Publicações relacionadas à zika
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In:
Nature
Author:
Erika Check Hayden
Publichealth officials say that the first human trials of a Zika vaccine could begin this year. But they caution that it will take until at least next year, and possibly much longer, to determine whether a vaccine works.
In the meantime, they are trying to avoid a repeat of their experience with the Ebola epidemic, during which most vaccine trials began too late — just as the rate of infection began to taper off. As a result, scientists missed out on the chance to prove that the vaccines prevent people from becoming infected.
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In:
The New England Journal of Medicine
Authors:
Peter Sands, M.P.A., Carmen Mundaca-Shah, M.D., Dr.P.H., and Victor J. Dzau, M.D.
Pandemics and epidemics have ravaged human societies throughout history. The plague, cholera, and smallpox killed tens of millions of people and destroyed civilizations. In the past 100 years, the “Spanish Flu” of 1918–1919 and HIV–AIDS caused the deaths of nearly 100 million people.
Advances in medicine have transformed our defenses against the threat of infectious disease. Better hygiene, antibiotics, diagnostics, and vac- cines have given us far more effective tools for preventing and responding to outbreaks. Yet the severe acute respiratory syndrome (SARS), the Middle East respiratory syndrome (MERS), and the recent West African Ebola outbreak show that we cannot be complacent (Fig. 1). Infectious- disease outbreaks that turn into epidemics and potential pandemics can cause massive loss of life and huge economic disruption.
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In:
Emerging Infectious Diseases
Authors:
Dennis Tappe, Stephan Nachtigall, Annette Kapaun, Paul Schnitzler, Stephan Günther, Jonas Schmidt-Chanasit
Zika virus (ZIKV), a mosquito-borne flavivirus, causes Zika fever, a self-limiting febrile and exanthematic arthralgia syndrome closely resembling dengue fever. Most often, signs and symptoms are macu- lopapular rash, fever, arthralgia, myalgia, headache, and conjunctivitis; edema, sore throat, cough, and vomiting occur less frequently (1). The virus, which was initially isolated from a rhesus monkey (Macaca mulatta) in 1947 in Uganda, has come to attention recently after a large outbreak occurred in the western Pacific region, including French Polynesia, New Caledonia, Easter Island, and the Cook Islands (2). Travel-related imported infections have thus been increasingly reported from the western Pacific and sporadically also in travelers to other regions of the world, including Thailand, Indonesia, and Senegal (2,3). ZIKV is transmitted by different Aedes mosquito species, and nonhuman primates play a role as reservoirs (1). After the beginning of the ZIKV epidemic in late 2013, a 20-fold increase of Guillain-Barré syndrome incidence was noted in French Polynesia; 1 patient was infected a week before neurologic symptoms started (4). We report an acute ZIKV infection in a traveler returning from Malaysian Borneo who experienced bilateral hearing difficulties during the course of illness.
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In:
The Lancet
Authors:
Jennifer J Adibi, Ernesto T A Marques Jr, Abigail Cartus, Richard H Beigi
The mechanism by which the Zika virus can cause fetal microcephaly is not known. Reports indicate that Zika is able to evade the normal immunoprotective responses of the placenta. Microcephaly has genetic causes, some associated with maternal exposures including radiation, tobacco smoke, alcohol, and viruses. Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly conveys the Zika virus to the early embryo or fetus. Alternatively, the placenta itself might be mounting a response to the exposure; this response might be contributing to or causing the brain defect. This distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies to prevent Zika-induced teratogenesis.
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In:
Medical Microbiology and Immunology
Authors:
Dennis Tappe · José Vicente Pérez‐Girón · Lorenzo Zammarchi · Jürgen Rissland · Davis F. Ferreira · Thomas Jaenisch · Sergio Gómez‐Medina · Stephan Günther · Alessandro Bartoloni · César Muñoz‐Fontela · Jonas Schmidt‐Chanasit
Abstract
Zika virus is an emerging mosquito-borne flavi- virus currently causing large epidemics in the Pacific Ocean region and Brazil. Clinically, Zika fever resembles dengue fever, but is less severe. Whereas the clinical syndrome and laboratory diagnostic procedures have been described, little attention was paid to the immunology of the disease and its possible use for clinical follow-up of patients. Here, we investigate the role of cytokines in the pathogenesis of Zika fever in travelers returning from Asia, the Pacific, and Bra- zil. Polyfunctional T cell activation (Th1, Th2, Th9, and Th17 response) was seen during the acute phase character- ized by respective cytokine level increases, followed by a decrease in the reconvalescent phase.
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