Zika virus infection histories in brain development

Area of Science:

• Neuroscience
• Virology
• Developmental Biology

Background:

• The Zika virus (ZIKV) outbreak in Brazil highlighted its teratogenic effects, specifically microcephaly.
• ZIKV infection in utero causes significant reduction in neuron numbers and neuronal death in the developing central nervous system (CNS).

Approach:

• This review synthesizes data from human, molecular, cellular, and animal model studies.
• It focuses on understanding the natural history of ZIKV within the embryonic CNS.
• The study examines the timing and pathways of ZIKV infection and spread.

Key Points:

• Intraneuronal viral transport is proposed as the primary mechanism for ZIKV spread within the embryonic brain.
• This mechanism is linked to the majority of congenital ZIKV syndrome (CZVS) cases.
• Viral transport across the blood-brain barrier and cerebrospinal fluid may cause more severe ZIKV-induced CNS malformations.

Conclusions:

• Understanding ZIKV's embryonic CNS infection dynamics is crucial for explaining CZVS phenotypic diversity.
• Intraneuronal transport is key to ZIKV pathogenesis in the developing brain.
• Further research into viral spread pathways can inform strategies to mitigate severe congenital malformations.