Guillain-Barré Syndrome

Ansar, Vibhuti; Valadi, Nojan

doi:10.1016/j.pop.2015.01.001

Cited by 40 publications

(34 citation statements)

References 10 publications

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“…2, 3 ZIKV has also been linked to Guillain–Barré syndrome (GBS), an autoimmune disease that causes paralysis. 4 The severity of the diseases associated with Zika and its rapid spread have triggered an urgent need to understand this virus.…”

Section: Introductionmentioning

confidence: 99%

Zika virus genome biology and molecular pathogenesis

Wang

Thurmond

Islas

et al. 2017

Emerging Microbes & Infections

106

103

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Zika virus (ZIKV) is an emerging RNA virus in the widespread Flavivirus genus. Recently, ZIKV has rapidly spread around the world and has been implicated in human disease, including neurological disorders, triggering public and scientific attention. Understanding how ZIKV causes disease is the highest priority, yet little is known about this virus. Here we examine the currently published data from ZIKV studies to provide the latest understanding of ZIKV genome biology and molecular pathogenesis. The ZIKV genome evolved rapidly from the Flavivirus genus and diverged from the members of this genus, even within the dengue virus cluster to which ZIKV belongs. Genome variations and divergences also exist among ZIKV strains/isolates. These genome divergences might account for the uniqueness of Zika disease. ZIKV infection activates not only the antiviral immune response but also the pro-inflammatory responses associated with disease symptoms. Strikingly, ZIKV activates protein complexes that are functionally associated with disease process, such as glial cell activation and proliferation (for example, Toll-like receptors), apoptosis and cell death, and inflammation. The activation of these complexes may critically contribute to Zika disease. The novel insights into ZIKV genome divergence and disease mechanisms summarized in this review will help accelerate the development of anti-ZIKV strategies.

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Section: Introductionmentioning

confidence: 99%

Zika virus genome biology and molecular pathogenesis

Wang

Thurmond

Islas

et al. 2017

Emerging Microbes & Infections

106

103

View full text Add to dashboard Cite

show abstract

“…An additional concern is the association of ZIKV infection and Guillain-Barré syndrome (GBS). GBS is an autoimmune polyradiculoneuropathy that can result in weakness, paralysis, and death [23–25], and was first associated with ZIKV infection during the 2013–2014 outbreak in French Polynesia. Cases of a diffuse demyelinating disorder consistent with GBS that are temporally associated with ZIKV infection have been reported in Brazil, El Salvador, Colombia, and Venezuela [26].…”

Section: Introductionmentioning

confidence: 99%

Neuropathogenesis of Zika Virus in a Highly Susceptible Immunocompetent Mouse Model after Antibody Blockade of Type I Interferon

et al. 2017

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Animal models are needed to better understand the pathogenic mechanisms of Zika virus (ZIKV) and to evaluate candidate medical countermeasures. Adult mice infected with ZIKV develop a transient viremia, but do not demonstrate signs of morbidity or mortality. Mice deficient in type I or a combination of type I and type II interferon (IFN) responses are highly susceptible to ZIKV infection; however, the absence of a competent immune system limits their usefulness for studying medical countermeasures. Here we employ a murine model for ZIKV using wild-type C57BL/6 mice treated with an antibody to disrupt type I IFN signaling to study ZIKV pathogenesis. We observed 40% mortality in antibody treated mice exposed to ZIKV subcutaneously whereas mice exposed by intraperitoneal inoculation were highly susceptible incurring 100% mortality. Mice infected by both exposure routes experienced weight loss, high viremia, and severe neuropathologic changes. The most significant histopathological findings occurred in the central nervous system where lesions represent an acute to subacute encephalitis/encephalomyelitis that is characterized by neuronal death, astrogliosis, microgliosis, scattered necrotic cellular debris, and inflammatory cell infiltrates. This model of ZIKV pathogenesis will be valuable for evaluating medical countermeasures and the pathogenic mechanisms of ZIKV because it allows immune responses to be elicited in immunologically competent mice with IFN I blockade only induced at the time of infection.

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“…Several treatments exist, such as plasma exchange and the administration of intravenous immunoglobulin (IVIG). 2 As is well-known, MG and GBS are different autoimmune disorders, affecting the neuromuscular junction and peripheral nerve, respectively. However, the exact pathophysiological process of both MG and GBS remains unclear.…”

mentioning

confidence: 99%