Axonal spread of neuroinvasive viral infections

Taylor, Matthew P.; Enquist, Lynn W.

doi:10.1016/j.tim.2015.01.002

Cited by 67 publications

(54 citation statements)

References 72 publications

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“…In neurotropic viral infections, intra-and interneuronal spread is considered to be a mechanism of immune evasion (51,52). However, our results do not support this assumption for L. monocytogenes.…”

Section: Discussioncontrasting

confidence: 88%

Listeria monocytogenes Spreads within the Brain by Actin-Based Intra-Axonal Migration

et al. 2015

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e Listeria monocytogenes rhombencephalitis is a severe progressive disease despite a swift intrathecal immune response. Based on previous observations, we hypothesized that the disease progresses by intra-axonal spread within the central nervous system. To test this hypothesis, neuroanatomical mapping of lesions, immunofluorescence analysis, and electron microscopy were performed on brains of ruminants with naturally occurring rhombencephalitis. In addition, infection assays were performed in bovine brain cell cultures. Mapping of lesions revealed a consistent pattern with a preferential affection of certain nuclear areas and white matter tracts, indicating that Listeria monocytogenes spreads intra-axonally within the brain along interneuronal connections. These results were supported by immunofluorescence and ultrastructural data localizing Listeria monocytogenes inside axons and dendrites associated with networks of fibrillary structures consistent with actin tails. In vitro infection assays confirmed that bacteria were moving within axon-like processes by employing their actin tail machinery. Remarkably, in vivo, neutrophils invaded the axonal space and the axon itself, apparently by moving between split myelin lamellae of intact myelin sheaths. This intra-axonal invasion of neutrophils was associated with various stages of axonal degeneration and bacterial phagocytosis. Paradoxically, the ensuing adaxonal microabscesses appeared to provide new bacterial replication sites, thus supporting further bacterial spread. In conclusion, intra-axonal bacterial migration and possibly also the innate immune response play an important role in the intracerebral spread of the agent and hence the progression of listeric rhombencephalitis. Due to its resistance to hostile conditions, the Gram-positive bacterium Listeria monocytogenes is ubiquitously distributed in the environment and commonly contaminates food and animal feed (1-3). Upon oral uptake, L. monocytogenes may turn into an intracellular pathogen causing listeriosis, one of the deadliest foodborne infections in humans and ruminants (1,(4)(5)(6). Clinical syndromes associated with L. monocytogenes infection include febrile gastroenteritis, mastitis, septicemia, abortion, and central nervous system (CNS) infection, the latter accounting for the high mortality rates associated with listeriosis (1, 5-9). In most human patients, neurolisteriosis manifests as meningitis or meningoencephalitis, and L. monocytogenes is listed among the most common pathogens of bacterial meningitis (10-13). Further forms of neurolisteriosis include brainstem encephalitis (rhombencephalitis) occurring in 25% of cases and brain abscesses accounting for a further 10% of cases with CNS infection (11,14). Neurolisteriosis in ruminants occurs almost exclusively as rhombencephalitis (1, 15-17) and mimics its human counterpart in many respects (17, 18), lending itself as a spontaneous animal model.Although the intracellular life cycle of L. monocytogenes has been elegantly deciphered by in vitro st...

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Section: Discussioncontrasting

confidence: 88%

Listeria monocytogenes Spreads within the Brain by Actin-Based Intra-Axonal Migration

et al. 2015

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“…Previous authors have shown that US9 is involved in anterograde transport of viral capsids and glycoproteins to axonal termini in related alphaherpesviruses, such as pseudorabies virus (PRV) (58–60). However the role of US9 in anterograde transport of HSV-1 is less clear (61–64).…”

Section: Discussionmentioning

confidence: 99%

Viral forensic genomics reveals the relatedness of classic herpes simplex virus strains KOS, KOS63, and KOS79

et al. 2016

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Herpes simplex virus 1 (HSV-1) is a widespread global pathogen, of which the strain KOS is one of the most extensively studied. Previous sequence studies revealed that KOS does not cluster with other strains of North American geographic origin, but instead clustered with Asian strains. We sequenced a historical isolate of the original KOS strain, called KOS63, along with a separately isolated strain attributed to the same source individual, termed KOS79. Genomic analyses revealed that KOS63 closely resembled other recently sequenced isolates of KOS and was of Asian origin, but that KOS79 was a genetically unrelated strain that clustered in genetic distance analyses with HSV-1 strains of North American/European origin. These data suggest that the human source of KOS63 and KOS79 could have been infected with two genetically unrelated strains of disparate geographic origins. A PCR RFLP test was developed for rapid identification of these strains.

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“…In addition, 'shingles' as a skin manifestation may reflect subsequent repeated subclinical reactivation of VZV, sometimes in cranial nerves that have a more direct effect on the cerebral arteries [18]. It is possible that the reactivated VZV spreads transaxonally in a centripetal direction like rabies [19], and reaches the cerebral arteries, and this is followed by transmural spread of the virus. Another possible mechanism is that zoster itself or post-herpetic neuralgia increases sympathetic status and adverse emotional reactions, theoretically increasing cerebrovascular risk [20].…”

Section: Discussionmentioning

confidence: 99%

Risk of stroke and transient ischaemic attack after herpes zoster

Kwon

Yun

Kim

et al. 2016

Clinical Microbiology and Infection

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We assessed the association of herpes zoster (HZ) with stroke/transient ischaemic attack (TIA) in the general population according to age with controlling risk factors for stroke, using a nationwide representative cohort. The study was based on a prospective dynamic cohort consisting of 1 million Koreans representing all age groups, genders and geographical areas in the Korea Health Insurance Database. New events of stroke/TIA and HZ were identified using the diagnostic codes in the International Classification of Diseases, tenth revision. The risk for stroke/TIA after HZ was compared with HZ-free stroke/TIA individuals according to age group. A total of 766 179 adults were followed up for 11 years from 2003. The incidence of the first-diagnosed HZ cases was 9.40 per 1000 person-years, and that of the first-diagnosed stroke/TIA cases was 9.77 per 1000 person-years. The risk for stroke/TIA was higher in patients who had previous HZ episodes than in those who had never experienced HZ (incidence rate ratio 1.90; 95% CI 1.85-1.95). In addition, this risk persisted for several years after HZ. The risk of stroke/TIA after HZ gradually decreased with age; adjusted hazard ratio (HR) 2.04 in 18- to 30-year-olds, HR 1.74 in 30- to 40-year-olds, HR 1.43 in 40- to 50-year-olds, HR 1.23 in 50- to 60-year-olds, HR 1.24 in 60- to 70-year-olds, and HR 1.29 in those >70 years old, after controlling risk factors for stroke/TIA. Our findings provide evidence that HZ carries an increased risk of stroke or TIA and that the effect of HZ on stroke decreases with increasing age.

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Axonal spread of neuroinvasive viral infections

Cited by 67 publications

References 72 publications

Listeria monocytogenes Spreads within the Brain by Actin-Based Intra-Axonal Migration

Listeria monocytogenes Spreads within the Brain by Actin-Based Intra-Axonal Migration

Viral forensic genomics reveals the relatedness of classic herpes simplex virus strains KOS, KOS63, and KOS79

Risk of stroke and transient ischaemic attack after herpes zoster

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