February 21, 2008Journal of VirologyOpen Access

Theiler's Virus-Induced Intrinsic Apoptosis in M1-D Macrophages Is Bax Mediated and Restricts Virus Infectivity: a Mechanism for Persistence of a Cytolytic Virus

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Population

M1-D macrophages and BHK-21 cells

Design

Preclinical

Follow-up

up to 24 hours postinfection

Authors

KSKyung‐No SonUniversity of Michigan RBRobert P. BeckerUniversity of Illinois Chicago PKPatricia KallioNorthwestern University

Discussion

Member takes

Implication

Apoptosis may restrict TMEV replication in macrophages; leaves open caspase inhibition as a modulator of neurovirulence.

Structured PICO

Population

M1-D macrophages and BHK-21 cells

Intervention

Pan-caspase inhibitors (qVD-OPh, zVAD-fmk) and Bcl-2 expression

Outcome

Virus replication kinetics and apoptotic signaling events (Bax translocation, cytochrome c efflux, caspase 9 and 3 activation)surrogate

BeAn virus infection in M1-D macrophages induces intrinsic apoptosis, which restricts virus replication and provides a potential mechanism for modulating TMEV neurovirulence.

Cite This Study

Son et al. (2008) studied this question.

synapsesocial.com/papers/6a910185aa0a5bd9a2e1b1d8 https://doi.org/10.1128/jvi.02349-07

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Theiler's Virus-Induced Intrinsic Apoptosis in M1-D Macrophages Is Bax Mediated and Restricts Virus Infectivity: a Mechanism for Persistence of a Cytolytic Virus

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Theiler's Virus-Induced Intrinsic Apoptosis in M1-D Macrophages Is Bax Mediated and Restricts Virus Infectivity: a Mechanism for Persistence of a Cytolytic Virus

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider