Chikungunya virus–associated encephalitis

Gérardin, Patrick; Couderc, Thérèse; Bintner, M.; Tournebize, Patrice; Renouil, M; Lemant, Jérôme; Boisson, Véronique; Borgherini, Gianandréa; Staïkowsky, F.; Schramm, Frédéric; Lecuit, Marc; Michault, Alain

doi:10.1212/wnl.0000000000002234

Cited by 150 publications

(86 citation statements)

References 37 publications

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Section: Introductionmentioning

confidence: 99%

“…Arthritogenic Old World alphaviruses also can cause encephalitis, but this occurs primarily in neonates (23). Between March 2005 and December 2006, a widespread outbreak of CHIKV occurred on the La Réunion Island in the Indian Ocean, infecting over one-third of the island population, causing at least 9 confirmed cases of neonatal encephalitis (23). Although some reports suggested that perinatal transmission of CHIKV may have occurred in the birth canal ( 24, 25 ), the presence of CHIKV RNA in the human placenta was confirmed in one case (26), although the cell type(s) targeted by the virus was not evaluated.…”

Section: Introductionmentioning

confidence: 99%

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Zika virus–related neurotropic flaviviruses infect human placental explants and cause fetal demise in mice

et al. 2018

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Although Zika virus (ZIKV) infection in pregnant women can cause placental damage, intrauterine growth restriction, microcephaly, and fetal demise, these disease manifestations only became apparent in the context of a large epidemic in the Americas. We hypothesized that ZIKV is not unique among arboviruses in its ability to cause congenital infection. To evaluate this, we tested the capacity of four emerging arboviruses (West Nile virus, WNV; Powassan virus, POWV; chikungunya virus, CHIKV; and Mayaro virus, MAYV) from related (flavivirus) and unrelated (alphavirus) genera to infect the placenta and fetus in immunocompetent, wild-type mice. Whereas all four viruses caused placental infection, only infection with the neurotropic flaviviruses (WNV and POWV) resulted in fetal demise. WNV and POWV also replicated efficiently in second-trimester human maternal (decidua) and fetal (chorionic villi and fetal membrane) explants whereas CHIKV and MAYV replicated less efficiently. In mice, RNA in situ hybridization and histopathological analysis revealed that WNV infected the placenta and fetal central nervous system, causing injury to the developing brain. In comparison, CHIKV and MAYV did not cause substantive placental or fetal damage despite evidence of vertical transmission. Based on the susceptibility of human maternal and fetal tissue explants and pathogenesis experiments in immunocompetent mice, other emerging neurotropic flaviviruses may share with ZIKV the capacity for transplacental transmission, and subsequent infection and injury to the developing fetus.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Zika virus–related neurotropic flaviviruses infect human placental explants and cause fetal demise in mice

et al. 2018

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“…In up to 57% of the cases, musculoskeletal pain may persist for years234. Rarely, fatal cases occur and this is typically in patients with underlying conditions56789. The host’s innate immune response plays an important role in the control as well as the pathogenesis of CHIKV infection.…”

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confidence: 99%

Mechanism and role of MCP-1 upregulation upon chikungunya virus infection in human peripheral blood mononuclear cells

Silva

Ende-Metselaar

Mulder

et al. 2016

Sci Rep

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Monocyte chemoattractant protein-1 (MCP-1/CCL2)-mediated migration of monocytes is essential for immunological surveillance of tissues. During chikungunya virus (CHIKV) infection however, excessive production of MCP-1 has been linked to disease pathogenesis. High MCP-1 serum levels are detected during the viremic phase of CHIKV infection and correlate with the virus titre. In vitro CHIKV infection was also shown to stimulate MCP-1 production in whole blood; yet the role and the mechanism of MCP-1 production upon infection of human peripheral blood mononuclear cells remain unknown. Here we found that active CHIKV infection stimulated production of MCP-1 in monocytes. Importantly however, we found that communication with other leukocytes is crucial to yield MCP-1 by monocytes upon CHIKV infection. Indeed, blocking interferon-α/β receptor or the JAK1/JAK2 signalling downstream of the receptor abolished CHIKV-mediated MCP-1 production. Additionally, we show that despite the apparent correlation between IFN type I, CHIKV replication and MCP-1, modulating the levels of the chemokine did not influence CHIKV infection. In summary, our data disclose the complexity of MCP-1 regulation upon CHIKV infection and point to a crucial role of IFNβ in the chemokine secretion. We propose that balance between these soluble factors is imperative for an appropriate host response to CHIKV infection.

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“…Atypical presentations of CHIKV infection can involve almost every organ system, as seen in Table 2. Even though the most common extra-articular manifestations reported in the literature involve the nervous system 25– 27 and the eye 17 ; alterations in the gastrointestinal tract, liver 16 , kidney, muscles, mucous membranes and skin and hematologic cells have been evidenced, as well as in hemostasis and coagulation processes. Cardiovascular compromise is worthy of mentioning because of its usually fatal outcomes 10, 28 .…”

Section: Resultsmentioning

confidence: 99%

Cardiovascular involvement and manifestations of systemic Chikungunya virus infection: A systematic review

et al. 2017

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Background: In the last three years, chikungunya virus disease has been spreading, affecting particularly the Americas, producing more than two million cases. In this setting, not only new disease-related epidemiological patterns have been found, but also new clinical findings have been reported by different research groups. These include findings on the cardiovascular system, including clinical, electrocardiographic and echocardiographic alterations. Methods: We performed a systematic review looking for reports about cardiovascular compromise during chikungunya disease. Cardiac compromise is not so common in isolated episodes; but countries where chikungunya virus is an epidemic should be well informed about this condition. We used 6 bibliographical databases as resources: Medline/Pubmed, Embase, ScienceDirect, ClinicalKey, Ovid and SciELO. Dengue reports on cardiovascular affectation were included as well, to compare both arbovirus’ organic affectations. Articles that delved mainly into the rheumatic articular and cutaneous complications were not considered, as they were not in line with the purpose of this study. The type of articles included were reviews, meta-analyses, case-controls, cohort studies, case reports and case series. Results: Originally based on 737 articles, our reviewed selected 40 articles with 54.2% at least mentioning CHIKV cardiovascular compromise within the systemic affectation. Cardiovascular manifestations can be considered common and have been reported in France, India, Sri Lanka, Malaysia, Colombia, Venezuela and USA, including mainly, but no limited to: hypotension, shock and circulatory collapse, Raynaud phenomenon, arrhythmias, murmurs, myocarditis, dilated cardiomyopathy, congestive insufficiency, heart failure and altered function profile (Troponins, CPK). Conclusions: Physicians should be encouraged to keep divulgating reports on the cardiovascular involvement of chikungunya virus disease, to raise awareness and ultimately encourage suitable diagnosis and intervention worldwide.

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Chikungunya virus–associated encephalitis

Abstract: In the context of a large outbreak, CHIKV is a significant cause of CNS disease. As with other etiologies, CHIKV-associated encephalitis case distribution by age follows a U-shaped parabolic curve.

Cited by 150 publications

References 37 publications

Zika virus–related neurotropic flaviviruses infect human placental explants and cause fetal demise in mice

Zika virus–related neurotropic flaviviruses infect human placental explants and cause fetal demise in mice

Mechanism and role of MCP-1 upregulation upon chikungunya virus infection in human peripheral blood mononuclear cells

Cardiovascular involvement and manifestations of systemic Chikungunya virus infection: A systematic review

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