Isolation, identification and genomic characterization of the Asian lineage Zika virus imported to China

Deng, Yong-Qiang; Zhao, Hui; Li, Xiaofeng; Zhang, Nana; Liu, Zhong-Yu; Jiang, Tao; Gu, Dayong; Shi, Lei; He, Jianan; Wang, Hongjiang; Sun, Zewen; Ye, Qing; Xie, Dongyang; Cao, Wu‐Chun; Qin, Cheng‐Feng

doi:10.1007/s11427-016-5043-4

Cited by 91 publications

(83 citation statements)

References 9 publications

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“…We reviewed 20 items [21–28, 48, 50, 53, 59, 62, 69–71, 82–84, 87] (S4 Table). Studies in the 1950s–1970s show that experimental inoculation of Zika virus resulted in illness, cerebral lesions, and viral replication in the brain in some but not all species tested [21–25, 27, 28].…”

Section: Resultsmentioning

confidence: 99%

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

et al. 2017

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BackgroundThe World Health Organization (WHO) stated in March 2016 that there was scientific consensus that the mosquito-borne Zika virus was a cause of the neurological disorder Guillain–Barré syndrome (GBS) and of microcephaly and other congenital brain abnormalities based on rapid evidence assessments. Decisions about causality require systematic assessment to guide public health actions. The objectives of this study were to update and reassess the evidence for causality through a rapid and systematic review about links between Zika virus infection and (a) congenital brain abnormalities, including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in any population, and to describe the process and outcomes of an expert assessment of the evidence about causality.Methods and FindingsThe study had three linked components. First, in February 2016, we developed a causality framework that defined questions about the relationship between Zika virus infection and each of the two clinical outcomes in ten dimensions: temporality, biological plausibility, strength of association, alternative explanations, cessation, dose–response relationship, animal experiments, analogy, specificity, and consistency. Second, we did a systematic review (protocol number CRD42016036693). We searched multiple online sources up to May 30, 2016 to find studies that directly addressed either outcome and any causality dimension, used methods to expedite study selection, data extraction, and quality assessment, and summarised evidence descriptively. Third, WHO convened a multidisciplinary panel of experts who assessed the review findings and reached consensus statements to update the WHO position on causality. We found 1,091 unique items up to May 30, 2016. For congenital brain abnormalities, including microcephaly, we included 72 items; for eight of ten causality dimensions (all except dose–response relationship and specificity), we found that more than half the relevant studies supported a causal association with Zika virus infection. For GBS, we included 36 items, of which more than half the relevant studies supported a causal association in seven of ten dimensions (all except dose–response relationship, specificity, and animal experimental evidence). Articles identified nonsystematically from May 30 to July 29, 2016 strengthened the review findings. The expert panel concluded that (a) the most likely explanation of available evidence from outbreaks of Zika virus infection and clusters of microcephaly is that Zika virus infection during pregnancy is a cause of congenital brain abnormalities including microcephaly, and (b) the most likely explanation of available evidence from outbreaks of Zika virus infection and GBS is that Zika virus infection is a trigger of GBS. The expert panel recognised that Zika virus alone may not be sufficient to cause either congenital brain abnormalities or GBS but agreed that the evidence was sufficient to recommend increased public health measures. Weaknesses are the limited assessment of ...

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Section: Resultsmentioning

confidence: 99%

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

et al. 2017

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“…Especially, our results demonstrate that viral RNA was abundant in lacrimal fluids in ZIKV-infected adult macaques, supporting the use of tears or lacrimal fluids for clinical diagnosis. ZIKV-associated damages have been documented in babies with microcephaly (de Paula Freitas et al, 2016, Ventura et al, 2016a, Ventura et al, 2016b), and conjunctivitis is also a common symptom in adult ZIKV patients (Dasgupta et al, 2016, Deng et al, 2016, Duffy et al, 2009). Whether the level of viral RNA in body fluids associated with disease severity remains unknown.…”

Section: Discussionmentioning

confidence: 99%

“…ZIKV stocks were propagated in Aedes albopictus C6/36 cells and titrated by plaque forming assay on BHK-21 cells (Dai et al, 2016, Deng et al, 2016). Studies with infectious ZIKV were conducted under biosafety level 2 (BSL-2) facilities at Beijing Institute of Microbiology and Epidemiology.…”

Section: Methodsmentioning

confidence: 99%

Characterization of a 2016 Clinical Isolate of Zika Virus in Non-human Primates

et al. 2016

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Animal models are critical to understand disease and to develop countermeasures for the ongoing epidemics of Zika virus (ZIKV). Here we report a non-human primate model using a 2016 contemporary clinical isolate of ZIKV. Upon subcutaneous inoculation, rhesus macaques developed fever and viremia, with robust excretion of ZIKV RNA in urine, saliva, and lacrimal fluid. Necropsy of two infected animals revealed that systematic infections involving central nervous system and visceral organs were established at the acute phrase. ZIKV initially targeted the intestinal tracts, spleen, and parotid glands, and retained in spleen and lymph nodes till 10 days post infection. ZIKV-specific immune responses were readily induced in all inoculated animals. The non-human primate model described here provides a valuable platform to study ZIKV pathogenesis and to evaluate vaccine and therapeutics.

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“…The mouse neurovirulence model of ZIKV has been well established previously (39,40). We further tested the neurovirulence of rGZ01 and compared it with the parental GZ01.…”

mentioning

confidence: 99%

Characterization of cis -Acting RNA Elements of Zika Virus by Using a Self-Splicing Ribozyme-Dependent Infectious Clone

Liu

Huang

et al. 2017

J Virol

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Zika virus (ZIKV) has caused significant outbreaks and epidemics in the Americas recently, raising global concern due to its ability to cause microcephaly and other neurological complications. A stable and efficient infectious clone of ZIKV is urgently needed. However, the instability and toxicity of flavivirus cDNA clones in Escherichia coli hosts has hindered the development of ZIKV infectious clones. Here, using a novel self-splicing ribozyme-based strategy, we generated a stable infectious cDNA clone of a contemporary ZIKV strain imported from Venezuela to China in 2016. The constructed clone contained a modified version of the group II self-splicing intron P.li.LSUI2 near the junction between the E and NS1 genes, which were removed from the RNA transcripts by an easy-to-establish in vitro splicing reaction. Transfection of the spliced RNAs into BHK-21 cells led to the production of infectious progeny virus that resembled the parental virus. Finally, potential cis-acting RNA elements in ZIKV genomic RNA were identified based on this novel reverse genetics system, and the critical role of 5=-SLA promoter and 5=-3= cyclization sequences were characterized by a combination of different assays. Our results provide another stable and reliable reverse genetics system for ZIKV that will help study ZIKV infection and pathogenesis, and the novel self-splicing intron-based strategy could be further expanded for the construction of infectious clones from other emerging and reemerging flaviviruses.IMPORTANCE The ongoing Zika virus (ZIKV) outbreaks have drawn global concern due to the unexpected causal link to fetus microcephaly and other severe neurological complications. The infectious cDNA clones of ZIKV are critical for the research community to study the virus, understand the disease, and inform vaccine design and antiviral screening. A panel of existing technologies have been utilized to develop ZIKV infectious clones. Here, we successfully generated a stable infectious clone of a 2016 ZIKV strain using a novel self-splicing ribozyme-based technology that abolished the potential toxicity of ZIKV cDNA clones to the E. coli host. Moreover, two crucial cis-acting replication elements (5=-SLA and 5=-CS) of ZIKV were first identified using this novel reverse genetics system. This novel self-splicing ribozyme-based reverse genetics platform will be widely utilized in future ZIKV studies and provide insight for the development of infectious clones of other emerging viruses.

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Isolation, identification and genomic characterization of the Asian lineage Zika virus imported to China

Cited by 91 publications

References 9 publications

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

Characterization of a 2016 Clinical Isolate of Zika Virus in Non-human Primates

Characterization of cis -Acting RNA Elements of Zika Virus by Using a Self-Splicing Ribozyme-Dependent Infectious Clone

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