Disrupted spatial memory is a consequence of picornavirus infection

Buenz, Eric J.; Rodriguez, Moses; Howe, Charles L.

doi:10.1016/j.nbd.2006.07.003

Cited by 50 publications

(70 citation statements)

References 49 publications

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“…In Alzheimer's disease and ischemic injury, the PyNs in CA1 (9) sustain damage. Picornaviruses, including Theiler's murine encephalomyelitis virus (TMEV) (14,21) and encephalomyocarditis virus (22,23), target CA1 neurons in a way similar to that adopted by kainic acid in the same area (24). BDV also induces CA1 lesions but only in interferon-g-deficient knockout mice (18).…”

Section: Discussionmentioning

confidence: 99%

“…Bystander involvement of the hippocampal PyNs was observed during TMEV infection, during which neutrophil- (14) or transforming growth factor (TGF)-b-(21) mediated immunopathology was suggested as a cause of apoptosis. However, these reports did not discuss differences in distribution or expression patterns of these pathogenic factors in the hippocampal subregions.…”

Section: Discussionmentioning

confidence: 99%

“…It has also been studied in experimental animal diseases induced by hypoxic injury (13) or neurovirulent viruses, such as picornaviruses (14), measles virus (15), sindbis virus (16), HSV (17), and Borna disease virus (BDV) (18), or in injuries induced by a chemical agent (19). Depending on the causative agents and methods adopted to induce hippocampal injury, the injured subregions in the hippocampus vary; however, the reason for this selective vulnerability remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

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Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

2014

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SUMMARY:The mutant virus Mu-3 was isolated from the soluble receptor-resistant mutant 7 virus (srr7), which is a neuropathogenic strain of the mouse hepatitis virus JHMV, and cloned as a soluble receptor-resistant mutant from the highly neuropathogenic JHMV strain cl-2 virus (cl-2). In order to identify specific characteristcs of Mu-3, the pathology of Mu-3-infected mice was compared with that of srr7-and cl-2-infected mice. The neuropathology after Mu-3 infection exhibited a mixed pattern comparable to that induced by srr7 and cl-2 infections. In addition, Mu-3 infection caused marked apoptotic lesions in the hippocampal region, particularly in the CA2 and CA3 subregions, in the brains of all infected mice. In contrast, in cl-2 infection, 10-20z of the infected mice exhibited apoptosis in the hippocampus, which was primarily observed in the CA1 subregion. Apoptosis also occurred in the pyramidal neurons and CD11b-bearing cells. The apoptotic cells, indicated by caspase 3-activation, were a mixed population of infected and a higher number of uninfected cells. These data indicated that apoptosis observed in Mu-3 infection could be induced by the indirect effects of infection in addition to direct effects of the infected cells occurring in a cell-autonomous manner.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

2014

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“…CVB3 may influence normal CNS development by inducing apoptosis in both infected stem cells and neurons (22,24). Potential disruption of normal neurogenic activity might lead to developmental defects and CNS deficiencies, such as cognitive dysfunction (10). An extended immunopathology in the CNS following CVB3 infection may adversely affect normal CNS development and function.…”

Section: Vol 83 2009 Coxsackievirus Chronic Immunopathology In the mentioning

confidence: 99%

“…For example, in 1996, approximately 10 to 15 million diagnosed cases of enterovirus infection occurred in the United States alone (49). Few studies have been done to determine if enteroviruses, or their close relatives, have the ability to persist and cause longterm damage in the CNS (10,56) or whether previous infection of neurons may indirectly lead to the degeneration of aging motor neurons.…”

mentioning

confidence: 99%

Viral Persistence and Chronic Immunopathology in the Adult Central Nervous System following Coxsackievirus Infection during the Neonatal Period

Feuer

Ruller

et al. 2009

J Virol

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Coxsackieviruses are significant human pathogens, and the neonatal central nervous system (CNS) is a major target for infection. Despite the extreme susceptibility of newborn infants to coxsackievirus infection and viral tropism for the CNS, few studies have been aimed at determining the long-term consequences of infection on the developing CNS. We previously described a neonatal mouse model of coxsackievirus B3 (CVB3) infection and determined that proliferating stem cells in the CNS were preferentially targeted. Here, we describe later stages of infection, the ensuing inflammatory response, and subsequent lesions which remain in the adult CNS of surviving animals. High levels of type I interferons and chemokines (in particular MCP-5, IP10, and RANTES) were upregulated following infection and remained at high levels up to day 10 postinfection (p.i). Chronic inflammation and lesions were observed in the hippocampus and cortex of surviving mice for up to 9 months p.i. CVB3 RNA was detected in the CNS up to 3 months p.i at high abundance (ϳ10 6 genomes/mouse brain), and viral genomic material remained detectable in culture after two rounds of in vitro passage. These data suggest that CVB3 may persist in the CNS as a low-level, noncytolytic infection, causing ongoing inflammatory lesions. Thus, the effects of a relatively common infection during the neonatal period may be long lasting, and the prognosis for newborn infants recovering from acute infection should be reexplored.

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A high‐throughput 3‐parameter flow cytometry‐based cell death assay

2007

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Apoptosis plays a role in many disease states, and the evaluation of novel therapeutics that alters the apoptotic cascade is an area of intense investigation. However, many generally available methods to evaluate cell death are either time consuming, imprecise, or both. We report a system that permits simultaneous evaluation of three apoptotic markers (cell membrane integrity, mitochondrial membrane potential, and cell cycle progression) with minimal technical manipulation. This system is particularly wellsuited for toxicologic evaluation of novel compounds and profiling of new apoptosis-inducing agents. q 2007 International Society for Analytical Cytology

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Disrupted spatial memory is a consequence of picornavirus infection

Cited by 50 publications

References 49 publications

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

Viral Persistence and Chronic Immunopathology in the Adult Central Nervous System following Coxsackievirus Infection during the Neonatal Period

A high‐throughput 3‐parameter flow cytometry‐based cell death assay

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