Zika virus infection, a new public health challenge

Campos, Gubio S.; Sardi, Silvia Inês; Sarno, Manoel; Brites, Carlos

doi:10.1016/j.bjid.2016.05.001

Cited by 12 publications

(10 citation statements)

References 5 publications

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“…In the present study abnormalities were confirmed at 25 weeks. In Brazil investigators, observed abnormalities at early as 21 weeks of gestation [3, 9]. Although microcephaly was confirmed by ultrasonography at week 25, the mother decided not to interrupt her pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…Between 2010 and 2017, neurologic complications (microcephaly) in French Polynesia Brazil and Colombia have increased dramatically [4, 5, 9, 10]. These brain malformations in those countries coincided with Zika virus outbreaks [10–12].…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, it is too soon to establish the exact incidence of microcephaly in the already pregnant women in Colombia. Brazilian officials have detected fetal abnormalities in 12/42 (29%) of Zika virus-positive women, but we do not know whether this rate will be similar in Colombia [4, 7, 9]. The cost of treatment to improve neurodevelopmental deficiencies in children due to Zika mediated neuronal cell death remains a major concern for Colombia.…”

Section: Discussionmentioning

confidence: 99%

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Case report: microcephaly associated with Zika virus infection, Colombia

et al. 2017

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BackgroundRecently there has been a large outbreak of Zika virus infections in Colombia, South America. The epidemic began in September 2015 and continued to April 2017, for the total number of Zika cases reported of 107,870. For those confirmed Zika cases, there were nearly 20,000 (18.5%) suspected to be pregnant women, resulting in 157 confirmed cases of microcephaly in newborns reported by their health government agency. There is a clear under-estimation of the total number of cases and in addition no prior publications have been published to demonstrate the clinical aspects of the Zika infection in Colombia. We characterized one Zika presentation to be able to compare and contrast with other cases of Zika infection already reported in the literature.Case presentationIn this case report, we demonstrate congenital microcephaly at week 19 of gestation in a 34-year-old mother who showed symptoms compatible with Zika virus infection from Sincelejo, State of Sucre, in the Colombian Caribbean. Zika virus RNA was detected in the placenta using real-time reverse transcriptase polymerase chain reaction (RT-PCR). At week 25, the fetus weigh estimate was 770 g, had a cephalic perimeter of 20.2 cm (5th percentile), ventriculomegaly on the right side and dilatation of the fourth ventricle. At week 32, the microcephaly was confirmed with a cephalic perimeter of 22 cm, dilatation of the posterior atrium to 13 mm, an abnormally small cerebellum (29 mm), and an augmented cisterna magna. At birth (39 weeks by cesarean section), the head circumference was 27.5 cm, and computerized axial tomography (Siemens Corp, 32-slides) confirmed microcephaly with calcifications.ConclusionWe report a first case of maternal Zika virus infection associated with fetal microcephaly in Colombia and confirmed similar presentation to those observed previous in Brazil, 2015–2016.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Case report: microcephaly associated with Zika virus infection, Colombia

et al. 2017

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“…A mosquito-borne flavivirus similar to dengue virus (DENV) and West Nile virus (WNV), Zika virus (ZIKV) has drawn global attention due to its rapid spread across the Pacific to the Americas (1, 2) and growing reports of fetal microcephaly and other congenital abnormalities (3, 4). Although infection is most often asymptomatic (5–7), the causal relationship between ZIKV infection during pregnancy and fetal microcephaly is now proven (6, 8–10).…”

Section: Introductionmentioning

confidence: 99%

PARP12 suppresses Zika virus infection through PARP-dependent degradation of NS1 and NS3 viral proteins

Zhao

Liu

et al. 2018

Sci. Signal.

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Zika virus infection stimulates a type I interferon (IFN) response in host cells, which suppresses viral replication. Type I IFNs exert antiviral effects by inducing the expression of hundreds of IFN-stimulated genes (ISGs). To screen for antiviral ISGs that restricted Zika virus replication, we individually knocked out 21 ISGs in A549 lung cancer cells and identified PARP12 as a strong inhibitor of Zika virus replication. Our findings suggest that PARP12 mediated the ADP-ribosylation of NS1 and NS3, nonstructural viral proteins that are involved in viral replication and modulating host defense responses. This modification of NS1 and NS3 triggered their proteasome-mediated degradation. These data increase our understanding of the antiviral activity of PARP12 and suggest a molecular basis for the potential development of therapeutics against Zika virus.

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“…Zika virus (ZIKV) spread in the Americas has been linked to unique severe adverse outcomes such as fetal loss (1), congenital Zika syndrome (CZS) (2), Guillain-Barré syndrome (GBS) (3), and rare cases of encephalopathy (4), meningoencephalitis (5), myelitis (6), uveitis (7), and severe thrombocytopenia (8). Previous studies have shown that prior exposure to a single serotype of dengue virus (DENV) predisposes individuals to severe disease upon secondary heterologous DENV infection.…”

mentioning

confidence: 99%

Significant control of Zika infection in macaques depends on the elapsing time after dengue exposure

Serrano-Collazo

Pantoja

et al. 2019

Preprint

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29Prior exposure to a single serotype of dengue virus (DENV) predisposes individuals to severe 30 disease upon secondary heterologous DENV infection. Here we show that the length of time 31 between DENV/Zika (ZIKV) infections has a qualitative impact on controlling ZIKV replication. 32We identified limited but significant differences in the magnitude of the early humoral immune 33 response associated with a period of twelve months but not three months of DENV 34 convalescence. However, their role limiting ZIKV replication is not conclusive. There was no 35 evidence of in vivo antibody-dependent amplification of ZIKV by DENV immunity in any group. 36We are also showing that the significant differences among groups may be linked to a pre-37 existing polyfunctional CD4+ T cells response (increased IFN-g and Cd107a before ZIKV 38 infection) and to an early and continuous expansion of the CD4+ effector memory cells early on 39 after ZIKV infection. Those significant differences were associated with a period of 12 months 40 after DENV infection that were not observed in a span of 3-months. These results suggest that 41 there is a window of optimal cross-protection between ZIKV and DENV with significant 42 consequences. These results have pivotal implications while interpreting ZIKV pathogenesis in 43 flavivirus-experimented populations, diagnostic results interpretation and vaccine designs 44 among others. 45 46 Author Summary 47impact on controlling the ZIKV infection. In this study, as in our prior work we did not observe 100 evidence of ZIKV disease enhancement associated with prior DENV exposure. We also 101 confirmed that the significant differences among groups are mediated by the pre-existence of a 102 robust effector memory T cell (TEM) and cytotoxic activity mainly mediated by CD4 + T cells 103 more than qualitative differences in the humoral immune response. However, by conducting a 104 detailed study of the ZIKV-neutralizing titers vs. ZIKV RNAemia at early time points after 105 infection, we were able to determine a possible contribution of the neutralizing antibodies 106 limiting the ZIKV replication at 7 days after infection in the animals with 12 months but not 3 107 months of DENV immunity or in the control group. Overall, we demonstrated that exposure to 108 ZIKV 12 months after DENV infection afford a high level of T cell-mediated cross protection than 109 it was observed at the 3-month span. Based on our previous study we believe this protection 110 wanes as macaques exposed to ZIKV 2.8 years after DENV were not afforded this protection. 111These results suggest that there is a window of optimal T cell cross-protection between ZIKV 112 and DENV. 113 114 Results 115

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Zika virus infection, a new public health challenge

Cited by 12 publications

References 5 publications

Case report: microcephaly associated with Zika virus infection, Colombia

Case report: microcephaly associated with Zika virus infection, Colombia

PARP12 suppresses Zika virus infection through PARP-dependent degradation of NS1 and NS3 viral proteins

Significant control of Zika infection in macaques depends on the elapsing time after dengue exposure

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