Experimental Herpes Zoster

Teague, Oscar; Goodpasture, Ernest W.

doi:10.1001/jama.1923.02650050031010

Cited by 34 publications

(8 citation statements)

References 1 publication

(1 reference statement)

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“…In the course of acute ganglionic infection with HSV-1, some productively infected neurons can give rise to infectious viral progeny that travel by anterograde axonal transport either to the brainstem or out to the periphery and back again (via retrograde axonal transport) to the TG, a process referred to as round-trip spread (8,32,49,53,55,57). In order to determine whether the preferential establishment of HSV-1 latent infection in A5-positive neurons is due to round-trip spread, we evaluated the distribution of latent HSV-1 infection in the mouse TG following ocular inoculation with US9…”

Section: Preferential Establishment Of Latent Hsv Infections Is Not Vmentioning

confidence: 99%

Investigation of the Mechanism by Which Herpes Simplex Virus Type 1 LAT Sequences Modulate Preferential Establishment of Latent Infection in Mouse Trigeminal Ganglia

Imai

Apakupakul

Krause

et al. 2009

J Virol

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We previously demonstrated that herpes simplex virus type 1 (HSV-1) preferentially establishes latent infection in monoclonal antibody (MAb) A5-positive ganglionic neurons and that a 2.8-kb portion of the HSV-1 genome, corresponding to the 5 end of the LAT (latency-associated transcript) coding region, is responsible for this phenotype (38, 65). In the current study we carried out further genetic mapping of this latency phenotype and investigated some of the mechanisms that might be responsible. Studies with the chimeric virus HSV-1 17syn؉/LAT2, an HSV-1 virus engineered to express HSV-2 LAT, demonstrated that this virus exhibited an HSV-2 latency phenotype, preferentially establishing latency in MAb KH10-positive neurons. This result is complementary to that previously described for the chimeric virus HSV-2 333/LAT1 and indicate that the HSV-1 latency phenotype can be changed to that of HSV-2 by substitution of a 2. Primary infection with herpes simplex virus (HSV) is characterized by local viral replication at the site of inoculation as well as retrograde axonal transport of the virus to regional sensory ganglia where a latent infection may be established. Sensory ganglia are comprised of a heterogeneous population of neurons, and work in our laboratory has demonstrated that different subpopulations of murine ganglionic neurons have different outcomes of infection with HSV (38,39,65). Of the subpopulations of ganglionic neurons that we have studied, those neurons recognized by monoclonal antibodies (MAbs) A5 (specific for a population of neurons expressing Gal␤1-4GlcNAc-R epitopes) and KH10 (specific for a different population of ganglionic neurons expressing Gal␣1-3Gal␤1-4NAc-R epitopes) have the most distinct susceptibility phenotypes (19,22,65). Although all neuronal subpopulations appear to be capable of supporting a productive infection with either HSV type 1 (HSV-1) or HSV-2, as assayed by in situ hybridization for the latency-associated transcripts (LAT), HSV-1 preferentially establishes a latent infection in A5-positive neurons whereas HSV-2 preferentially establishes a latent infection in KH10-positive neurons (38), a pattern that is observed following both ocular and footpad inoculation.In the mouse trigeminal ganglion (TG) MAbs A5 and KH10 recognize functionally distinct neuronal populations. Most A5-positive neurons are immunoreactive for neuropeptides and the high affinity nerve growth factor receptor (and terminate in lamina I and IIa of the dorsal horn of the spinal cord), whereas KH10-positive neurons colabel with the lectin BSL-IB 4 (Bandeiraea simplicifolia isolectin B 4 ), identifying them as a population of small-diameter, peripherin-positive, glial cell line-derived neurotrophic factor-responsive, but vanilloid receptor-negative neurons that terminate largely in lamina IIb of the dorsal horn of the spinal cord (3,19,38,42,52,67). These observations highlight the importance of studying the interaction of HSV with different sensory neuronal subtypes in order to gain a complete understanding ...

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Section: Preferential Establishment Of Latent Hsv Infections Is Not Vmentioning

confidence: 99%

Investigation of the Mechanism by Which Herpes Simplex Virus Type 1 LAT Sequences Modulate Preferential Establishment of Latent Infection in Mouse Trigeminal Ganglia

Imai

Apakupakul

Krause

et al. 2009

J Virol

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“…Growths appeared earlier in the treated skin, were more numerous, tended to be more pigmented, 1 The tar came from the Ostergasfabrik of Amsterdam, and was the generous gift of Dr. Karl Landsteiner. It has been employed in much work in this laboratory.…”

Section: Influence Of Carcinogenic Agents To Alter Skin Susceptibilitymentioning

confidence: 99%

Cell State as Affecting Susceptibility to a Virus

Friedewald

1942

Journal of Experimental Medicine

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Rabbit skin can be rendered abnormally susceptible to papilloma virus infection by preliminary treatments with a variety of agents. The most effective agents thus far found are 0.3 per cent methylcholanthrene in benzene and a mixture in equal parts of turpentine and acetone, applied four or five times at 2 day intervals. When virus is inoculated into skin altered by these agents, either intradermally or by inunction after scarification, papillomas appear earlier and in greater number than on normal skin, and much higher dilutions give rise to growths. The method provides a means of detecting amounts of virus which cause no papillomas upon inoculation into normal skin. Papilloma virus material which is rubbed into scarified normal or hyperplastic skin is largely lost in the scabbing which ensues, and nearly all of it fails to reach susceptible cells. The preparatory agents which increase the effectiveness of the virus bring about marked epidermal hyperplasia, and the hyperplastic tissue regenerates with greater rapidity when scarified. The agents evidently act in large part by providing young epidermal cells in quantity to the virus, as also by inducing a richer vascularization than ordinary in support of the papillomatous proliferation. It is possible that they also act by providing especially susceptible cells. The implications of the findings are discussed.

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“…Their excellent experiments (59) illustrate that peripheral lesions may induce lesions of the central nervous system and that the cause of the central lesions may be traced if we examine the possibility of spread from the periphery along the corresponding nerve trunks.…”

Section: Dissemination Of Micro-organisms and Their Products Along Nementioning

confidence: 99%

Dental Infection and Diseases of the Nervous System

Störtebecker

1960

Allergy

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Experimental Herpes Zoster

Cited by 34 publications

References 1 publication

Investigation of the Mechanism by Which Herpes Simplex Virus Type 1 LAT Sequences Modulate Preferential Establishment of Latent Infection in Mouse Trigeminal Ganglia

Investigation of the Mechanism by Which Herpes Simplex Virus Type 1 LAT Sequences Modulate Preferential Establishment of Latent Infection in Mouse Trigeminal Ganglia

Cell State as Affecting Susceptibility to a Virus

Dental Infection and Diseases of the Nervous System

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