A importância do bioetanol dentro do contexto brasileiro, comparação de sua síntese a partir de cana-de-açúcar e milho e bioetanol de segunda geração.

RESUMO. Diante da busca por alternativas à dependência dos combustíveis fósseis, o bioetanol representa no Brasil, com sua síntese principalmente a partir de cana-de-açúcar, modelo para o mundo em produção e desenvolvimento sustentável. Este trabalho objetivou avaliar sua importância para o país, sua produção como biocombustível de segunda geração (2G) e comparar sua síntese a partir de cana e milho. O bioetanol tem representado no Brasil importante papel econômico, social e ambiental, com estudos e políticas de sua expansão no país e para o resto do mundo, visando substituir a gasolina. A produção de bioetanol 2G tem potencial de dobrar a produção do biocombustível, sem aumentar a área agrícola. Além disso, sua produção a partir de cana e milho, pode aumentar a sustentabilidade do processo através da criação de usinas flex, que processam ambas matérias-primas. Dessa maneira, as novas tecnologias têm impulsionado o sucesso de bioetanol, tornando-o como referência ao se tratar de biocombustíveis.JORNACITEC 2019

Immunoglobulin response to Plasmodium falciparum RESA proteins in uncomplicated and severe malaria

Background: The three members of the ring-infected erythrocyte surface antigen (RESA) proteins family share high sequence homologies, which impair the detection and assignment to one or another protein of some pathogenic processes inherent to Plasmodium falciparum malaria. The present study was intended to determine if the antibody and inflammatory responses of children living in a malaria-endemic area varied depending on the RESA-1, RESA-2 or RESA-3 proteins and the severity of the disease, two groups of severe and uncomplicated malaria cases being considered. Methods: Two synthetic peptides representing predicted B cell epitopes were designed per RESA protein, all located outside of the 3' and 5' repetition blocks, in order to allow an antibody detection specific of each member of the family. Recombinant rRESA-1B and rRESA-3B proteins were also engineered. Two groups of Beninese children admitted to hospital in 2009 for either uncomplicated or severe malaria were compared for their plasma levels of IgG specifically recognizing each recombinant RESA protein or synthetic peptide, and for their plasma inflammatory cytokine levels (IFN-gamma, TNF-alpha and IL-10), taking into account host and parasite genetic factors. Results: The absence of IgG cross-reactivity between rRESA proteins and their protein carrier as well as between each RESA peptide and a non-epitopic RESA control peptide validated the use of the engineered recombinant proteins and peptides for the measurement of plasma IgG. Taking into account age, fever duration and parasitaemia, a multiple logistic regression performed on children clustered according to their antibody responses' profiles concluded to an increased risk of severe malaria for P2 (representative of RESA-1) responders (P = 0.007). Increased IL-10 plasma levels were found in children harbouring multiclonal P. falciparum infections on the basis of the T1526G resa2 gene polymorphism (P = 0.004). Conclusions: This study provided novel tools to dissect the seroreactivity against the three members of the RESA protein family and to describe its relation to protection against malaria. It suggested the measurement of plasma antibodies raised against specific peptides to serve as predictive immunologic markers for disease severity. Lastly, it reinforced previous observations linking the T1526G resa2 gene mutation to severe malaria

Genetic diversity and dynamics of the Noir Marron settlement in French Guyana : A study combining mitochondrial DNA, Y chromosome and HTLV-1 genotyping [Abstract]

The Noir Marron are the direct descendants of thousands of African slaves deported to the Guyanas during the Atlantic Slave Trade and later escaped mainly from Dutch colonial plantations. Six ethnic groups are officially recognized, four of which are located in French Guyana: the Aluku, the Ndjuka, the Saramaka, and the Paramaka. The aim of this study was: (1) to determine the Noir Marron settlement through genetic exchanges with other communities such as Amerindians and Europeans; (2) to retrace their origins in Africa. Buffy-coat DNA from 142 Noir Marron, currently living in French Guyana, were analyzed using mtDNA (typing of SNP coding regions and sequencing of HVSI/II) and Y chromosomes (typing STR and SNPs) to define their genetic profile. Results were compared to an African database composed by published data, updated with genotypes of 82 Fon from Benin, and 128 Ahizi and 63 Yacouba from the Ivory-Coast obtained in this study for the same markers. Furthermore, the determination of the genomic subtype of HTLV-1 strains (env gp21 and LTR regions), which can be used as a marker of migration of infected populations, was performed for samples from 23 HTLV-1 infected Noir Marron and compared with the corresponding database. MtDNA profiles showed a high haplotype diversity, in which 99% of samples belonged to the major haplogroup L, frequent in Africa. Each haplotype was largely represented on the West African coast, but notably higher homologies were obtained with the samples present in the Gulf of Guinea. Y Chromosome analysis revealed the same pattern, i.e. a conservation of the African contribution to the Noir Marron genetic profile, with 98% of haplotypes belonging to the major haplogroup E1b1a, frequent in West Africa. The genetic diversity was higher than those observed in African populations, proving the large Noir Marron’s fatherland, but a predominant identity in the Gulf of Guinea can be suggested. Concerning HTLV-1 genotyping, all the Noir Marron strains belonged to the large Cosmopolitan A subtype. However, among them 17/23 (74%) clustered with the West African clade comprizing samples originating from Ivory-Coast, Ghana, Burkina-Fasso and Senegal, while 3 others clustered in the Trans-Sahelian clade and the remaining 3 were similar to strains found in individuals in South America. Through the combined analyses of three approaches, we have provided a conclusive image of the genetic profile of the Noir Marron communities studied. The high degree of preservation of the African gene pool contradicts the expected gene flow that would correspond to the major cultural exchanges observed between Noir Marron, Europeans and Amerindians. Marital practices and historical events could explain these observations. Corresponding to historical and cultural data, the origin of the ethnic groups is widely dispatched throughout West Africa. However, all results converge to suggest an individualization from a major birthplace in the Gulf of Guinea

Individual variation in levels of haptoglobin-related protein in children from Gabon

Background: Haptoglobin related protein (Hpr) is a key component of trypanosome lytic factors (TLF), a subset of highdensity lipoproteins (HDL) that form the first line of human defence against African trypanosomes. Hpr, like haptoglobin (Hp) can bind to hemoglobin (Hb) and it is the Hpr-Hb complexes which bind to these parasites allowing uptake of TLF. This unique form of innate immunity is primate-specific. To date, there have been no population studies of plasma levels of Hpr, particularly in relation to hemolysis and a high prevalence of ahaptoglobinemia as found in malaria endemic areas. Methods and Principal Findings: We developed a specific enzyme-linked immunosorbent assay to measure levels of plasma Hpr in Gabonese children sampled during a period of seasonal malaria transmission when acute phase responses (APR), malaria infection and associated hemolysis were prevalent. Median Hpr concentration was 0.28 mg/ml (range 0.03-1.1). This was 5-fold higher than that found in Caucasian children (0.049 mg/ml, range 0.002-0.26) with no evidence of an APR. A general linear model was used to investigate associations between Hpr levels, host polymorphisms, parasitological factors and the acute phase proteins, Hp, C-reactive protein (CRP) and albumin. Levels of Hpr were associated with Hp genotype, decreased with age and were higher in females. Hpr concentration was strongly correlated with that of Hp, but not CRP

Relation between Plasmodium falciparum asymptomatic infection and malaria attacks in a cohort of Senegalese children

© 2008 Le Port et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Multiplicity of Plasmodium falciparum infection in asymptomatic children in Senegal: relation to transmission, age and erythrocyte variants

<p>Abstract</p> <p>Background</p> <p>Individuals living in malaria endemic areas generally harbour multiple parasite strains. Multiplicity of infection (MOI) can be an indicator of immune status. However, whether this is good or bad for the development of immunity to malaria, is still a matter of debate. This study aimed to examine the MOI in asymptomatic children between two and ten years of age and to relate it to erythrocyte variants, clinical attacks, transmission levels and other parasitological indexes.</p> <p>Methods</p> <p>Study took place in Niakhar area in Senegal, where malaria is mesoendemic and seasonal. Three hundred and seventy two asymptomatic children were included. Sickle-cell trait, G6PD deficiency (A- and Santamaria) and α⁺-thalassaemia (-α^3.7type) were determined using PCR. Multiplicity of <it>Plasmodium falciparum </it>infection, i.e. number of concurrent clones, was defined by PCR-based genotyping of the merozoite surface protein-2 (<it>msp2</it>), before and at the end of the malaria transmission season. The χ²-test, ANOVA, multivariate linear regression and logistic regression statistical tests were used for data analysis.</p> <p>Results</p> <p>MOI was significantly higher at the end of transmission season. The majority of PCR positive subjects had multiple infections at both time points (64% before and 87% after the transmission season). MOI did not increase in α-thalassaemic and G6PD mutated children. The ABO system and HbAS did not affect MOI at any time points. No association between MOI and clinical attack was observed. MOI did not vary over age at any time points. There was a significant correlation between MOI and parasite density, as the higher parasite counts increases the probability of having multiple infections.</p> <p>Conclusion</p> <p>Taken together our data revealed that α-thalassaemia may have a role in protection against certain parasite strains. The protection against the increase in MOI after the transmission season conferred by G6PD deficiency is probably due to clearance of the malaria parasite at early stages of infection. The ABO system and HbAS are involved in the severity of the disease but do not affect asymptomatic infections. MOI was not age-dependent, in the range of two to ten years, but was correlated with parasite density. However some of these observations need to be confirmed including larger sample size with broader age range and using other <it>msp2 </it>genotyping method.</p

Genome wide linkage study, using a 250K SNP map, of Plasmodium falciparum infection and mild malaria attack in a Senegalese population

Multiple factors are involved in the variability of host's response to P. falciparum infection, like the intensity and seasonality of malaria transmission, the virulence of parasite and host characteristics like age or genetic make-up. Although admitted nowadays, the involvement of host genetic factors remains unclear. Discordant results exist, even concerning the best-known malaria resistance genes that determine the structure or function of red blood cells. Here we report on a genomewide linkage and association study for P. falciparum infection intensity and mild malaria attack among a Senegalese population of children and young adults from 2 to 18 years old. A high density single nucleotide polymorphisms (SNP) genome scan (Affimetrix GeneChip Human Mapping 250K-nsp) was performed for 626 individuals: i.e. 249 parents and 377 children out of the 504 ones included in the follow-up. The population belongs to a unique ethnic group and was closely followed-up during 3 years. Genome-wide linkage analyses were performed on four clinical and parasitological phenotypes and association analyses using the family based association tests (FBAT) method were carried out in regions previously linked to malaria phenotypes in literature and in the regions for which we identified a linkage peak. Analyses revealed three strongly suggestive evidences for linkage: between mild malaria attack and both the 6p25.1 and the 12q22 regions (empirical p-value = 5 x 10(-5) and 96 x 10(-5) respectively), and between the 20p11q11 region and the prevalence of parasite density in asymptomatic children (empirical p-value = 1.5 x 10(-4)). Family based association analysis pointed out one significant association between the intensity of plasmodial infection and a polymorphism located in ARHGAP26 gene in the 5q31-q33 region (p-value = 3.7 x 10(-5)). This study identified three candidate regions, two of them containing genes that could point out new pathways implicated in the response to malaria infection. Furthermore, we detected one gene associated with malaria infection in the 5q31-q33 region

Hepatitis C Virus Infection May Lead to Slower Emergence of P. falciparum in Blood

International audienceBACKGROUND: Areas endemic for Plasmodium falciparum, hepatitis B virus (HBV) and hepatitis C virus (HCV) overlap in many parts of sub-Saharan Africa. HBV and HCV infections develop in the liver, where takes place the first development stage of P. falciparum before its further spread in blood. The complex mechanisms involved in the development of hepatitis may potentially influence the development of the liver stage of malaria parasites. Understanding the molecular mechanisms of these interactions could provide new pathophysiological insights for treatment strategies in Malaria. METHODOLOGY: We studied a cohort of 319 individuals living in a village where the three infections are prevalent. The patients were initially given a curative antimalarial treatment and were then monitored for the emergence of asexual P. falciparum forms in blood, fortnightly for one year, by microscopy and polymerase chain reaction. PRINCIPAL FINDINGS: At inclusion, 65 (20.4%) subjects had detectable malaria parasites in blood, 36 (11.3%) were HBV chronic carriers, and 61 (18.9%) were HCV chronic carriers. During follow-up, asexual P. falciparum forms were detected in the blood of 203 patients. The median time to P. falciparum emergence in blood was respectively 140 and 120 days in HBV- and HBV+ individuals, and 135 and 224 days in HCV- and HCV+ individuals. HCV carriage was associated with delayed emergence of asexual P. falciparum forms in blood relative to patients without HCV infection. CONCLUSIONS: This pilot study represents first tentative evidence of a potential epidemiological interaction between HBV, HCV and P. falciparum infections. Age is an important confounding factor in this setting however multivariate analysis points to an interaction between P. falciparum and HCV at the hepatic level with a slower emergence of P. falciparum in HCV chronic carriers. More in depth analysis are necessary to unravel the basis of hepatic interactions between these two pathogens, which could help in identifying new therapeutic approaches against malaria