, nei neuroni e nelle hiPSCs, causando un tipico effetto citopatico e morte cellulare per apoptosi. L’infezione ha indotto un significativo aumento dell’espressione dei geni dell’immunità innata, in particolare dei geni MDA5 (the cellular pattern recognition receptor (PRR) IFH1 gene), IFIT1 (IFN-induced protein with tetratricopeptide repeats 1) e IFIT2. I corpi embrioidi sono stati distrutti dal virus e le hiPSCs e le NSCs infettate sono morte prima di completare il differenziamento neurale. L’efficienza di replicazione di ZIKV nelle NSCs era maggiore rispetto a quella di DENV-2 e USUV, ma minore rispetto al WNV. Infatti, WNV replicava in modo più efficiente, induceva una maggiore morte cellulare e stimolava una più elevata risposta antivirale rispetto a ZIKV nei diversi tipi cellulari. Conclusione: ZIKV infetta e replica nelle NSCs, inducendo morte cellulare e impedendo lo sviluppo neurale, ma in modo meno efficiente rispetto al WNV. E’ probabile quindi che l’infezione di altri tipi cellulari sia determinante per il danno al sistema nervoso fetale indotto in modo specifico da ZIKV.
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Rückert, Claudia. "Alphavirus and flavivirus infection of Ixodes tick cell lines : an insight into tick antiviral immunity." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/10063.
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Arthropod-borne viruses, arboviruses, have the ability to replicate in both vertebrates and invertebrates and are transmitted to susceptible vertebrate hosts by vectors such as mosquitoes and ticks. Ticks are important vectors of many highly pathogenic arboviruses, including the flavivirus tick-borne encephalitis virus (TBEV) and the nairovirus Crimean-Congo haemorrhagic fever virus. In contrast, alphaviruses are principally mosquito-borne and have been isolated only rarely from ticks; ticks have not been implicated as their vectors. Nevertheless, the alphavirus Semliki Forest virus (SFV) replicates in cell lines derived from many different tick species, including those of the genus Ixodes, which includes vectors of TBEV and its lesspathogenic relative Langat virus (LGTV). In vertebrate cells, arboviruses generally cause cytopathic effects; however, arbovirus infection of arthropod cells usually results in a persistent low-level infection without cell death. While little is known about antiviral immunity in tick cells, the immune system of other arbovirus vectors such as mosquitoes has been studied extensively over the last decade. In insects, pathways such as RNA interference (RNAi), JAK/STAT, Toll, Imd and melanisation have been implicated in controlling arbovirus infection, with RNAi being considered the most important antiviral mechanism. In tick cells, RNAi has been shown to have an antiviral effect, but current knowledge of other immunity pathways is limited and none have been implicated in the antiviral response. In the present study, SFV and LGTV replication in selected Ixodes spp. tick cell lines was characterised and the Ixodes scapularis-derived cell line IDE8 was identified as a suitable cell line for this project. Potential antiviral innate immunity pathways were investigated; putative components of the tick JAK/STAT, Toll and Imd pathways were identified by BLAST search using available sequences from well-studied arthropods including the fruit fly Drosophila melanogaster. Using gene silencing, an attempt was made to determine whether these pathways play a role in controlling SFV and LGTV infection in tick cell lines. Selected genes were silenced in IDE8 cells using long target-specific dsRNA and cells were subsequently infected with either SFV or LGTV. Effects of gene silencing on virus replication were assessed by quantitative real time PCR (qPCR) or luciferase reporter assay. Effects on infectious virus production were measured by plaque assay. Replication of the orbivirus St Croix River virus (SCRV), which chronically infects IDE8 cells, was also quantified by qPCR after silencing of selected genes. Interestingly, SFV or LGTV infection of IDE8 cells resulted in a significant increase in SCRV replication, possibly as a result of interference with antiviral pathways by SFV and LGTV or possibly due to diversion of cellular responses from sole control of SCRV. No evidence for an antiviral role for the JAK/STAT or Toll pathways was found in IDE8 cells. However, an antiviral effect was observed for protein orthologues putatively involved in the RNAi response. Argonaute proteins play an important role in translation inhibition and target degradation mediated by RNAi, and silencing of selected Argonaute proteins resulted in a significant increase in SFV and SCRV replication. The carboxypeptidase CG4572 is essential for an efficient antiviral response in D. melanogaster, and supposedly involved in the systemic RNAi response. A putative tick orthologue of CG4572 was identified and this appeared to be involved in the antiviral response in IDE8 tick cells. When expression of CG4572 was silenced and cells subsequently infected with SFV or LGTV, replication of both viruses was significantly increased. In addition, it was shown that three mosquito orthologues of CG4572 also had an antiviral role against SFV in Aedes mosquito cells. In conclusion, of the tick cell lines investigated, IDE8 provided a suitable model system for investigating tick cell responses against arboviruses and new insight into the nature of the tick cell antiviral response was gained.
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Youseff, Brian. "The Role of Tumor Necrosis Factor Receptor-Associated Factor 6 in Tick-Borne Flavivirus Infection." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco155691388498993.
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Pettersson, John H. O. "The Origin of the Genus Flavivirus and the Ecology of Tick-Borne Pathogens." Doctoral thesis, Uppsala universitet, Systematisk biologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-211090.
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The present thesis examines questions related to the temporal origin of the Flavivirus genus and the ecology of tick-borne pathogens. In the first study, we date the origin and divergence time of the Flavivirus genus. It has been argued that the first flaviviruses originated after the last glacial maximum. This has been contradicted by recent analyses estimating that the tick-borne flaviviruses emerged at least before 16,000 years ago. It has also been argued that the Powassan virus was introduced into North America at the time between the opening and splitting of the Beringian land bridge. Supported by tip date and biogeographical calibration, our results suggest that this genus originated circa 120,000 (156,100–322,700) years ago if the Tamana bat virus is included in the genus, or circa 85,000 (63,700–109,600) years ago excluding the Tamana bat virus. In the second study we estimate the prevalence of tick-borne encephalitis virus (TBEV) in host-seeking Ixodes ricinus from 29 localities in Sweden and compare our data with those of neighbouring countries. Nymphs and adult ticks were screened for TBEV using a real-time PCR assay. The mean TBEV prevalence for all tick stages combined was 0.26% for Sweden and 0.28% for all Scandinavian countries, excluding Iceland. The low prevalence of TBEV in nature may partly be explained by the fact that TBEV occurs in spatially small foci and that the inclusion of ticks from non-infected foci will reduce the prevalence estimate. In the third and fourth study, we conducted the first large-scale investigations to estimate the prevalence and geographical distribution of Anaplasma spp. and Rickettsia spp. in host-seeking larvae, nymphs and adults of I. ricinus ticks in Sweden. Ticks were collected from several localities in central and southern Sweden and were subsequently screened for the presence of Anaplasma spp. and Rickettsia spp. using a real-time PCR assay. For all active tick stages combined, the mean prevalence of Anaplasma spp. and Rickettsia spp. in I. ricinus in Sweden was estimated to 1.1% and 4.8%, respectively. It was also shown that A. phagocytophilum and R. helvetica are the main Anaplasma and Rickettsia species occurring in Sweden.
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Courtney, Sean C. "Functional Analysis of Host Cell Proteins and Stress Responses that Inhibit West Nile Virus Infection." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/biology_diss/101.
Повний текст джерелаАнотація:
Resistance to flavivirus-induced disease is conferred by a single gene that encodes oligoadenylate synthetase (Oas) 1b (Oas1b). Oas1b is not a functional synthetase suggesting its anti-flavivirus mechanism is RNase L-independent and that it may be mediated by interactions with other host cell protein(s). A yeast two-hybrid screen was used to identify host cell binding partners of Oas1b. Candidate partners were confirmed by yeast co-transformation and co-immunoprecipitation analyses. Oxysterol binding protein-related 1L (ORP1L) and ATP binding cassette subfamily F 3 (ABCF3) were found to interact with Oas1b. RNAi knockdown studies suggested that ORP1L and ABCF3 form a tripartite complex with Oas1b that is critical for the flavivirus-induced disease resistance mechanism.
Stresses including oxidation, nutrient starvation, and viral infections often induce the formation of stress granules (SGs) in eukaryotic cells. In response to stress, eIF2α kinases phosphorylate eIF2α leading to stalled 48S pre-initiation complexes and SG formation. West Nile virus (WNV) Eg101 infections were previously shown not to induce the formation of SGs. Infections with viruses of other natural WNV strains, as well as a WNV lineage 1/2-based infectious clone (W956IC) were analyzed and only W956IC infections were found to induce SGs. eIF2α kinase knockout MEFs were used to show that the W956IC-induced SGs were PKR-dependent. WNV chimeras were made by inserting Eg101 genes into the W956IC backbone. Chimeras replacing NS5 or NS1 and NS5 or NS1 and NS3 and NS4a reduced SG formation as well as early viral RNA synthesis similar to Eg101 infections. W956IC infections but not Eg101 infections were shown to produce exposed viral dsRNA at early times after infection. The data suggest that natural WNV infections evade the cell SG response by suppressing the amplification of viral RNA until cytoplasmic membranes have been remodeled to protect replication complexes from detection.
It was previously reported that WNV Eg101 infections inhibited the formation of arsenite-induced SGs. The ability of other natural WNV strain infections to inhibit SG formation by arsenite (HRI), DTT (PERK), W956IC co-infection (PKR), and heat shock treatments was assessed. WNV infections only inhibited arsenite-induced SG formation suggesting that WNV infections specifically suppress the response to oxidative intermediates.
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Riccetti, Silvia. "In vitro modelling of patient-specific susceptibility to neurotropic flavivirus infection by using induced pluripotent stem cells." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422230.
Повний текст джерелаАнотація:
Background: A characteristic feature of many infections is that only a portion of exposed individuals develop clinical disease. These include mosquito-borne flaviviruses such as West Nile virus (WNV), Zika virus (ZIKV) and Usutu virus (USUV) infections, which generally cause mild illness or asymptomatic infections in humans. Nonetheless, WNV can cause serious neuroinvasive diseases in less than 1% of infected patients, mainly elderly and immunocompromised subjects; ZIKV may cause fetal microcephaly in about 5% of infections acquired during pregnancy and 1 in 10,000 infected adults develop Guillain-Barré syndrome; USUV seems less pathogenic than WNV and most human infections described so far were asymptomatic, with rare cases of encephalitis or meningitis.
Aim of the study: The different infection outcomes or progression to severe disease can be partly explained by host genetic variations, but the genetic traits associated with susceptibly to severe infection remain poorly understood. Aim of this study was to develop a patient-specific in vitro platform, based on human induced pluripotent stem cells (hiPSCs), to investigate the mechanisms of variations in human susceptibility to severe flavivirus infection.
Methods: iPSCs were generated from erythroblasts of two blood donors with asymptomatic WNV infection (controls) and from two patients who developed WNV encephalitis but had no co-morbidity or other risk factors (cases). Patient-specific iPSCs were differentiated into neural stem cells (NSCs) and infected with WNV lineage 1 (GU011992), ZIKV Asian lineage (KU853013), and USUV lineage Europe 1 (AY453411) at different MOIs. Time course experiments were performed to evaluate viral replication kinetics in infected NSCs, cell viability and cell death following infection, and expression of genes involved in antiviral innate immunity. Next-generation sequencing of 2,600 genes related to immune system in iPSCs of cases and controls was performed to detects mutations potentially associated with increased susceptibility to neuroinvasive disease.
Results: USUV and WNV replicated more efficiently, yielding 10 and 100-fold higher viral load and inducing 40% and 70% higher cell mortality, respectively, in NSCs derived from cases than in NSCs derived from controls. WNV induced 3-fold higher caspase 3 activity in infected NSC derived from encephalitis patients than in NSCs derived from asymptomatic donors. Several genes involved in the antiviral IFN pathway were significantly upregulated after USUV, ZIKV and WNV infection (in particular, type 3 IFNs genes), but the general trend indicated an attenuated response in NSCs derived from WNV encephalitis cases, which showed significantly lower mRNA levels of IFN pathway regulators such as TLR3, MAVS and IRF7. Exome sequencing analysis identified heterozygous inactivating mutations in the PSIP1 and DDX58 genes of cases, but not in controls, as polymorphism in other genes that could play a role in disease susceptibility.
Conclusions: Patient-specific iPSCs are useful tools to model individual susceptibility to viral infectious diseases and allowed to demonstrate that WNV and USUV and, to a lesser extent, ZIKV, replicated more efficiently and induced more cell death and apoptosis in NSCs derived from patients with WNV encephalitis than in cells derived from blood donors with asymptomatic infection. This increased susceptibility to neurotropic flaviviruses was associated with a significantly attenuated innate antiviral response. Exome sequencing revealed inactivating mutations in genes that represent good candidates for further investigation.
Книги з теми "Flavivirus Infection"
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Gregory, Bock, Goode Jamie, Novartis Foundation, and Novartis Institute for Tropical Diseases., eds. New treatment strategies for dengue and other flaviviral diseases. Chichester: John Wiley & Sons, 2006.
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Shi, Pei-Yong. Molecular virology and control of flaviviruses. Norfolk, UK: Caister Academic Press, 2012.
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3
Monath, Thomas P., and J. Erin Staples. Yellow fever. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0045.
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Yellow fever is an acute mosquito-borne flavivirus infection characterized in its full-blown form by fever, jaundice, albuminuria, and haemorrhage. Two forms are distinguished: urban yellow fever in which the virus is spread from person to person by peridomestic Aedes aegypti mosquitoes and jungle (sylvan) yellow fever transmitted by tree-hole breeding mosquitoes between non-human primates and sometimes humans. Yellow fever is endemic and epidemic in tropical areas of the Americas and Africa but has never appeared in Asia or the Pacific region. Prevention and control are effected principally through yellow fever vaccination.
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Mesquita, Emersom C., and Fernando A. Bozza. Diagnosis and management of viral haemorrhagic fevers in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0293.
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In a globalized scenario where widespread international travel allows viral agents to migrate from endemic to non-endemic areas, health care providers and critical care specialists must be able to readily recognize a suspected case of viral haemorrhagic fever (VHF). Early suspicion is pivotal for improving patient outcome and to ensure that appropriate biosafety measures be applied. VHFs are acute febrile illnesses marked by coagulation disorders and organ specific syndromes. VHFs represent a great medical challenge because diseases are associated with a high mortality rate and many VHFs have the potential for person-to-person transmission (Filoviruses, Arenavioruses, and Bunyaviroses). Dengue is the most frequent haemorrhagic viral disease and re-emergent infection in the world and, due to its public health relevance, severe dengue will receive special attention in this chapter. The diagnosis of VHFs is made by detecting specific antibodies, viral antigens (ELISA) and viral nucleic acid (RT-PCR) on blood samples. Supportive care is the cornerstone in the treatment of VHFs. Ribavirin should be started as soon as a case of VHF is suspected and discontinued if a diagnosis of Filovirus or Flavivirus infection is established. Adjunctive antimicrobial therapy is usually implemented to treat co-existing or secondary infections. Antimalarial treatment should also be initiated if a malaria test (thick blood films) is not quickly available and/or reliable and patients travel history is compatible. It is always recommended to apply appropriate biosafety measures and notify local infection control unit and state and national authorities.
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Keshav, Satish, and Palak Trivedi. Viral hepatitis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0212.
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Hepatitis means ‘inflammation of the liver’ and is manifest with symptoms that include malaise, anorexia, fever, flu-like symptoms, and pain in the right upper quadrant of the abdomen, with the pain being caused by swelling of the liver and its capsule. Elevations in circulating hepatic enzymes, particularly aspartate transaminase and alanine transaminase, are common, with jaundice occurring some time after the onset of other symptoms and signs. There are five viruses that primarily cause viral hepatitis: hepatitis A, B, C, D, and E viruses, abbreviated HAV, HBV, HCV, HDV, and HEV, respectively. These viruses are all hepatotrophic, in that the liver is the primary site of infection. HAV, HBV, and HEV are usually acute, self-limiting infections that may, nonetheless, cause morbidity and, in the case of HEV, fatality. However, HBV and, more so, HCV can cause chronic carriage of the virus over many years, as well as the development of chronic hepatitis. HDV is only pathogenic in conjunction with HBV. After recovery from acute infection with HAV, individuals have long-lasting immunity against further infection. The same holds true for the majority of individuals with acute HBV infection. There seems to be little natural immunity to HCV infection, and a significant proportion of cases result in chronic hepatitis. Immunity to HEV is not long-lasting, and repeated infections are possible. Many other viruses can cause hepatitis, of which cytomegalovirus, herpes simplex virus, Epstein–Barr virus, and flaviviruses such as dengue and yellow fever are the most important. The liver, however, is not their primary site of replication or cellular damage.
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Казачинская, Е. И. ВИРУС ДЕНГЕ. Академическое изд-во «Гео», 2021. http://dx.doi.org/10.21782/b978-5-6043022-6-2.
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The review is devoted to the analysis of literature data on the history research of dengue fever, the discovery of the etiological infectious agent of this disease-dengue virus and its serotypes. A taxonomic overview of the }lavivirus family, genome organization, structure and function of viral proteins, mosquito species-viral vectors and virus transmission cycles, theories of its origin are presented. As well as the evolution, characteristics and epidemiology of viral serotypes, cellular receptors for dengue virus penetration, pathogenicity for human and factors for the development of severe disease, induced immunity, applied methods and markers for diagnosis, principles of disease treatment and drug development (more information about monoclonal antibodies-potential therapeutic drugs), vaccine options and their effectiveness are considered. The book is intended for students, graduate students, employees of research institutions and universities, as well as doctors involved in the study of }laviviruses and the problem of differential diagnosis of flavivirus infections.
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Osterholm, Michael T., and Mark Olshaker. Deadliest Enemy: Our War Against Killer Germs. Hodder & Stoughton, 2020.
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Osterholm, Michael T., and Mark Olshaker. Deadliest Enemy: Our War Against Killer Germs. Little Brown & Company, 2017.
Знайти повний текст джерелаЧастини книг з теми "Flavivirus Infection"
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El Adl, Salma, and Alaa Badawi. "Nuclear Receptor Ligands in Flavivirus Infection Control." In Nuclear Receptors, 483–502. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78315-0_18.
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Campos, Rafael K., Mariano A. Garcia-Blanco, and Shelton S. Bradrick. "Roles of Pro-viral Host Factors in Mosquito-Borne Flavivirus Infections." In Roles of Host Gene and Non-coding RNA Expression in Virus Infection, 43–67. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/82_2017_26.
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Reid, Hugh W., Herbert Weissenböck, and Károly Erdélyi. "Flavivirus Infections." In Infectious Diseases of Wild Mammals and Birds in Europe, 128–45. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118342442.ch9.
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Tan, Kah Hin, Kitti Chan Wing Ki, Satoru Watanabe, Subhash G. Vasudevan, and Manoj Krishnan. "Cell-Based Flavivirus Infection (CFI) Assay for the Evaluation of Dengue Antiviral Candidates Using High-Content Imaging." In Dengue, 99–109. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0348-1_7.
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Johnson, Barbara W. "Neurotropic Flaviviruses." In Neurotropic Viral Infections, 229–58. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33133-1_9.
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Brinton, M. "Flaviviruses." In Clinical and Molecular Aspects of Neurotropic Virus Infection, 69–99. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1675-6_3.
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Thomas, Stephen J., Timothy P. Endy, and Alan L. Rothman. "Flaviviruses: Dengue." In Viral Infections of Humans, 351–81. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7448-8_15.
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Thomas, Stephen J., Timothy P. Endy, and Alan L. Rothman. "Flaviviruses: Dengue." In Viral Infections of Humans, 1–65. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-4939-9544-8_15-1.
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Griffin, Diane E. "Alphaviruses, Flaviviruses, and Bunyaviruses." In Infectious Agents and Pathogenesis, 255–74. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4684-5886-2_13.
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Modis, Yorgo, and Vinod Nayak. "Molecular Mechanisms of Flaviviral Membrane Fusion." In West Nile Encephalitis Virus Infection, 265–86. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79840-0_12.
Повний текст джерелаТези доповідей конференцій з теми "Flavivirus Infection"
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Rodrigues, Francisco, Andre Campino, and Patricia Coelho. "Epidemiology of dengue in Portugal – a portrait." In III SEVEN INTERNATIONAL MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/seveniiimulti2023-226.
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Dengue is a systemic infectious disease of viral etiology transmitted through the bite of female hematophagous mosquitoes of the genus Aedes, with Aedes aegypti and Aedes albopictus being the most competent species for its transmission [1-4]. Dengue virus (VDEN) taxonomically belongs to the family Flaviviridae and the genus flavivirus [5-8]. To date, four antigenically differentiated serotypes - VDEN-1, VDEN-2, VDEN-3 and VDEN-4 - have been reported based on biological, immunological and molecular criteria [8,9]. Among all arboviruses, VDEN is by far the pathogen that most affects humans [10-13]. According to the World Health Organization (WHO) in the last 50 years the incidence of Dengue cases has increased by about 30 times, and it is estimated that there are currently between 50 and 100 million infections annually [10]. The disease is widespread in all tropical and subtropical regions of the planet, with a growing incidence in Asia, Africa, Latin America and the Pacific region [10,14]. It is estimated that approximately 2.5 billion people live at risk of contracting the disease in endemic countries [10,13]. Around 120 million people travel to affected areas each year, with travellers playing a key role in the geographical spread of the disease (the return of infected travellers from Dengue-endemic countries can establish autochthonous cycles of infection) [15,16, 17].