Zika virus (ZIKV) has recently caused a pandemic disease, and many cases of ZIKV infection in pregnant women resulted in abortion, stillbirth, deaths and congenital defects including microcephaly, which now has been proposed as ZIKV congenital syndrome. This study aimed to investigate the in situ immune response profile and mechanisms of neuronal cell damage in fatal Zika microcephaly cases. Brain tissue samples were collected from 15 cases, including 10 microcephalic ZIKV-positive neonates with fatal outcome and five neonatal control flavivirus-negative neonates that died due to other causes, but with preserved central nervous system (CNS) architecture. In microcephaly cases, the histopathological features of the tissue samples were characterized in three CNS areas (meninges, perivascular space, and parenchyma). The changes found were mainly calcification, necrosis, neuronophagy, gliosis, microglial nodules, and inflammatory infiltration of mononuclear cells. The in situ immune response against ZIKV in the CNS of newborns is complex. Despite the predominant expression of Th2 cytokines, other cytokines such as Th1, Th17, Treg, Th9, and Th22 are involved to a lesser extent, but are still likely to participate in the immunopathogenic mechanisms of neural disease in fatal cases of microcephaly caused by ZIKV.

BackgroundIn December 2013, an outbreak of Chikungunya virus (CHIKV) caused by the Asian genotype was notified in the Caribbean. The outbreak has since spread to 38 regions in the Americas. By September 2014, the first autochthonous CHIKV infections were confirmed in Oiapoque, North Brazil, and in Feira de Santana, Northeast Brazil.MethodsWe compiled epidemiological and clinical data on suspected CHIKV cases in Brazil and polymerase-chain-reaction-based diagnostic was conducted on 68 serum samples from patients with symptom onset between April and September 2014. Two imported and four autochthonous cases were selected for virus propagation, RNA isolation, full-length genome sequencing, and phylogenetic analysis. We then followed CDC/PAHO guidelines to estimate the risk of establishment of CHIKV in Brazilian municipalities.ResultsWe detected 41 CHIKV importations and 27 autochthonous cases in Brazil. Epidemiological and phylogenetic analyses indicated local transmission of the Asian CHIKV genotype in Oiapoque. Unexpectedly, we also discovered that the ECSA genotype is circulating in Feira de Santana. The presumed index case of the ECSA genotype was an individual who had recently returned from Angola and developed symptoms in Feira de Santana. We estimate that, if CHIKV becomes established in Brazil, transmission could occur in 94% of municipalities in the country and provide maps of the risk of importation of each strain of CHIKV in Brazil.ConclusionsThe etiological strains associated with the early-phase CHIKV outbreaks in Brazil belong to the Asian and ECSA genotypes. Continued surveillance and vector mitigation strategies are needed to reduce the future public health impact of CHIKV in the Americas.Electronic supplementary materialThe online version of this article (doi:10.1186/s12916-015-0348-x) contains supplementary material, which is available to authorized users.

Virus–host interactions determine an infection outcome. The Asian lineage of Zika virus (ZIKV), responsible for the recent epidemics, has fixed a mutation in the NS1 gene after 2012 that enhances mosquito infection. Here we report that the same mutation confers NS1 to inhibit interferon-β induction. This mutation enables NS1 binding to TBK1 and reduces TBK1 phosphorylation. Engineering the mutation into a pre-epidemic ZIKV strain debilitates the virus for interferon-β induction; reversing the mutation in an epidemic ZIKV strain invigorates the virus for interferon-β induction; these mutational effects are lost in IRF3-knockout cells. Additionally, ZIKV NS2A, NS2B, NS4A, NS4B, and NS5 can also suppress interferon-β production through targeting distinct components of the RIG-I pathway; however, for these proteins, no antagonistic difference is observed among various ZIKV strains. Our results support the mechanism that ZIKV has accumulated mutation(s) that increases the ability to evade immune response and potentiates infection and epidemics.

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Resumo A febre amarela é doenca infecciosa não-contagiosa causada por um arbovírus mantido em ciclos silvestres em que macacos atuam como hospedeiros amplificadores e mosquitos dos gêneros Aedes na África, e Haemagogus e Sabethes na América, são os transmissores. Cerca de 90% dos casos da doença apresentam-se com formas clínicas benignas que evoluem para a cura, enquanto 10% desenvolvem quadros dramáticos com mortalidade em torno de 50%. O problema mostra-se mais grave em África onde ainda há casos urbanos. Nas Américas, no período de 1970-2001, descreveram- Abstract Yellow fever is an infectious and non-contagious disease caused by an arbovirus, the yellow fever virus. The agent is maintained in jungle cycles among primates as vertebrate hosts and mosquitoes, especially Aedes in Africa, and Haemagogus and Sabethes in America. Approximately 90% of the infections are mild or asymptomatic, while 10% course to a severe clinical picture with 50% case-fatality rate. Yellow fever is largely distributed in Africa where urban epidemics are still reported. In South America, between 1970-2001, 4,543 cases were reported, mostly from Peru (51.5%), Bolivia (20.1%) and Brazil (18.7%). The disease is diagnosed by serology (detection of IgM), virus isolation, immunohistochemistry and RT-PCR. Yellow fever is a zoonosis and cannot be eradicated, but it is preventable in man by using the 17D vaccine. A single dose is enough to protect an individual for at least 10 years, after which revaccination is recommended. In this paper, the main concepts about yellow fever as well as the fatal adverse effects of the vaccine are updated. Key-words: Yellow fever. Jaundice. Vaccine. Aedes. Hepatitis. A febre amarela é uma doença infecciosa não contagiosa que se mantém endêmica ou enzoótica nas florestas tropicais da América e África causando periodicamente surtos isolados ou epidemias de maior ou menor impacto em saúde pública, sendo transmitida ao homem mediante a picada de insetos hematófagos da família Culicidae, em especial dos gêneros Aedes e Haemagogus 31 52 . Em África, também tem sido registrado o isolamento viral a partir de carrapatos Amblyoma variegatum, em áreas secas, o que pode indicar o papel secundário desses insetos na cadeia de transmissão da virose em que se demonstrou transmissão transovariana e para macacos 67 . Insere-se o vírus da febre amarela no grupo dos arbovírus (do inglês arthropod borne virus) e ele apresenta-se em sua forma clássica com febre hemorrágica de elevada letalidade. A febre amarela constitui a febre hemorrágica viral original, a primeira descrita no mundo, a que mais temor provoca na sociedade moderna 31 52 . Sob o ponto de vista epidemiológico divide-se a febre amarela em duas formas, rural e urbana que diferem

SUMMARY The emergence of Zika virus (ZIKV) and its association with congenital malformations has prompted the rapid development of vaccines. Although efficacy with nucleic acid or inactivated viral vaccine platforms has been established in animals, no study has addressed protection during pregnancy. We tested in mice two vaccine platforms, a lipid nanoparticle-encapsulated modified mRNA vaccine encoding ZIKV prM and E genes and a live-attenuated ZIKV strain encoding an NS1 protein without glycosylation, for their ability to protect against transmission to the fetus. Vaccinated dams challenged with a heterologous ZIKV strain at embryo day 6 (E6) and evaluated at E13 showed markedly diminished levels of viral RNA in maternal, placental, and fetal tissues, which resulted in protection against placental damage and fetal demise. As modified mRNA and live-attenuated vaccine platforms can restrict in utero transmission of ZIKV in mice, their further development in humans to prevent congenital ZIKV syndrome is warranted.

Yellow fever virus (YFV) causing a deadly viral disease is transmitted by the bite of infected mosquitoes. In Brazil, YFV is restricted to a forest cycle maintained between non-human primates and forest-canopy mosquitoes, where humans can be tangentially infected. Since late 2016, a growing number of human cases have been reported in Southeastern Brazil at the gates of the most populated areas of South America, the Atlantic coast, with Rio de Janeiro state hosting nearly 16 million people. We showed that the anthropophilic mosquitoes Aedes aegypti and Aedes albopictus as well as the YFV-enzootic mosquitoes Haemagogus leucocelaenus and Sabethes albiprivus from the YFV-free region of the Atlantic coast were highly susceptible to American and African YFV strains. Therefore, the risk of reemergence of urban YFV epidemics in South America is major with a virus introduced either from a forest cycle or by a traveler returning from the YFV-endemic region of Africa.

A total of 187 different species of arboviruses and other viruses in vertebrates were identified at the Evandro Chagas Institute (IEC) from