Microcephaly caused by congenital Zika virus infection and viral detection in maternal urine during pregnancy

Regadas, Vanessa Couras; Silva, Márcio de Castro e; Abud, Lucas Giansante; Labadessa, Luiz Mario Pereira Lopes; Oliveira, Rafael Gouvêa Gomes de; Miyake, Cecília Hissae; Queiroz, Rodolfo Mendes

doi:10.1590/1806-9282.64.01.11

Cited by 9 publications

(8 citation statements)

References 8 publications

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“…The main sign observed in these pregnant women was rash and the most common symptoms were myalgia, headache and pruritus. On the other hand, fever was not a frequent symptom, revealing a similar profile to national 9 and international studies 10 .…”

supporting

confidence: 71%

The role of pregnant women with rash in the Zika virus sentinel surveillance

Martins

Saad

Ignácio

et al. 2019

Rev. Soc. Bras. Med. Trop.

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Introduction: The state of São Paulo has been monitoring cases of microcephaly and pregnant women presenting with acute rash, through CeVeSP. Methods: This was a descriptive study focusing on pregnant women with rash and the outcome of their pregnancy, based on the notifications through the CeVeSP. Results: During 2016, 2,209 cases of pregnant women with rash were reported and investigated. Of these, 36.6% were confirmed. Of the pregnant women who tested positive for ZIKV, 6.4% did not have a favorable outcome. Conclusions: Our results allowed the characterization of pregnant women exposed to ZIKV and the outcome of pregnancy.

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supporting

confidence: 71%

The role of pregnant women with rash in the Zika virus sentinel surveillance

Martins

Saad

Ignácio

et al. 2019

Rev. Soc. Bras. Med. Trop.

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“…Traveller/non-traveller populations: In this update, we found further evidence that congenital abnormalities occurred in infants born to women travellers returning from ZIKV-affected areas and women remaining in those areas. In total, 25 publications report on 272 congenital abnormalities due to ZIKV infection in travellers 27, 29, 30, 32, 34, 36, 38, 42, 45, 56, 58, 61, 89, 94, 98, 109, 117, 122, 123, 137, 140, 151, 153, 166, 173 , with 109 publications reporting congenital abnormalities due to ZIKV in 2652 non travellers 24– 26, 28, 31, 33, 35, 37, 39– 41, 43, 44, 46– 48, 50, 51, 54, 57, 60, 62– 79, 81, 83– 85, 87, 88, 90– 93, 95– 97, 100, 101, 104– 106, 110– 113, 115, 116, 118, 119, 121, 124– 135, 142– 147, 149, 152, 154, 156– 164, 167, 168, 171, 172, 175– 180, 182, …”

Section: Resultsmentioning

confidence: 99%

Zika virus infection as a cause of congenital brain abnormalities and Guillain-Barré syndrome: A living systematic review

et al. 2019

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Background: The Zika virus (ZIKV) caused a large outbreak in the Americas leading to the declaration of a Public Health Emergency of International Concern in February 2016. A causal relation between infection and adverse congenital outcomes such as microcephaly was declared by the World Health Organization (WHO) informed by a systematic review structured according to a framework of ten dimensions of causality, based on the work of Bradford Hill. Subsequently, the evidence has continued to accumulate, which we incorporate in regular updates of the original work, rendering it a living systematic review. Methods: We present an update of our living systematic review on the causal relation between ZIKV infection and adverse congenital outcomes and between ZIKV and GBS for four dimensions of causality: strength of association, dose-response, specificity, and consistency. We assess the evidence published between January 18, 2017 and July 1, 2019. Results: We found that the strength of association between ZIKV infection and adverse outcomes from case-control studies differs according to whether exposure to ZIKV is assessed in the mother (OR 3.8, 95% CI: 1.7-8.7, I2=19.8%) or the foetus/infant (OR 37.4, 95% CI: 11.0-127.1, I2=0%). In cohort studies, the risk of congenital abnormalities was 3.5 times higher after ZIKV infection (95% CI: 0.9-13.5, I2=0%). The strength of association between ZIKV infection and GBS was higher in studies that enrolled controls from hospital (OR: 55.8, 95% CI: 17.2-181.7, I2=0%) than in studies that enrolled controls at random from the same community or household (OR: 2.0, 95% CI: 0.8-5.4, I2=74.6%). In case-control studies, selection of controls from hospitals could have biased results. Conclusions: The conclusions that ZIKV infection causes adverse congenital outcomes and GBS are reinforced with the evidence published between January 18, 2017 and July 1, 2019.

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“…Most clinical studies have demonstrated that high level of ZIKV viral loads can be detected in the urine samples of both adult and infant patients (7, 8). Previous studies show that ZIKV can infect glomerular parenchymal cells and renal proximal tubular epithelial cells, which may serve as potential reservoirs for ZIKV in kidney (9, 10).…”

Section: Introductionmentioning

confidence: 99%

Zika Virus Infection Induces Acute Kidney Injury Through Activating NLRP3 Inflammasome Via Suppressing Bcl-2

Liu

Tang

et al. 2019

Front. Immunol.

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Zika virus (ZIKV) is a newly emerging flavivirus that broadly exhibits in various bodily tissues and fluids, especially in the brain, and ZIKV infection often causes microcephaly. Previous studies have been reported that ZIKV can infect renal cells and can be detected in the urine samples of infected individuals. However, whether ZIKV infection causes renal diseases and its pathogenic mechanisms remains unknown. Here, we identified that ZIKV infection resulted in acute kidney injury (AKI) in both newborn and adult mouse models by increasing the levels of AKI-related biomarkers [e.g., serum creatinine (Scr), kidney injury molecular−1 (Kim-1), and neutrophil gelatinase-associated lipocalin (NGAL)]. ZIKV infection triggered the inflammatory response and renal cell injury by activating Nod-like receptor 3 (NLRP3) inflammasome and secreting interleukin-1β (IL-1β). IL-1β inhibited aquaporins expression and led to water re-absorption disorder. Furthermore, ZIKV infection induced a decreased expression of B-cell lymphoma-2 (Bcl-2) in the kidney. Overexpression of Bcl-2 attenuated ZIKV-induced NLRP3 inflammasome activation in renal cells and down-regulated PARP/caspase-3-mediated renal apoptosis. Overall, our findings demonstrated that ZIKV infection induced AKI by activating NLRP3 inflammasome and apoptosis through suppressing Bcl-2 expression, which provided potential therapeutic targets for ZIKV-associated renal diseases.

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Microcephaly caused by congenital Zika virus infection and viral detection in maternal urine during pregnancy

Cited by 9 publications

References 8 publications

The role of pregnant women with rash in the Zika virus sentinel surveillance

The role of pregnant women with rash in the Zika virus sentinel surveillance

Zika virus infection as a cause of congenital brain abnormalities and Guillain-Barré syndrome: A living systematic review

Zika Virus Infection Induces Acute Kidney Injury Through Activating NLRP3 Inflammasome Via Suppressing Bcl-2

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