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Poliovirus replication and spread in primary neuron cultures.

Abstract：

:While some neurotropic viruses cause rapid central nervous system (CNS) disease upon entry into the brain parenchyma, other viruses that are cytolytic in the periphery either result in little neuropathology or are associated with a protracted course of CNS disease consistent with persistent infection. One such virus, poliovirus (PV), is an extremely lytic RNA virus that requires the expression of CD155, the poliovirus receptor (PVR), for infection. To compare the kinetics of PV infection in neuronal and non-neuronal cell types, primary hippocampal neurons and fibroblasts were isolated from CD155+ transgenic embryos and infected with the Mahoney and Sabin strains of PV. Despite similar levels of infection in these ex vivo cultures, PV-infected neurons produced 100-fold fewer infectious particles as compared to fibroblasts throughout infection, and death of PV-infected neurons was delayed approximately 48 h. Spread in neurons occurred primarily by trans-synaptic transmission and was CD155-dependent. Together, these results demonstrate that the magnitude and speed with which PV replication, spread, and subsequent cell death occur in neurons is decreased as compared to non-neuronal cells, implicating cell-specific effects on replication that may then influence viral pathogenesis.

journal_name

Virology

journal_title

Virology

authors

Daley JK,Gechman LA,Skipworth J,Rall GF

doi

10.1016/j.virol.2005.05.032

subject

Has Abstract

pub_date

2005-09-15 00:00:00

pages

10-20

issue

1

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(05)00322-3

journal_volume

340

pub_type

杂志文章

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