Top PDF Phylogeography of Japanese encephalitis virus: genotype is associated with climate.

Phylogeography of Japanese encephalitis virus: genotype is associated with climate.

Phylogeography of Japanese encephalitis virus: genotype is associated with climate.

The circulation of vector-borne zoonotic viruses is largely determined by the overlap in the geographical distributions of virus-competent vectors and reservoir hosts. What is less clear are the factors influencing the distribution of virus-specific lineages. Japanese encephalitis virus (JEV) is the most important etiologic agent of epidemic encephalitis worldwide, and is primarily maintained between vertebrate reservoir hosts (avian and swine) and culicine mosquitoes. There are five genotypes of JEV: GI-V. In recent years, GI has displaced GIII as the dominant JEV genotype and GV has re-emerged after almost 60 years of undetected virus circulation. JEV is found throughout most of Asia, extending from maritime Siberia in the north to Australia in the south, and as far as Pakistan to the west and Saipan to the east. Transmission of JEV in temperate zones is epidemic with the majority of cases occurring in summer months, while transmission in tropical zones is endemic and occurs year-round at lower rates. To test the hypothesis that viruses circulating in these two geographical zones are genetically distinct, we applied Bayesian phylogeographic, categorical data analysis and phylogeny-trait association test techniques to the largest JEV dataset compiled to date, representing the envelope (E) gene of 487 isolates collected from 12 countries over 75 years. We demonstrated that GIII and the recently emerged GI-b are temperate genotypes likely maintained year-round in northern latitudes, while GI-a and GII are tropical genotypes likely maintained primarily through mosquito-avian and mosquito-swine transmission cycles. This study represents a new paradigm directly linking viral molecular evolution and climate.
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The Molecular Epidemiology and Evolution of Murray Valley Encephalitis Virus: Recent Emergence of Distinct Sub-lineages of the Dominant Genotype 1.

The Molecular Epidemiology and Evolution of Murray Valley Encephalitis Virus: Recent Emergence of Distinct Sub-lineages of the Dominant Genotype 1.

Murray Valley encephalitis virus (MVEV; genus Flavivirus, family Flaviviridae) is the most important cause of arboviral encephalitis in Australia. It is a member of the Japanese encephali- tis (JE) serocomplex, along with other medically important flaviviruses such as JE virus (JEV) and West Nile virus (WNV), which also circulate in the Australasian region [1]. MVEV exists in zoonotic cycles between Culex species mosquitoes and water birds (reviewed in [2]). It is enzootic in northern parts of Australia, including the Kimberley region of Western Australia and northern areas of the Northern Territory, with frequent spillovers into the Pilbara and Gascoyne regions of Western Australia, and occasional spread to southern areas of the North- ern Territory and northern Queensland [3–5]. MVEV very occasionally spreads into south- eastern Australia following periods of heavy and prolonged rainfall, where it has caused major epidemics in the last century, centred in the Murray Valley region [2,3,6]. Since the last nation- wide epidemic of MVE in 1974, there have been approximately 127 human cases, with the majority occurring in Western Australia or the Northern Territory. Outside Australia, MVEV is believed to be endemic in Papua New Guinea (PNG), where human cases, serological evi- dence of infection, and virus isolations have been reported [7–9]. In addition to human disease, MVEV can cause fatal encephalitis in horses [10,11].
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The effect of vaccination coverage and climate on Japanese encephalitis in Sarawak, Malaysia.

The effect of vaccination coverage and climate on Japanese encephalitis in Sarawak, Malaysia.

The four major limitation of this study were 1) highly focused and small scale nature of the original pilot hospital-based surveillance study, which only used a single hospital and a passive surveillance method; 2) the reporting bias from the relatively higher peak of JE cases in Sarawak in 1998, which also coincided with the Nipah virus outbreak in Malaysia and led to greater effort to accurately identify encephalitic cases relative to the other years; 3) a very limited time series (i.e. 10 years) during which there was only one relatively large JE outbreak peak, only 3 ENSO events (2 El Nin˜o and 1 La Nin˜a) and only 4 years when there was no vaccine; and 4) because West Nile (Kunjin) virus has been isolated from mosquitoes in Sarawak [38] patients may have been misdiagnosed due to cross-reactivity between West Nile virus (WN) virus (WNV) and JEV. Because we focused on a single hospital in Sarawak, which was the main referral hospital in the area, and collected accurate data, we are confident we have a less biased sample that is providing a lucid picture of JEV infection trends. A study demonstrated the high peak in 1998 during the Nipah outbreak was for the whole Sarawak state, while the peak for Sibu during the same period was not substantially different from the other years [19], suggesting that the data collected for Sibu are less prone to clinician awareness bias since even the heightened reporting for encephalitis cases in 1998/1999 did not change the reporting pattern in Sibu. With such a short time period and the reduction of disease cases with vaccination, it is difficult to say with certainty whether the patterns seen in the study are regular predictable phenomena or random events; therefore, longer studies with pig or mosquito JE incidence may be useful in future studies. Whilst the serological tests employed in the study
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Molecular identification of Saint Louis encephalitis virus genotype IV in Colombia

Molecular identification of Saint Louis encephalitis virus genotype IV in Colombia

The results allow us to postulate the existence of an enzootic cycle of SLEV lineage IV transmission with- out discarding the possible existence of other genotypes circulating in this zone. Genotypes VA/III/II are widely dispersed, probably by migratory birds, in Brazil, USA, Mexico and Argentina (Kramer & Chandler 2001, Au- guste et al. 2009, Díaz et al. 2011). Interestingly, geno- type IV has not been associated with geographic disper- sion or equine/human cases of encephalitis and has not been detected in countries other than Panama and Co- lombia. This finding suggests that genotype IV, similar to other genotypes, has low virulence for equines and humans, which is consistent with previous observations of SLEV isolated from the Palenque region (Mexico) (Kopp et al. 2013) and could explain the absence of neu- rological disease in SLEV seropositive equines in the Córdoba (Mattar et al. 2005, 2011) with the exception of the recent isolation of SLEV-genotype VB from a neuro- logically ill horse in Brazil (Rosa et al. 2013).
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Abrogated inflammatory response promotes neurogenesis in a murine model of Japanese encephalitis.

Abrogated inflammatory response promotes neurogenesis in a murine model of Japanese encephalitis.

duration and intensity of the inflammatory response. One of the best characterised neurogenic niches is SVZ [40], the endogenous brain compartment housing the self-renewing NSPCs, which have immense potential of tissue repair upon CNS injury [41,42]. Functional impairment of the SVZ germinal niche has been shown following either cranial irradiation [43], or LPS-mediated acute inflammation [44] or EAE-induced persistent inflammation [45]. Inflammation associated with ischemic insults and stroke compro- mise the survivability of the newly formed striatal neurons that are generated from the SVZ after stroke [46,47]. Our investigation also revealed a significant reduction in the actively replicating cells including those belonging to the neuronal lineage in the JEV- infected SVZ niche. Administration of the anti-inflammatory compound minocycline was able to restore the NSPC population back to that in control SVZ. Minocycline readily crosses the BBB and suppress microglial activation in a number of neurodegener- ative disorders as well as virus infections [30,48]. Similarly, in models of LPS inflammation and stroke, minocycline decreased microglial activation, accounting for the potentiation of NSPC pool and neurogenesis [14,28]. However, no direct effect of minocycline in stimulating endogenous neurogenesis in control animals has been reported, which is corroborated by our in vivo findings. Minocycline administration to control animals did not result in any significant increase in the number of proliferating cells in the neurogenic niche, i.e. the SVZ. Hence, it is plausible that minocycline has no direct effect on neurogenesis. Inflamma- tory blockade usually is accompanied by a broad spectrum of effects which promote neurogenesis, like reduction of cell death of new born neurons [14], attenuation of HPA axis activation [49], or the decrease in pro-inflammatory cytokines and serum glucocorticoid levels [15,50].
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The Potential Use of Wolbachia-Based Mosquito Biocontrol Strategies for Japanese Encephalitis.

The Potential Use of Wolbachia-Based Mosquito Biocontrol Strategies for Japanese Encephalitis.

Although climate change could further increase the geographical range of JEV transmission, in a similar way as predicted for DENV [31,32], the potential impact is yet to be determined. It is predicted that climate change will lead to increases in mosquito vector density, incursion of exotic mosquito species into novel areas, changes in agricultural practices, and migration of host reservoir birds. In particular, rice fields in JEV-endemic areas would likely become more arid and the subsequent increase in flooding, either through irrigation or extreme weather events, would provide optimal breeding conditions for Cx. tritaeniorhynchus [2]. Rapid out- breaks of JE are difficult to control, with traditional methods such as space spraying of insecti- cides having little impact because of the unpredictability and infrequency of outbreaks. Climate change may also influence migration patterns of birds, which may result in long-dis- tance JEV dissemination in new areas. WNV is a closely related zoonotic flavivirus that has a similar enzootic transmission cycle with reservoir migratory birds. The introduction of the closely related WNV to novel areas has been strongly associated with bird migration [33,34], and climate change is likely to influence WNV outbreaks [35,36]. As there is very little known about the particular migration patterns of the avian reservoirs for JEV, the likely impact of cli- mate change remains unknown [37]. In recent years, significant advances have been made in the potential use of the bacterial endosymbiont Wolbachia for mosquito biocontrol. This has included the successful transinfection of Cx. quinquefasciatus to create a wPip strain variant su- perinfection [38]. Wolbachia transinfection of Cx. tritaeniorhynchus could provide the basis for an environmentally friendly and cost-effective biocontrol strategy that could significantly impact JEV transmission (Box 1), which is likely to remain applicable even if JEV-endemic re- gions expand in the future as a result of climate change.
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Low Protective Efficacy of the Current Japanese Encephalitis Vaccine against the Emerging Genotype 5 Japanese Encephalitis Virus.

Low Protective Efficacy of the Current Japanese Encephalitis Vaccine against the Emerging Genotype 5 Japanese Encephalitis Virus.

Japanese encephalitis (JE), probably the world’s most frequently occurring viral encephalitis, is a neurological infectious disease caused by Japanese encephalitis virus (JEV), transmitted via mosquito bite [1]. The mortality rate of JE patients is 30–35% and 50% of JE survivors live with neurological sequelae. Therefore, JE is considered a disease with significant public health and economic burdens [2, 3]. JE, prevalent in 24 Asia-Pacific countries, is a mosquito-borne zoo- notic natural focal disease with an estimated 67,900 cases each year. Approximately, 30 million people live in JE-endemic areas [4]. In addition, with increased international travel and busi- ness to these areas, more people are at risk of JE infection [5, 6], presenting a potentially serious international public health problem.
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SOROPREVALÊNCIA DE ANTICORPOS E PADRONIZAÇÃO DO TESTE ELISA SANDUÍCHE INDIRETO PARA 19 TIPOS DE ARBOVÍRUS EM HERBÍVOROS DOMÉSTICOS ALEXANDRE DO ROSÁRIO CASSEB

SOROPREVALÊNCIA DE ANTICORPOS E PADRONIZAÇÃO DO TESTE ELISA SANDUÍCHE INDIRETO PARA 19 TIPOS DE ARBOVÍRUS EM HERBÍVOROS DOMÉSTICOS ALEXANDRE DO ROSÁRIO CASSEB

The brazilian Amazon region maintains the largest variety of arboviruses and the state of Pará is responsible for 26% of this territory, so the major goal of this work was to determine the prevalence and distribution of HI antibodies to 19 domestic arbovirus in domestic herbivores in the state of Pará and to standardize an indirect sandwich IgG ELISA test to serum samples of equines, cattle, buffaloes and sheep. In all species studied and throughout the State of Pará a large prevalence of HI antibodies to all arbovirus analyzed was observed and SLEV, ILHV, EEEV, MAGV and WEEV, showed higher prevalence, where the SLEV was the most prevalent. Regarding the virus families HI antibodies to MAGV was the most prevalent Bunyaviridae in all species, the most prevalent Flaviviridae was SLEV in all species and in the family Togaviridae the EEEV was more prevalent in horses. In order to analyze the prevalence of HI antibodies by animal species was observed that horses did not show significant differences compared to buffaloes, however, showed significant difference compared to cattle and sheep; there was not observed significant difference between the ruminant species. Using sandwich indirect IgG ELISA a large number of crossed reactions were found. This enzymatic test can be used to detect IgG antibodies among families of arboviruses studied.
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Distinct dictation of Japanese encephalitis virus-induced neuroinflammation and lethality via triggering TLR3 and TLR4 signal pathways.

Distinct dictation of Japanese encephalitis virus-induced neuroinflammation and lethality via triggering TLR3 and TLR4 signal pathways.

TLRs function as intermediates by interacting with products of viral replication, and transmitting signals to a cascade of adaptors and kinases that ultimately lead to the activation of transcription of cytokines and type I IFN genes. TLR3 recruits the adaptor molecule TRIF to induce type I IFN gene via interactions with TRAF3, TBK1, and IKKe, which, in turn, activate the latent transcription factors IRF-3 and IRF-7, whereas other TLRs associating with the adaptor protein MyD88 form a complex with TRAF6, IRAK1, and IRAK4 to activate kinases that regulate IRF-5 and IRF-7. Notably, TLR4 signal pathway uses both adaptor molecules MyD88 and TRIF to initiate the production of cytokine and type I IFN proteins. In viral infection, four TLRs, including TLR3, TLR7, TLR8 and TLR9, seem to play critical roles in the recognition of viral nucleic acid components, and TLR2 and TLR4 were shown to detect viral components such as envelope glycoproteins [22–26]. We have previously shown that JEV can modulate innate immune responses and subsequent adaptive responses in MyD88-dependent and independent path- ways [27], which indicate that JEV may be recognized by certain TLR signal pathways, thereby affecting the outcome of JEV- induced neurological diseases. Therefore, we aimed to determine whether each TLR signal pathway modulated neurological disease caused by JEV infection, using several TLR-deficient mice (TLR2, TLR3, TLR4, TLR7, TLR9). Surprisingly, among the tested TLR-deficient mouse strains we found a contrasting result in TLR3 2/2 and TLR4 2/2 mice, i.e. TLR3 2/2 mice were highly susceptible to JE, whereas TLR4 2/2 mice showed markedly enhanced resistance to JE. Subsequently, we investigated the pathologic feature, type I IFN innate and adaptive immunity of TLR3 2/2 and TLR4 2/2 mice during JE progression. TLR3 2/2 mice displayed severe neuroinflammatory reactions as well as enhanced BBB permeability by failure of the early control of viral replication, whereas TLR4 2/2 mice elicited the effective regula- tion of viral replication and subsequent inflammatory reaction by inducing potent type I IFN innate immune responses against JEV. Notably, our data revealed that TLR4 ablation provided potent type I IFN innate responses through enhanced induction of antiviral ISG genes by alternative activation of IRF-3 and NF-kB in myeloid-derived DCs and macrophages. Also, TLR4 2/2 mice showed an alteration of plasmacytoid DC subpopulation and CD4 +
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Biological stability of a strain of Cowpea severe mosaic virus over 20 years

Biological stability of a strain of Cowpea severe mosaic virus over 20 years

Abstract - Cowpea (Vigna unguiculata) is an important crop of the traditional agriculture system in the Northeast of Brazil. It can be infected by more than 20 virus species and Cowpea severe mosaic virus (CPSMV) is one of the most important pathogens that naturally infect cowpea in Brazil. Several CPSMV isolates were obtained and characterized in the Plant Virus Laboratory at the Federal University of Ceará: CPSMV-CE - the first characterized isolate of the virus obtained from cowpea in the State of Ceará; CPSMV-AL - isolated from cowpea in Alagoas; CPSMV-PE - isolated from cowpea in Pernambuco; CPSMV-PR - obtained from soybean (Glycine max) in Paraná and CPSMV-CROT - isolated from Crotalaria paulinea, in Maranhão. An isolate of CPSMV with the property to infect the cv. Macaibo, a cowpea cultivar immune to most of CPSMV isolates was also biologically and serologically characterized as a new strain of the virus (CPSMV-MC). The CPSMV-MC was isolated in January 1990 and has been evaluated over 20 years by host range studies and maintenance in vivo by periodical mechanical inoculations in cowpea. The results of this periodical evaluation revealed that the biological integrity and the serological properties of CPSMV-MC were preserved over 20 years, indicating that the genetic preservation of a virus strain could occur over the years. Molecular studies involving part of the coat protein (CP) gene of CPSMV-MC and five other Brazilian CPSMV isolates indicated a high degree of conservation, with 92-100% nucleotide sequence identity among the isolates.
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Laboratorial Diagnosis of Lymphocytic Meningitis

Laboratorial Diagnosis of Lymphocytic Meningitis

Central Nervous System (CNS) infections classically are classified as meningitis and encephalitis [1]. Meningitis is the most common infectious CNS syndrome, defined as an inflammation of the meninges. The clinical symptoms are fever, malaise, vomiting, and in some cases, petechial rashes. Signs of meningeal irritation include neck stiffness, Kernig’s sign, (an inflection of the knee when the limb is placed at a certain degree of relative inflection to the trunk), and Brudzinski’s sign, (an involuntary inflection of the limb following a head inflection). These signs are poorly sensed in adults. In one study of adults, both Kernig and Brudzinski signs had a sensitivity of only 5%, while the sensitivity of nuchal rigidity was 30%. The non- specific nature of the symptoms and clinical signs means that we often over-treat and look to other exams to confirm the diagnosis [2].
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Bispidine-amino acid conjugates act as a novel scaffold for the design of antivirals that block Japanese encephalitis virus replication.

Bispidine-amino acid conjugates act as a novel scaffold for the design of antivirals that block Japanese encephalitis virus replication.

Effect of bispidine conjugates on JEV production We tested for the anti-viral property of bispidine-conjugates using JEV replication model in N2A cells. Cells were infected with JEV and after the adsorption of the virus, cells were grown in medium containing bispidine conjugates and at 22 h pi viral titers in the infected cell supernatants were measured by performing plaque assays. Cells treated with the leucine derivative, BLB, consistently reduced viral titers by hundred to thousand-fold compared to cells treated with DMSO. The removal of N- protecting groups (BLdp) led to complete loss of anti-JEV activity. Changing the terminal group from a t-butyloxycarbonyl group (BLB) to benzyloxycarbonyl (BLZ) on the terminal of leucine lowered the viral inhibition efficiency while the hexapeptide derivative (B(GLV)2) showed a decrease in anti-JEV activity indicating the dependence on the nature of the amino acid unit on the inhibitory properties of these compounds (Figure 2A). We next assessed if the observed effect of BLB on JEV titers is due to reduced cell numbers as a result of cell death. BLB treatment was found not to affect cell viability (by trypan blue exclusion, data not shown) or induce cytotoxicity at the concentration used for viral inhibition (Figure 2B). JEV infects a wide-variety of species and cell type, therefore, we next tested whether BLB was capable of inhibiting JEV replication in cell lines from different species. Huh7 and C6/36 cells were infected with JEV and treated with BLB as mentioned above. We found that BLB inhibited JEV infection by more than ten-fold in both these cell lines indicating that the target of BLB could be one of the viral protein/s or a host factor which is conserved across species and which plays a role in JEV replication (Figure 2C). The inhibitory effect in these cell lines appears to be less than that observed in N2A cells suggesting that the cells of neuronal origin are probably more sensitive to the action of BLB. Previous reports of JEV inhibition using peptide-conjugated morpholino oligomer also showed a similar cell-type dependent effect [11].
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SORL1 is genetically associated with late-onset Alzheimer's disease in Japanese, Koreans and Caucasians.

SORL1 is genetically associated with late-onset Alzheimer's disease in Japanese, Koreans and Caucasians.

Funding: This study was supported by a Grants-in-Aid for Scientific Research on Priority Areas, ‘Advanced Brain Science Project’ (Y.I.), ‘Comprehensive Genomics’ (R.K., K.T. and K.Y.), and ‘Applied Genomics’ (S.T.) and ‘Integrated Database Project’ (A.K.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan, ‘Japanese Alzheimer’s Disease Neuroimaging Initiative’ (R.K.) by New Energy and Industrial Technology Development Organization (NEDO) in Japan, and by a grant from the Korea Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (A120030). The United States National Institutes of Health (NIH), National Institute on Aging (NIH-NIA) supported this work through the following grants: ADGC, U01 AG032984, RC2 AG036528; NACC, U01 AG016976; NCRAD, U24 AG021886; NIA LOAD, U24 AG026395, U24 AG026390; BU ADC P30; MIRAGE R01 AG025259; Banner Sun Health Research Institute P30 AG019610; Boston University, P30 AG013846, U01 AG10483, R01 CA129769, R01 MH080295, R01 AG017173, R01AG33193; Columbia University, P50 AG008702, R37 AG015473; Duke University, P30 AG028377, AG05128; Emory University, AG025688; Group Health Research Institute, UO1 AG06781, UO1 HG004610; Indiana University, P30 AG10133; Johns Hopkins University, P50 AG005146, R01 AG020688; Massachusetts General Hospital, P50 AG005134; Mayo Clinic, P50 AG016574; Mount Sinai School of Medicine, P50 AG005138, P01 AG002219; New York University, P30 AG08051, MO1RR00096, and UL1 RR029893; Northwestern University, P30 AG013854; Oregon Health & Science University, P30 AG008017, R01 AG026916; Rush University, P30 AG010161, R01 AG019085, R01 AG15819, R01 AG17917, R01 AG30146; TGen, R01 NS059873; University of Alabama at Birmingham, P50 AG016582, UL1RR02777; University of Arizona, R01 AG031581; University of California, Davis, P30 AG010129; University of California, Irvine, P50 AG016573, P50, P50 AG016575, P50 AG016576, P50 AG016577; University of California, Los
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Rev. Soc. Bras. Med. Trop.  vol.50 número3

Rev. Soc. Bras. Med. Trop. vol.50 número3

Following the uneventful reversion of sedation and extubation, there was no evidence of neurological motor disorders. However, important cognitive-behavioral changes were observed, including affective disorders, infantile behavior, as well as different types of apraxia, particularly regarding personal care activities and writing. Laboratory tests indicated an increased natremia (30mEq/L) over 24 hours. A further brain magnetic resonance imaging (MRI) study showed bilateral and symmetric high signal intensity on T2-weighted luid attenuated inversion recovery (T2 FLAIR) in the caudate and putamen nucleus, which was interpreted as osmotic demyelination syndrome (Figure 2). There was no diffusion restriction or enhancement following intravenous contrast.
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DETECTION OF A NEUTROPHIL CHEMOTACTIC FACTOR IN JAPANESE ENCEPHALITIS PATIENTS

DETECTION OF A NEUTROPHIL CHEMOTACTIC FACTOR IN JAPANESE ENCEPHALITIS PATIENTS

Japanese encephalitis virus (JEV, an arthropod-borne flavivirus) infection remains one of the major causes of encephalitis with significant mortality among children in India. The principal vector is Culex mosquito (C.tritaenorhynchus), which breeds extensively in rice fields. The natural cycle of JEV consists of pig mosquito pig or bird mosquito bird cycle, with pigs being the most important biological amplifiers and reservoirs 1-3 . JEV is transmitted to humans through the bite of infected mosquitoes. But humans are accidental, dead end hosts and human JE cases imported into non-endemic areas represent a minimal risk for subsequent transmission of the virus 4 . The infection with JEV ranges from nonspecific febrile illness to a severe meningoencephalomyelitis illness. After entry into the host, JEV replicates in a number of organs and generates a rapid inflammatory response in humans and in experimental animals with mononuclear and polymorphonuclear infiltration 5 . Neutrophils increase in number during second week of JEV infection 6 and it has been reported earlier that this increase coincides with the production of a chemotactic protein (MDF) by JEV-primed splenic macrophages in mice 7 , with development of hypoglycemia 8 . MDF has been shown to play a role in the pathogenesis of JEV infection 2,6 . So it was thought important to investigate this aspect in human cases also and to look for any correlation with the illness.
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WATER RETENTION AND AVAILABILITY IN SOILS OF THE STATE OF SANTA CATARINA-BRAZIL: EFFECT OF TEXTURAL CLASSES, SOIL CLASSES AND LITHOLOGY

WATER RETENTION AND AVAILABILITY IN SOILS OF THE STATE OF SANTA CATARINA-BRAZIL: EFFECT OF TEXTURAL CLASSES, SOIL CLASSES AND LITHOLOGY

The retention and availability of water in the soil vary according to the soil characteristics and determine plant growth. Thus, the aim of this study was to evaluate water retention and availability in the soils of the State of Santa Catarina, Brazil, according to the textural class, soil class and lithology. The surface and subsurface horizons of 44 profiles were sampled in different regions of the State and different cover crops to determine field capacity, permanent wilting point, available water content, particle size, and organic matter content. Water retention and availability between the horizons were compared in a mixed model, considering the textural classes, the soil classes and lithology as fixed factors and profiles as random factors. It may be concluded that water retention is greater in silty or clayey soils and that the organic matter content is higher, especially in Humic Cambisols, Nitisols and Ferralsol developed from igneous or sedimentary rocks. Water availability is greater in loam-textured soils, with high organic matter content, especially in soils of humic character. It is lower in the sandy texture class, especially in Arenosols formed from recent alluvial deposits or in gravelly soils derived from granite. The greater water availability in the surface horizons, with more organic matter than in the subsurface layers, illustrates the importance of organic matter for water retention and availability.
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Characterisation of divergent flavivirus NS3 and NS5 protein sequences detected in Rhipicephalus microplus ticks from Brazil

Characterisation of divergent flavivirus NS3 and NS5 protein sequences detected in Rhipicephalus microplus ticks from Brazil

Only 0.025% of the reads exhibited identity with con- tig sequences 401 and 317. Although viral RNA sequenc- es from MGTV were underrepresented, we found two RNA-seq contigs, 1,961 and 2,579, with greater than 90% nt identity with the tick cDNA library contigs (Supple- mentary data, Table SII, highlighted rows). Both contigs exhibited significant similarity to the TABV polyprotein. RNA-seq contigs 1,961 (2,993 nt) and 2,579 (2,721 nt) were similar to the Flavivirus NS5 and NS3 NS proteins, respectively. Several contigs exhibited intermediate sim- ilarity with other Flavivirus structural and NS proteins (Supplementary data, Fig. S6). However, because most of these contigs represented short consensus sequences, we were unable to build a proper scaffold genome for MGTV. Therefore, RNA-seq contigs 1,961 and 2,579 were the only ones confirmed as MGTV-derived sequences. Al- though the complete genomic sequence could not be identified through deep sequencing, the complete NS3 and NS5 sequences from MGTV were obtained. Because NS3 and NS5 are the two largest and most conserved Fla- vivirus proteins (Chambers et al. 1990), we performed a comparative sequence analysis between these two MGTV proteins and NS3 and NS5 from Flaviviridae vi- ruses to confirm our findings concerning the presence of Flavivirus-like transcripts in R. microplus ticks and to investigate the relationship between this presumed flavi- virus and other members of the Flaviviridae family.
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Which body mass index is best associated with risk of diabetes mellitus and hypertension in a Japanese-Brazilian population?

Which body mass index is best associated with risk of diabetes mellitus and hypertension in a Japanese-Brazilian population?

The data used in the current study are from a co- hort-type population study initiated in 1993, fol- lowing a demographic survey, with the purpose of identifying the prevalence of diabetes mellitus (based on the oral glucose tolerance test) and as- sociated diseases in first-generation Japanese- Brazilians (Issei, or born in Japan) and second- generation (Nisei, or born in Brazil) from 40 to 79 years of age, both males and females, resid- ing in the municipality of Bauru, São Paulo. De- tails on the population selection, recruiting, and characteristics have been described elsewhere
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Determinants of Arbovirus Vertical Transmission in Mosquitoes.

Determinants of Arbovirus Vertical Transmission in Mosquitoes.

Our analysis found striking differences in eVT rates across virus and mosquito taxa. Overall, Aedes mosquitoes displayed higher eVT rates than Culex mosquitoes. Aedes eggs are generally more resistant to desiccation than Culex eggs [23], which may confer a selective advantage to vertically transmitted viruses. In addition, Aedes mosquitoes had higher eVT rates in nature under arid climatic conditions compared to equatorial or warm temperate climatic conditions. This supports the hypothesis that VT could be a maintenance mechanism during the adverse season. In agreement with earlier observations [7,24,25], orthobunyaviruses such as LACV and CEV were vertically transmitted better than flaviviruses and alphaviruses. Orthobunyaviruses are assumed to achieve higher VT rates because they are vertically transmitted by TOT, a more efficient VT mechanism than trans-egg VT of flaviviruses [12]. It is noteworthy that the Flavi- virus genus includes several insect-specific flaviviruses that are primarily maintained by VT in nature [26]. Unlike dual-host flaviviruses [12], insect-specific flaviviruses display high rates of VT that are assumed to result from TOT [27], suggesting that different VT mechanisms may have evolved in the same viral genus. TOT relies on viral infection of developing oocytes, which results in close to 100% infection in the subsequent generations [24]. Such “stabilized” infections have been described for several members of the Orthobunyavirus genus such as CEV in Ae. dorsalis [28] and San Angelo virus in Ae. albopictus [29]. Note that even when TOT rates are close to 100%, prevalence in the vector population is expected to remain low unless the virus confers an evolutionary advantage to the infected subpopulation. TOT may not be required for trans-generational persistence of arboviral infection in the vector, as patterns con- sistent with stabilized infections were also reported for the flaviviruses DENV1 in Ae. albopic- tus [30] and DENV3 in Ae. aegypti [31]. A fourfold increase in DENV3 eVT rate indicated that selection could be involved [31]. Interestingly, we found that prior DENV amplification in invertebrate host cells enhanced subsequent eVT, supporting the idea that stabilized infections require adaptation. Because systemic dissemination of the virus acquired by HT during blood feeding is a prerequisite for VT, stabilized infections are also more likely to be established dur- ing later gonotrophic cycles. VT efficiency could be underestimated in studies that focus on the first gonotrophic cycle and therefore do not account for stabilized infections [24]. When a sta- bilized infection is established, however, VT is expected to occur as soon as the first gono- trophic cycle.
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How do viral and host factors modulate the sexual transmission of HIV? Can transmission be blocked?

How do viral and host factors modulate the sexual transmission of HIV? Can transmission be blocked?

From top to bottom: The epithelial lining of the vagina forms an effi cient barrier to viral penetration when intact. Cervical mucus may serve to strengthen this barrier by physically trapping virions [25]. HIV crosses the epithelial barrier either because of epithelial damage (e.g., microabrasions and traumatic breaches or lesions caused by STDs), or capture by intra- epithelial DCs that convey the virus to target cells deeper in the mucosa [9]. In the lumen of the vagina, continuous with the cervical canal, virions with two kinds of tropism are illustrated: (i) X4 virus (orange) uses the co-receptor CXCR4 (rarely found early after transmission) and (ii) R5 virus (green) utilizing the co-receptor CCR5 (preferentially found early after transmission). Why R5 virus comes to dominate in the newly infected host is not known; it may refl ect preferential amplifi cation at a stage after transmission (not shown) [26]. To the left, an R5 virion is shown bound to an embedded DC, which has CD4, CCR5, and C- type lectin receptors on its surface, all of which can interact with the surface glycoprotein of the virus. The DC may merely capture X4 or R5 virus and carry it across the epithelial barrier or get infected by R5 virus and produce progeny virus (virus budding from the cell surface is shown as half-circular sections studded with grey Env spikes) [9]. To the right, an R5 virion binds to and infects a T helper lymphocyte, which has both CD4 and CCR5 on its surface. Virus that has penetrated into the epithelium is also shown to infect a macrophage. Arrows indicate how virus infects the fi rst target cells and how progeny virus or DCs then migrate via the afferent lymphatics to reach the lymph nodes. Here, further amplifi cation occurs in an environment rich in CD4 + target cells.
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