Antibody Kinetics in Infants Exposed to Chikungunya Virus Infection During Pregnancy Reveals Absence of Congenital Infection

Ramful, Duksha; Sampériz, Sylvain; Fritel, Xavier; Michault, Alain; Jaffar‐Bandjee, Marie‐Christine; Rollot, Olivier; Boumahni, B.; Gérardin, Patrick

doi:10.1093/infdis/jit814

Cited by 34 publications

(42 citation statements)

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“…Exposure was able to identify with certainty, encephalopathy from other causes and embryofœtopathies were ruled out, unexposed children being randomly selected through the maternal CHIMERE cohort and the serological status of each infant was known [12]. The sera of exposed children were monitored until seroreversion to rule out misclassification of children infected early in pregnancy [55]. There was no residual participation bias driven by maternal situation while using a propensity scale of social disadvantage.…”

Section: Discussionmentioning

confidence: 99%

Neurocognitive Outcome of Children Exposed to Perinatal Mother-to-Child Chikungunya Virus Infection: The CHIMERE Cohort Study on Reunion Island

et al. 2014

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BackgroundLittle is known about the neurocognitive outcome in children exposed to perinatal mother-to-child Chikungunya virus (p-CHIKV) infection.MethodsThe CHIMERE ambispective cohort study compared the neurocognitive function of 33 p-CHIKV-infected children (all but one enrolled retrospectively) at around two years of age with 135 uninfected peers (all enrolled prospectively). Psychomotor development was assessed using the revised Brunet-Lezine scale, examiners blinded to infectious status. Development quotients (DQ) with subscores covering movement/posture, coordination, language, sociability skills were calculated. Predictors of global neurodevelopmental delay (GND, DQ≤85), were investigated using multivariate Poisson regression modeling. Neuroradiologic follow-up using magnetic resonance imaging (MRI) scans was proposed for most of the children with severe forms.ResultsThe mean DQ score was 86.3 (95%CI: 81.0–91.5) in infected children compared to 100.2 (95%CI: 98.0–102.5) in uninfected peers (P<0.001). Fifty-one percent (n = 17) of infected children had a GND compared to 15% (n = 21) of uninfected children (P<0.001). Specific neurocognitive delays in p-CHIKV-infected children were as follows: coordination and language (57%), sociability (36%), movement/posture (27%). After adjustment for maternal social situation, small for gestational age, and head circumference, p-CHIKV infection was found associated with GND (incidence rate ratio: 2.79, 95%CI: 1.45–5.34). Further adjustments on gestational age or breastfeeding did not change the independent effect of CHIKV infection on neurocognitive outcome. The mean DQ of p-CHIKV-infected children was lower in severe encephalopathic children than in non-severe children (77.6 versus 91.2, P<0.001). Of the 12 cases of CHIKV neonatal encephalopathy, five developed a microcephaly (head circumference <−2 standard deviations) and four matched the definition of cerebral palsy. MRI scans showed severe restrictions of white matter areas, predominant in the frontal lobes in these children.ConclusionsThe neurocognitive outcome of children exposed to perinatal mother-to-child CHIKV infection is poor. Severe CHIKV neonatal encephalopathy is associated with an even poorer outcome.

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Section: Discussionmentioning

confidence: 99%

Neurocognitive Outcome of Children Exposed to Perinatal Mother-to-Child Chikungunya Virus Infection: The CHIMERE Cohort Study on Reunion Island

et al. 2014

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“…One interpretation of this finding is that infants are seropositive due to transfer of maternal antibody. However, while there is evidence of maternal transfer of CHIKV antibody in humans, the rates are not 100% and antibody levels decay rapidly [36,37]. Additionally, maternal transfer would be unlikely to sustain infant seroprevalence over several years.…”

Section: Discussionmentioning

confidence: 99%

Role of monkeys in the sylvatic cycle of chikungunya virus in Senegal

Althouse

Guerbois

Cummings

et al. 2016

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Athropod-borne viruses (arboviruses) pose the greatest risk of spillover into humans of any class of pathogens. Such spillover may occur as a one-step jump from a reservoir host species into humans or as a two-step jump from the reservoir to a different amplification host species and thence to humans. Despite the widespread havoc wreaked by emerging arboviruses, little is known about their transmission dynamics in reservoir and amplification hosts. Here we used serosurveillance and mathematical modeling to elucidate the role of monkeys in the sylvatic, enzootic cycle of chikungunya virus (CHIKV). Over three years, 219 African green monkeys, 78 patas monkeys, and 440 Guinea baboons were captured in the region surrounding Kédougou, Senegal. The age of each animal was determined by anthropometry and dentition, and exposure to CHIKV was determined by detection of neutralizing antibodies. We estimate age-specific * To whom correspondence should be addressed. Email: balthouse@idmod.org † These authors contributed equally to this work.CHIKV seroprevalence, force of infection (FoI), and basic reproductive number (R 0 ) in each species. Among the different species, CHIKV FoI ranged from 0.13 to 1.12 (95% CI, 0.81-2.28) and R 0 ranged from 1.5 (95% CI, 1.3-1.9) to 6.6 (95% CI, 5.1-10.4). CHIKV infection of infant monkeys was detected even when the virus was not detected in a concurrent survey of primatophilic mosquitoes and when population seropositivity, and therefore immunity, was too high for monkeys themselves to support continuous CHIKV transmission. We therefore conclude that monkeys in this region serve primarily as amplification rather than reservoir hosts of CHIKV. Additional efforts are needed to identify other vertebrate hosts capable of supporting continuous circulation. keywords: chikungunya virus -sylvatic arbovirus -non-human primate -age-stratified serosurvey

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“…Most of the reports concerning the effect of CHIKV infection during pregnancy describe no major effect on pregnancy outcomes or newborns if the mother was infected before the peripartum period (248)(249)(250). However, CHIKV-specific IgM antibodies were detected in the cord blood of the infants, providing evidence for intrauterine transmission of the virus (249,250). In contrast, another study identified that in the case of a symptomatic mother (2 days before and 2 days following delivery), the neonate also developed CHIKV symptoms (251).…”

Section: Humansmentioning

confidence: 99%

Emerging Role of Zika Virus in Adverse Fetal and Neonatal Outcomes

et al. 2016

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SUMMARYThe rapid spread of the Zika virus (ZIKV) in the Americas and its potential association with thousands of suspected cases of microcephaly in Brazil and higher rates of Guillain-Barré syndrome meet the conditions for a Public Health Emergency of International Concern, as stated by the World Health Organization in February 2016. Two months later, the Centers for Disease Control and Prevention (CDC) announced that the current available evidence supports the existence of a causal relationship between prenatal Zika virus infection and microcephaly and other serious brain anomalies. Microcephaly can be caused by several factors, and its clinical course and prognosis are difficult to predict. Other pathogens with proven teratogenicity have been identified long before the current ZIKV epidemic. Despite the growing number of cases with maternal signs of infection and/or presence of ZIKV in tissues of affected newborns or fetuses, it is currently difficult to assess the magnitude of increase of microcephaly prevalence in Brazil, as well as the role of other factors in the development of congenital neurological conditions. Meanwhile, health agencies and medical organizations have issued cautious guidelines advising health care practitioners and expectant couples traveling to, returning from, or living in affected areas. Analogous to dengue virus (DENV) epidemics, ZIKV has the potential to become endemic in all countries infested byAedesmosquitoes, while new mutations could impact viral replication in humans, leading to increased virulence and consequently heightened chances of viral transmission to additional naive mosquito vectors. Studies are urgently needed to answer the questions surrounding ZIKV and its role in congenital neurological conditions.

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Antibody Kinetics in Infants Exposed to Chikungunya Virus Infection During Pregnancy Reveals Absence of Congenital Infection

Cited by 34 publications

References 14 publications

Neurocognitive Outcome of Children Exposed to Perinatal Mother-to-Child Chikungunya Virus Infection: The CHIMERE Cohort Study on Reunion Island

Neurocognitive Outcome of Children Exposed to Perinatal Mother-to-Child Chikungunya Virus Infection: The CHIMERE Cohort Study on Reunion Island

Role of monkeys in the sylvatic cycle of chikungunya virus in Senegal

Emerging Role of Zika Virus in Adverse Fetal and Neonatal Outcomes

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