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Biological sex is a significant determinant of host responses and disease outcomes during viral infection. Although males often exhibit more robust pathological inflammatory responses, the implications for immune responses within the central nervous system remain unclear. Given that many viral infections can lead to long-term neurological complications, it is crucial to understand how biological sex influences neuroinflammation. Using a mouse model of Zika virus infection, we find that males develop more severe clinical disease compared to females, despite comparable infectious viral loads. Our findings demonstrate that sexually dimorphic immune responses contribute to increased male susceptibility to virus-induced neuropathology.
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Mansour et al. (2026) studied this question.
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