Éditeur(s) : HAL CCSD Masson
Résumé : National audience
Started in 2015 in Brazil, an outbreak linked to a little known arbovirus, Zika virus spread throughout Latin America. This virus, considered until recently as responsible of only mild symptoms, made mention of previously unsuspected complications, with severe neurological manifestations in adults and malformations of the central nervous system, including microcephaly, in newborns of mother infected during the pregnancy. While the continent is more accustomed to the succession of arbovirus epidemics, suspected complications and the many unknowns keys of the latter arriving raise many public health issues. French Guiana, a French territory located in the north-east of the continent, combines both European level of resources and climate and issues specific to the Amazon region and Latin America. We discuss here the issues for 2016 Zika virus epidemic in our region, many of them are generalizable to neighboring countries.
ISSN: 0037-9085

inserm-01422054
http://www.hal.inserm.fr/inserm-01422054
http://www.hal.inserm.fr/inserm-01422054/document
http://www.hal.inserm.fr/inserm-01422054/file/2016%2C%20Epelboin%20-%20%C3%89pid%C3%A9mie%20de%20virus%20Zika%20en%20Am%C3%A9rique%20latine%20-%20quels%20enjeux%20pour%20la%20Guyane%20%281%29.pdf
DOI : 10.1007/s13149-016-0490-5

Éditeur(s) : HAL CCSD Wiley Online Library
Résumé : International audience
Zika virus is an Aedes-borne Flavivirus causing fever, arthralgia, myalgia rash, associated with Guillain-Barré syndrome and suspected to induce microcephaly in the fetus. We report here the complete coding sequence of the first characterized Caribbean Zika virus strain, isolated from a patient from Martinique in December, 2015.
ISSN: 2052-2975

hal-01331574
https://hal.archives-ouvertes.fr/hal-01331574
PUBMED : 27274849
PUBMEDCENTRAL : PMC4879239

Éditeur(s) : HAL CCSD American Society of Hematology
Résumé : International audience
Zika fever is an Aedes-borne disease caused by a flavivirus (Zika virus, ZIKV, genus Flavivirus). During the past years ZIKV spread in Polynesia, South-America and the Caribbean. Most ZIKV infections are asymptomatic or result in mild febrile disease with rash and conjunctivitis. Attention was recently drawn to non-vectored ZIKV transmission, including sexual, probable blood-borne and mother-to-fetus transmission, and to severe forms such as Guillain-Barré syndrome, acute neurological infections and fetal abnormalities (including microcephaly). Many aspects of Zika fever natural history remain unknown, e.g. the proportion of asymptomatic cases and the duration of viremia. Estimating the prevalence of Zika infections is difficult because a large proportion of infected individuals do not seek medical attention and seroprevalence studies are hampered by antigenic cross-reactivity with other flaviviruses, e.g. dengue virus. Here, we present a study of ZIKV infection in blooddonors from Martinique island (French West Indies, Caribbean region), with novel epidemiological, biological and clinical information that refine the picture of Zika fever in adults.
ISSN: 0006-4971

inserm-01415646
http://www.hal.inserm.fr/inserm-01415646
http://www.hal.inserm.fr/inserm-01415646/document
http://www.hal.inserm.fr/inserm-01415646/file/2016%2C%20Gallian%20et%20al%20-%20Zika%20virus%20in%20asymptomatic%20blood%20donors%2C%20Martinique%20%281%29.pdf
DOI : 10.1182/blood-2016-09-737981

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
Treacher Collins/Franceschetti syndrome (TCS; OMIM 154500) is a disorder of craniofacial development belonging to the heterogeneous group of mandibulofacial dysostoses. TCS is classically characterized by bilateral mandibular and malar hypoplasia, downward-slanting palpebral fissures, and microtia. To date, three genes have been identified in TCS:,TCOF1, POLR1D, and POLR1C. We report a clinical and extensive molecular study, including TCOF1, POLR1D, POLR1C, and EFTUD2 genes, in a series of 146 patients with TCS. Phenotype-genotype correlations were investigated for 19 clinical features, between TCOF1 and POLR1D, and the type of mutation or its localization in the TCOF1 gene. We identified 92/146 patients (63%) with a molecular anomaly within TCOF1, 9/146 (6%) within POLR1D, and none within POLR1C. Among the atypical negative patients (with intellectual disability and/or microcephaly), we identified four patients carrying a mutation in EFTUD2 and two patients with 5q32 deletion encompassing TCOF1 and CAMK2A in particular. Congenital cardiac defects occurred more frequently among patients with TCOF1 mutation (7/92, 8%) than reported in the literature. Even though TCOF1 and POLR1D were associated with extreme clinical variability, we found no phenotype-genotype correlation. In cases with a typical phenotype of TCS, 6/146 (4%) remained with an unidentified molecular defect.
ISSN: 1098-3600

hal-01134364
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01134364
DOI : 10.1038/gim.2015.29
PUBMED : 25790162