Autor: |
Pamela E. Capendale, Inés García-Rodríguez, Anoop T. Ambikan, Lance A. Mulder, Josse A. Depla, Eline Freeze, Gerrit Koen, Carlemi Calitz, Vikas Sood, Renata Vieira de Sá, Ujjwal Neogi, Dasja Pajkrt, Adithya Sridhar, Katja C. Wolthers |
Jazyk: |
angličtina |
Rok vydání: |
2024 |
Předmět: |
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Zdroj: |
Nature Communications, Vol 15, Iss 1, Pp 1-14 (2024) |
Druh dokumentu: |
article |
ISSN: |
2041-1723 |
DOI: |
10.1038/s41467-024-46634-9 |
Popis: |
Abstract 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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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