Database : MEDLINE
Search on : Alphavirus and Infections [Words]
References found : 2317 [refine]
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[PMID]: 29410416
[Au] Autor:Auerswald H; Boussioux C; In S; Mao S; Ong S; Huy R; Leang R; Chan M; Duong V; Ly S; Tarantola A; Dussart P
[Ad] Address:Virology Unit, Institut Pasteur du Cambodge, Institut Pasteur International Network, PO Box 983, Phnom Penh, Cambodia.
[Ti] Title:Broad and long-lasting immune protection against various Chikungunya genotypes demonstrated by participants in a cross-sectional study in a Cambodian rural community.
[So] Source:Emerg Microbes Infect;7(1):13, 2018 Feb 07.
[Is] ISSN:2222-1751
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chikungunya virus (CHIKV) is an alphavirus circulating worldwide. Its presence in Asia has been reported since the 1950s, constituting the Asian genotype. Since 2005, strains from the Eastern, Central, and Southern African (ECSA) genotype have caused several outbreaks across Asia. Viruses from the ECSA genotype were also detected in Cambodia in late 2011 and led to an outbreak in a rural community in 2012. A former investigation from 2012 found a higher risk of infection in people younger than 40 years, suggesting a pre-existing herd immunity in the older Cambodian population due to infection with an Asian genotype. In 2016, we collected serum from equivalent numbers of individuals born before 1975 and born after 1980 that were also part of the 2012 study. We analyzed the 154 serum samples from 2016 for neutralization against the Cambodian ECSA isolate and three strains belonging to the Asian genotype. This experiment revealed that 22.5% (18/80) of the younger study participants had no CHIKV antibodies, whereas 5.4% (4/74) of the older population remained naive. Study participants infected during the ECSA outbreak had twofold neutralizing titers against the ECSA and the most ancient Asian genotype virus (Thailand 1958) compared to the other two Asian genotype viruses. The neutralization data also support the older population's exposure to an Asian genotype virus during the 1960s. The observed cross-reactivity confirms that the investigated CHIKV strains belong to a single serotype despite the emergence of novel ECSA genotype viruses and supports the importance of the development of a Chikungunya vaccine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1038/s41426-017-0010-0

  2 / 2317 MEDLINE  
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[PMID]: 29512949
[Au] Autor:Zambaz C; Dan D
[Ad] Address:Service de rhumatologie, Département de l'appareil locomoteur, CHUV, 1011 Lausanne.
[Ti] Title:Arthrites virales. [Viral arthritis].
[So] Source:Rev Med Suisse;14(597):526-528, 2018 Mar 07.
[Is] ISSN:1660-9379
[Cp] Country of publication:Switzerland
[La] Language:fre
[Ab] Abstract:Arthritis and arthralgia during a viral infection are often polyarticular and symmetric and can mimic rheumatoid arthritis. Depending on germs, others signs and symptoms as fever, cutaneous rash (Parvovirus B19) or jaundice (hepatitis) can be present. Worldwide most common germs are Parvovirus B19, hepatitis B and C, HIV and alphavirus. There are significant differences throughout the world and epidemiology continues to evolve with a progression of vector-borne infections. Diagnosis of viral arthritis is often difficult and is based on epidemiological, clinical and serological data.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review

  3 / 2317 MEDLINE  
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[PMID]: 29263262
[Au] Autor:Martin NM; Griffin DE
[Ad] Address:W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
[Ti] Title:Interleukin-10 Modulation of Virus Clearance and Disease in Mice with Alphaviral Encephalomyelitis.
[So] Source:J Virol;92(6), 2018 Mar 15.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Alphaviruses are an important cause of mosquito-borne outbreaks of arthritis, rash, and encephalomyelitis. Previous studies in mice with a virulent strain (neuroadapted SINV [NSV]) of the alphavirus Sindbis virus (SINV) identified a role for Th17 cells and regulation by interleukin-10 (IL-10) in the pathogenesis of fatal encephalomyelitis (K. A. Kulcsar, V. K. Baxter, I. P. Greene, and D. E. Griffin, Proc Natl Acad Sci U S A 111:16053-16058, 2014, https://doi.org/10.1073/pnas.1418966111). To determine the role of virus virulence in generation of immune responses, we analyzed the modulatory effects of IL-10 on disease severity, virus clearance, and the CD4 T cell response to infection with a recombinant strain of SINV of intermediate virulence (TE12). The absence of IL-10 during TE12 infection led to longer morbidity, more weight loss, higher mortality, and slower viral clearance than in wild-type mice. More severe disease and impaired virus clearance in IL-10 mice were associated with more Th1 cells, fewer Th2 cells, innate lymphoid type 2 cells, regulatory cells, and B cells, and delayed production of antiviral antibody in the central nervous system (CNS) without an effect on Th17 cells. Therefore, IL-10 deficiency led to more severe disease in TE12-infected mice by increasing Th1 cells and by hampering development of the local B cell responses necessary for rapid production of antiviral antibody and virus clearance from the CNS. In addition, the shift from Th17 to Th1 responses with decreased virus virulence indicates that the effects of IL-10 deficiency on immunopathologic responses in the CNS during alphavirus infection are influenced by virus strain. Alphaviruses cause mosquito-borne outbreaks of encephalomyelitis, but determinants of outcome are incompletely understood. We analyzed the effects of the anti-inflammatory cytokine IL-10 on disease severity and virus clearance after infection with an alphavirus strain of intermediate virulence. The absence of IL-10 led to longer illness, more weight loss, more death, and slower viral clearance than in mice that produced IL-10. IL-10 influenced development of disease-causing T cells and entry into the brain of B cells producing antiviral antibody. The Th1 pathogenic cell subtype that developed in IL-10-deficient mice infected with a less virulent virus was distinct from the Th17 subtype that developed in response to a more virulent virus, indicating a role for virus strain in determining the immune response. Slow production of antibody in the nervous system led to delayed virus clearance. Therefore, both the virus strain and the host response to infection are important determinants of outcome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Data-Review

  4 / 2317 MEDLINE  
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[PMID]: 28455127
[Au] Autor:Camini FC; da Silva Caetano CC; Almeida LT; da Costa Guerra JF; de Mello Silva B; de Queiroz Silva S; de Magalhães JC; de Brito Magalhães CL
[Ad] Address:Núcleo de Pesquisas em Ciências Biológicas, NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
[Ti] Title:Oxidative stress in Mayaro virus infection.
[So] Source:Virus Res;236:1-8, 2017 05 15.
[Is] ISSN:1872-7492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Mayaro virus (MAYV) is a neglected tropical arbovirus that causes a febrile syndrome that is sometimes accompanied by incapacitating arthritis/arthralgia. The pathogenesis of MAYV has not been completely defined and oxidative stress mediated by an increase in reactive oxygen species (ROS) and/or depletion of antioxidant defences has been found to contribute to several aspects of viral disease. To investigate whether MAYV induced oxidative stress in host cells, we monitored ROS production, oxidative stress markers and antioxidant defences at different time points after infection. Our results show that MAYV induced significant oxidative stress in infected HepG2 cells, as indicated by the increase of malondialdehyde (MDA) and protein carbonyl levels, and by a significant decrease of the reduced versus oxidized glutathione (GSH/GSSG) ratio. Generally, MAYV-infected HepG2 cells also showed an increase in antioxidant defences. We observed an increase in the superoxide dismutase (SOD) and catalase (CAT) activities and the total glutathione content. To determine whether similar effects occurred in other cell types, we evaluated the ROS, MDA and SOD activity levels in J774 cells after MAYV infection. Similar to our observations in HepG2 cells, the J774 cells showed an increase in ROS, MDA and total SOD activity following MAYV infection. Thus, since the cellular redox environment is influenced by the production and removal of ROS, we hypothesize that the overproduction of ROS was responsible for the oxidative stress in response to the MAYV infection despite the increase in the antioxidant status. This study is the first report on the involvement of oxidative stress during MAYV infection. Collectively, our data shed light on some mechanisms that are operational in host cells following exposure to MAYV.
[Mh] MeSH terms primary: Alphavirus Infections/metabolism
Alphavirus/physiology
Oxidative Stress
[Mh] MeSH terms secundary: Alphavirus/genetics
Alphavirus Infections/genetics
Alphavirus Infections/virology
Catalase/metabolism
Glutathione/metabolism
Hep G2 Cells
Humans
Malondialdehyde/metabolism
Oxidation-Reduction
Reactive Oxygen Species/metabolism
Superoxide Dismutase/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Reactive Oxygen Species); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); GAN16C9B8O (Glutathione)
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[Js] Journal subset:IM
[Da] Date of entry for processing:170430
[St] Status:MEDLINE

  5 / 2317 MEDLINE  
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[PMID]: 29462879
[Au] Autor:Lim EXY; Supramaniam A; Lui H; Coles P; Lee WS; Liu X; Rudd PA; Herrero LJ
[Ad] Address:Institute for Glycomics, Griffith University, Gold Coast Campus, Southport, QLD 4215, Australia. elisa.lim@griffithuni.edu.au.
[Ti] Title:Chondrocytes Contribute to Alphaviral Disease Pathogenesis as a Source of Virus Replication and Soluble Factor Production.
[So] Source:Viruses;10(2), 2018 Feb 15.
[Is] ISSN:1999-4915
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Arthritogenic alphavirus infections often result in debilitating musculoskeletal disorders that affect the joints, muscle, and bone. In order to evaluate the infection profile of primary human skeletal muscle and chondrocyte cells to Ross River virus (RRV) in vitro, cells were infected at a multiplicity of infection (MOI) of 1 over a period of two days. Viral titers were determined by plaque assay and cytokine expression by Bio-Plex assays using the supernatants harvested. Gene expression studies were conducted using total RNA isolated from cells. Firstly, we show that RRV RNA is detected in chondrocytes from infected mice in vivo Both human primary skeletal muscle and chondrocyte cells are able to support productive RRV infection in vitro. We also report the production of soluble host factors including the upregulation of heparanase (HPSE) and inflammatory host factors such as interleukin-6 (IL-6), monocyte chemoattractant protein 1 (MCP-1), RANTES (regulated on activation, normal T cell expressed and secreted), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α), which are also present during clinical disease in humans. Our study is the first to demonstrate that human chondrocyte cells are permissive to RRV infection, support the production of infectious virus, and produce soluble factors including HPSE, which may contribute to joint degradation and the pathogenesis of disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180221
[Lr] Last revision date:180221
[St] Status:In-Data-Review

  6 / 2317 MEDLINE  
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[PMID]: 28744856
[Au] Autor:Chan YH; Ng LFP
[Ad] Address:Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore.
[Ti] Title:Age has a role in driving host immunopathological response to alphavirus infection.
[So] Source:Immunology;152(4):545-555, 2017 12.
[Is] ISSN:1365-2567
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Alphaviruses are a group of arthropod-borne pathogens capable of causing a wide spectrum of clinical symptoms, ranging from milder symptoms like rashes, fever and polyarthralgia, to life-threatening encephalitis. This genus of viruses is prevalent globally, and can infect patients across a wide age range. Interestingly, disease severity of virus-infected patients is wide-ranging. Definitions of the pathogenesis of alphaviruses, as well as the host factors influencing disease severity, remain limited. The innate and adaptive immune systems are important host defences against alphavirus infections. Several reports have highlighted the roles of specific immune subsets in contributing to the immune pathogenesis of these viruses. However, immunosenescence, a gradual deterioration of the immune system brought about by the natural advancement of age, affects the functional roles of these immune subsets. This phenomenon compromises the host's ability to defend against alphavirus infection and pathogenesis. In addition, the lack of maturity in the immune system in newborns and infants also results in more severe disease outcomes. In this review, we will summarize the subtle yet diverse physiological changes in the immune system during aging, and how these changes underlie the differences in disease severity for common alphaviruses.
[Mh] MeSH terms primary: Aging/immunology
Alphavirus Infections/immunology
Alphavirus/immunology
[Mh] MeSH terms secundary: Age Factors
Aging/pathology
Alphavirus Infections/mortality
Alphavirus Infections/pathology
Animals
Humans
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1711
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:170727
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12799

  7 / 2317 MEDLINE  
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[PMID]: 28461071
[Au] Autor:Langsjoen RM; Auguste AJ; Rossi SL; Roundy CM; Penate HN; Kastis M; Schnizlein MK; Le KC; Haller SL; Chen R; Watowich SJ; Weaver SC
[Ad] Address:Institute for Translational Science, University of Texas Medical Branch, Galveston, TX, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA.
[Ti] Title:Host oxidative folding pathways offer novel anti-chikungunya virus drug targets with broad spectrum potential.
[So] Source:Antiviral Res;143:246-251, 2017 07.
[Is] ISSN:1872-9096
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Alphaviruses require conserved cysteine residues for proper folding and assembly of the E1 and E2 envelope glycoproteins, and likely depend on host protein disulfide isomerase-family enzymes (PDI) to aid in facilitating disulfide bond formation and isomerization in these proteins. Here, we show that in human HEK293 cells, commercially available inhibitors of PDI or modulators thereof (thioredoxin reductase, TRX-R; endoplasmic reticulum oxidoreductin-1, ERO-1) inhibit the replication of CHIKV chikungunya virus (CHIKV) in vitro in a dose-dependent manner. Further, the TRX-R inhibitor auranofin inhibited Venezuelan equine encephalitis virus and the flavivirus Zika virus replication in vitro, while PDI inhibitor 16F16 reduced replication but demonstrated notable toxicity. 16F16 significantly altered the viral genome: plaque-forming unit (PFU) ratio of CHIKV in vitro without affecting relative intracellular viral RNA quantities and inhibited CHIKV E1-induced cell-cell fusion, suggesting that PDI inhibitors alter progeny virion infectivity through altered envelope function. Auranofin also increased the extracellular genome:PFU ratio but decreased the amount of intracellular CHIKV RNA, suggesting an alternative mechanism of action. Finally, auranofin reduced footpad swelling and viremia in the C57BL/6 murine model of CHIKV infection. Our results suggest that targeting oxidative folding pathways represents a potential new anti-alphavirus therapeutic strategy.
[Mh] MeSH terms primary: Antiviral Agents/pharmacology
Chikungunya Fever/virology
Chikungunya virus/drug effects
Chikungunya virus/physiology
Host-Pathogen Interactions/physiology
[Mh] MeSH terms secundary: Alphavirus Infections/virology
Animals
Auranofin/antagonists & inhibitors
Chikungunya Fever/mortality
Chikungunya virus/pathogenicity
Disease Models, Animal
Encephalitis Virus, Venezuelan Equine/drug effects
Flavivirus/drug effects
HEK293 Cells
Humans
Membrane Glycoproteins
Mice
Mice, Inbred C57BL
Protein Disulfide-Isomerases/pharmacology
Protein Folding
Thioredoxin-Disulfide Reductase/pharmacology
Viral Envelope Proteins/metabolism
Virus Replication/drug effects
Zika Virus/drug effects
Zika Virus Infection/virology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antiviral Agents); 0 (Membrane Glycoproteins); 0 (Viral Envelope Proteins); 3H04W2810V (Auranofin); EC 1.8.1.9 (Thioredoxin-Disulfide Reductase); EC 5.3.4.1 (Protein Disulfide-Isomerases)
[Em] Entry month:1712
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE

  8 / 2317 MEDLINE  
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[PMID]: 29244871
[Au] Autor:Haist KC; Burrack KS; Davenport BJ; Morrison TE
[Ad] Address:Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado, United States of America.
[Ti] Title:Inflammatory monocytes mediate control of acute alphavirus infection in mice.
[So] Source:PLoS Pathog;13(12):e1006748, 2017 Dec.
[Is] ISSN:1553-7374
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chikungunya virus (CHIKV) and Ross River virus (RRV) are mosquito-transmitted alphaviruses that cause debilitating acute and chronic musculoskeletal disease. Monocytes are implicated in the pathogenesis of these infections; however, their specific roles are not well defined. To investigate the role of inflammatory Ly6ChiCCR2+ monocytes in alphavirus pathogenesis, we used CCR2-DTR transgenic mice, enabling depletion of these cells by administration of diptheria toxin (DT). DT-treated CCR2-DTR mice displayed more severe disease following CHIKV and RRV infection and had fewer Ly6Chi monocytes and NK cells in circulation and muscle tissue compared with DT-treated WT mice. Furthermore, depletion of CCR2+ or Gr1+ cells, but not NK cells or neutrophils alone, restored virulence and increased viral loads in mice infected with an RRV strain encoding attenuating mutations in nsP1 to levels detected in monocyte-depleted mice infected with fully virulent RRV. Disease severity and viral loads also were increased in DT-treated CCR2-DTR+;Rag1-/- mice infected with the nsP1 mutant virus, confirming that these effects are independent of adaptive immunity. Monocytes and macrophages sorted from muscle tissue of RRV-infected mice were viral RNA positive and had elevated expression of Irf7, and co-culture of Ly6Chi monocytes with RRV-infected cells resulted in induction of type I IFN gene expression in monocytes that was Irf3;Irf7 and Mavs-dependent. Consistent with these data, viral loads of the attenuated nsP1 mutant virus were equivalent to those of WT RRV in Mavs-/- mice. Finally, reconstitution of Irf3-/-;Irf7-/- mice with CCR2-DTR bone marrow rescued mice from severe infection, and this effect was reversed by depletion of CCR2+ cells, indicating that CCR2+ hematopoietic cells are capable of inducing an antiviral response. Collectively, these data suggest that MAVS-dependent production of type I IFN by monocytes is critical for control of acute alphavirus infection and that determinants in nsP1, the viral RNA capping protein, counteract this response.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180128
[Lr] Last revision date:180128
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.ppat.1006748

  9 / 2317 MEDLINE  
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[PMID]: 29321325
[Au] Autor:LaPointe AT; Gebhart NN; Meller ME; Hardy RW; Sokoloski KJ
[Ad] Address:Department of Microbiology and Immunology, and the Center for Predictive Medicine for Biodefense and Emerging Infectious Diseases, University of Louisville School of Medicine, Louisville KY 40202, U.S.A.
[Ti] Title:The Identification and Characterization of Sindbis Virus RNA:Host Protein Interactions.
[So] Source:J Virol;, 2018 Jan 10.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Arthropod-borne viruses, such as the members of genus , are a significant concern to global public health. As obligate intracellular pathogens, RNA viruses must interact with the host cell machinery to establish, and complete, their viral lifecycles. Despite considerable efforts to define the host/pathogen interactions essential for alphaviral replication, an unbiased and inclusive assessment of alphaviral RNA:protein interactions has not been undertaken. Moreover, the biological and molecular importance of these interactions, in the full context of their molecular function as RNA-binding proteins, has not been fully realized. The data presented here introduces a robust viral RNA:protein discovery method to elucidate the Sindbis virus (SINV) RNA:Protein host interface. Cross-Link Assisted mRNP Purification (CLAMP) assessment reveals an extensive array of host/pathogen interactions centered on the viral RNAs (vRNAs). After prioritization of the host proteins associated with the vRNAs, we identified the site of Protein:vRNA interaction via a CLIP-seq approach and assessed the consequences of the RNA:protein binding event of hnRNP K, hnRNP I, and hnRNP M in regards to viral infection. Herein we demonstrate that mutation of the prioritized hnRNP:vRNA interaction sites effectively disrupted the hnRNP:vRNA interaction. Correlating with disrupted hnRNP:vRNA binding, SINV growth kinetics were reduced relative to wild type parental viral infections in a vertebrate and invertebrate tissue culture models of infection. The molecular mechanism leading to reduced viral growth kinetics were found to be dysregulated structural gene expression. Collectively, this study further defines the scope and importance of the alphavirus host/pathogen vRNA:protein interactions. Members of the genus Alphavirus are widely recognized for their potential to cause severe disease. Despite this recognition, there are no antiviral therapeutics, or safe and effective vaccines, currently available to treat alphaviral infection. Alphaviruses utilize the host cell machinery to efficiently establish and complete their viral lifecycle. However, the extent, and importance, of host/pathogen RNA:protein interactions is woefully under characterized. The efforts detailed in this study fulfill this critical gap; and the significance of this research is three-fold. First, the data presented here fundamentally expands the scope and understanding of alphavirus host/pathogen interactions. Secondly, this study identifies the site of interactions for several prioritized interactions and defines the contribution of the RNA:protein interaction at the molecular level. Finally, these studies build a strategy by which the importance of given host/pathogen interactions may be assessed, in the future, using a mouse model of infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180111
[Lr] Last revision date:180111
[St] Status:Publisher

  10 / 2317 MEDLINE  
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[PMID]: 29285673
[Au] Autor:Liu SQ; Li X; Zhang YN; Gao AL; Deng CL; Li JH; Jehan S; Jamil N; Deng F; Wei H; Zhang B
[Ad] Address:Chinese Academy of Sciences Key Laboratory of Special Pathogens and Biosafety, Center for Emerging Infectious Diseases, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
[Ti] Title:Detection, isolation, and characterization of chikungunya viruses associated with the Pakistan outbreak of 2016-2017.
[So] Source:Virol Sin;32(6):511-519, 2017 Dec.
[Is] ISSN:1995-820X
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:The chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus, which has infected millions of people in Africa, Asia, Americas, and Europe since it reemerged in India and Indian Ocean regions in 2005-2006. Starting in the middle of November 2016, CHIKV has been widely spread, and more than 4,000 cases of infections in humans were confirmed in Pakistan. Here, we report the first isolation and characterization of CHIKV from the Pakistan outbreak. Eight CHIKV strains were newly isolated from human serum samples using a cell culture procedure. A full-length genome sequence and eight complete envelope (E1) sequences of CHIKV from Pakistan were obtained in this study. Alignment of the CHIKV E1 sequences revealed that the eight new CHIKV isolates were highly homogeneous, with only two nonsynonymous substitutions found at generally conserved sites (E99 and Q235). Based on the comparison of 342 E1 sequences, the two nonsynonymous mutations were located in well-recognized domains associated with viral functions such as the cell fusion and vector specificity, suggesting their potential functional importance. Phylogenetic analysis indicated that the CHIKV strains from Pakistan originated from CHIKV circulating in the Indian region. This study helps elucidate the epidemics of CHIKV in Pakistan and also provides a foundation for studies of evolution and expansion of CHIKV in South Asia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180105
[Lr] Last revision date:180105
[St] Status:In-Process
[do] DOI:10.1007/s12250-017-4059-7


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