Abstract
Chikungunya virus (CHIKV) is an alphavirus that causes febrile illness punctuated by severe polyarthralgia. After the emergence of CHIKV in the Western Hemisphere, multiple reports of congenital infections were published that documented neurological complications, cardiac defects, respiratory distress, and miscarriage. The Western Hemisphere is endemic to several alphaviruses, and whether antigenic cross-reactivity can impact the course of infection has not been explored. Recent advances in biomedical engineering have produced cell co-culture models that replicate the cellular interface at the maternal fetal axis. We employed a trans-well assay to determine if cross-reactive antibodies affected the movement and replication of CHIKV across placental cells and into an embryoid body. The data showed that antibodies to Venezuelan equine encephalitis virus significantly reduced CHIKV viral load in embryoid bodies. The data highlighted the fact that viral pathogenesis can be cell-specific and that exploiting antigenic cross-reactivity could be an avenue for reducing the impact of congenital CHIKV infections.
Highlights
Chikungunya virus (CHIKV) is an alphavirus vectored by Aedes mosquitos and is an enveloped +
When CHIKV emerged in the Western Hemisphere, neuroinvasive disease and congenital infections were reported at rates much higher than the Eastern Hemisphere [4]
Reports of congenital infection were published in many CHIKV-endemic locations, the vast majority originated from South and Central America [4]
Summary
Chikungunya virus (CHIKV) is an alphavirus vectored by Aedes mosquitos and is an enveloped +positive sense single stranded RNA ssRNA virus with a 12 kb genome. Chikungunya virus (CHIKV) is an alphavirus vectored by Aedes mosquitos and is an enveloped +. CHIKV infection was thought to be self-limited, but increasing reports are showing that rheumatic and neurological sequelae can linger for years following infection [1,2,3]. When CHIKV emerged in the Western Hemisphere, neuroinvasive disease and congenital infections were reported at rates much higher than the Eastern Hemisphere [4]. After the emergence of CHIKV in the Western Hemisphere, multiple reports of congenital infections were published that documented neurological complications, cardiac defects, respiratory distress, and miscarriage [5,8,9]. Reports of congenital infection were published in many CHIKV-endemic locations, the vast majority originated from South and Central America [4]
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