Guillain-Barré Syndrome During Ongoing Zika Virus Transmission — Puerto Rico, January 1–July 31, 2016

Dirlikov, Emilio; Major, Chelsea G.; Mayshack, Marrielle; Medina, Nicole A.; Matos, Desiree; Ryff, Kyle; Torres-Aponte, Jomil; Alkis, Rebecca; Muñoz‐Jordán, Jorge L.; Colón-Sánchez, Candimar; Salinas, Jorge; Pastula, Daniel M.; Garcı́a, Myriam; Segarra, Marangely Olivero; Malave, Graciela; Thomas, Dana L.; Rodríguez–Vega, Gloria M.; Luciano, Carlos A.; Sejvar, James J.; Sharp, Tyler M.; Rivera-García, Brenda

doi:10.15585/mmwr.mm6534e1

Cited by 113 publications

(82 citation statements)

References 9 publications

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“…Our data thereby provide a compelling basis to investigate the role of T cells and BBB breakdown within ZIKV-induced neurological complications that follow ZIKV infection in humans 20 .…”

mentioning

confidence: 85%

Antiviral CD8 T cells induce Zika-virus-associated paralysis in mice

et al. 2017

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Zika virus (ZIKV) is an emerging, mosquito-borne RNA virus. The rapid spread of ZIKV within the Americas has unveiled microcephaly1 and Guillain-Barré syndrome 2,3 as ZIKV-associated neurological complications. Recent reports have further indicated other neurological manifestations to be associated with ZIKV including myelitis 4, meningoencephalitis 5 and fatal encephalitis6. Here, we investigate the neuropathogenesis of ZIKV infection in IFNAR knockout (Ifnar1−/−) mice, an infection model that exhibits high viral burden within the central nervous system (CNS). We show that systemic spread of ZIKV from the site of infection to the brain requires Ifnar1-deficiency in the hematopoietic compartment. However, spread of ZIKV within the CNS is supported by Ifnar1-deficient non-hematopoietic cells. Within this context, ZIKV infection of astrocytes results in breakdown of the blood-brain barrier and a large influx of CD8+ effector T cells. Further, we find antiviral activity of CD8+ T cells within the brain markedly limits ZIKV infection of neurons, but as a consequence instigates ZIKV-associated paralysis. Taken together, our study uncovers mechanisms underlying ZIKV-neuropathogenesis within a susceptible mouse model and suggests BBB breakdown and T cell mediated neuropathology as potential underpinnings of ZIKV-associated neurological complications in humans.

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“…Our data thereby provide a compelling basis to investigate the role of T cells and BBB breakdown within ZIKV-induced neurological complications that follow ZIKV infection in humans 20 .…”

mentioning

confidence: 85%

Antiviral CD8 T cells induce Zika-virus-associated paralysis in mice

et al. 2017

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“…Up to present, studies describing the role of ZIKV in GBS have focused on outbreak areas and symptomatic ZIKV patients 4, 5, 8, 9, 25, 26, 27. Interestingly, ZIKV infections are symptomatic in only an estimated 20% of cases and ZIKV will probably soon be endemic in most affected areas.…”

Section: Discussionmentioning

confidence: 99%

“…GBS is an acute polyradiculoneuropathy causing a rapidly progressive limb weakness and is triggered by various types of preceding infection 6. Recently, the association between ZIKV and GBS has also been reported in various Latin‐American countries following outbreaks of ZIKV 4, 7, 8, 9. In Asia, where ZIKV has been endemic for several decades,10, 11, 12 the occurrence of GBS and other neurological complications after ZIKV infection have thus far not been reported.…”

Section: Introductionmentioning

confidence: 99%

Zika virus and Guillain–Barré syndrome in Bangladesh

GeurtsvanKessel

Islam

et al. 2018

Ann Clin Transl Neurol

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ObjectivePrevious studies have associated Guillain–Barré syndrome (GBS) with Zika virus (ZIKV) outbreaks in South America and Oceania. In Asia, ZIKV is known to circulate widely, but the association with Guillain–Barré syndrome is unclear. We investigated whether endemic ZIKV infection is associated with the development of GBS.MethodsA prospective study was conducted from 2011 to 2015 in Bangladesh. A total of 418 patients and 418 healthy family controls were included in the study. Patients were diagnosed with GBS prior to inclusion according to established criteria. Detailed information on the epidemiology, clinical presentation, electrophysiology, diagnosis, disease severity, and clinical course were obtained during a follow‐up of 1 year using a predefined protocol.Results ZIKV‐neutralizing antibodies were detected in our study from 2013 onwards. The prevalence of ZIKV‐neutralizing antibodies was not significantly higher in patients with GBS compared to healthy controls (OR 2.23, P = 0.14, 95% CI 0.77–6.53). Serological evidence for prior ZIKV infection in patients with GBS was associated with more frequent cranial, sensory, and autonomic nerve involvement compared to GBS patients with Campylobacter jejuni, the predominant preceding infection in GBS worldwide. Nerve‐conduction studies revealed that ZIKV antibodies were associated with a demyelinating subtype of GBS, while C. jejuni infections were related to an axonal subtype.InterpretationNo significant association was found between ZIKV infection and GBS in Bangladesh, but GBS following ZIKV infection was characterized by a distinct clinical and electrophysiological subtype compared to C. jejuni infection. These findings indicate that ZIKV may precede a specific GBS subtype but the risk is low.

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“…During the past year, the Puerto Rico Department of Health and CDC established an enhanced surveillance system for GBS in Puerto Rico. Initial analyses have demonstrated that among 56 patients with suspected GBS during January 1-July 31, 2016, a total of 26 (47%) had confirmed (n = 10, 18%) or presumptive (16, 29%) Zika virus infection (41). Other work related to GBS includes retrospective case-control investigations in Puerto Rico, Brazil, and Colombia, which will help improve understanding of the association between Zika virus infection and GBS.…”

Section: Improving Understanding Of the Link Between Guillain-barré Smentioning

confidence: 99%