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Capendale, Pamela E; García-Rodríguez, Inés; Ambikan, Anoop T; Mulder, Lance A; Depla, Josse A; Freeze, Eline; Koen, Gerrit; Calitz, Carlemi; Sood, Vikas; Vieira de Sá, Renata; Neogi, Ujjwal; Pajkrt, Dasja; Sridhar, Adithya; Wolthers, Katja C
Nature communications, 03/2024, Letnik: 15, Številka: 1Journal Article
Picornaviruses are a leading cause of central nervous system (CNS) infections. While genotypes such as parechovirus A3 (PeV-A3) and echovirus 11 (E11) can elicit severe neurological disease, the highly prevalent PeV-A1 is not associated with CNS disease. Here, we expand our current understanding of these differences in PeV-A CNS disease using human brain organoids and clinical isolates of the two PeV-A genotypes. Our data indicate that PeV-A1 and A3 specific differences in neurological disease are not due to infectivity of CNS cells as both viruses productively infect brain organoids with a similar cell tropism. Proteomic analysis shows that PeV-A infection significantly alters the host cell metabolism. The inflammatory response following PeV-A3 (and E11 infection) is significantly more potent than that upon PeV-A1 infection. Collectively, our findings align with clinical observations and suggest a role for neuroinflammation, rather than viral replication, in PeV-A3 (and E11) infection.
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in: SICRIS
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