Herpes Simplex Virus-1 and Varicella-Zoster Virus Latency in Ganglia

Mitchell, Bradley M.; Bloom, David; Cohrs, Randall J.; Gilden, Donald H.; Kennedy, Peter G. E.

doi:10.1080/713831492

Cited by 27 publications

(40 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Virus then spreads along the sensory nerves to sensory root ganglia where latency is established in ganglionic neurons. [9][10][11]13 HSV-1 was detected in four of eight cases. In two cases, HSV-1 was detected only in neural tissues (dorsal root ganglion, spinal cord, sympathetic ganglion, and peripheral nerve), whereas in two other cases, HSV-1 was detected in multiple tissues.…”

Section: Discussionmentioning

confidence: 90%

“…Primary HSV-1 infection of immunocompetent persons is characterized by lesions of the oral mucosa, followed by latent persistence within neurons of cervical and cranial nerve sensory ganglia. [3][4][5][6][7][8][9][10][11] In some cases, HSV-1 and HSV-2 can be found in brain tissue. 12 Viral reactivation can lead to recurrent mucocutaneous disease, whereas dissemination may lead to widespread organ involvement, including esophagus, lower gastrointestinal tract, trachea, lungs, brain, eyes, and skin.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11][13][14][15][16] Dissemination may lead to widespread organ involvement, including the eye, brain, lung, myocardium, and liver. Primary VZV infection, most often acquired in early childhood, is characterized by fever and a diffuse maculopapular rash.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Anatomical mapping of human herpesvirus reservoirs of infection

Chen

Hudnall

2006

Modern Pathology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Anatomical mapping of human herpesvirus reservoirs of infection

Chen

Hudnall

2006

Modern Pathology

View full text Add to dashboard Cite

“…Primary infection, usually in children, causes varicella (Bchickenpox^), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis [1,2]. In latently infected human ganglia, VZV is located in neurons [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…However, the consistent detection by several groups of other VZV transcripts (VZV open reading frames 4, 21, 29, 62, 63 and 66) after this time may possibly reflect agonal attempts at VZV reactivation [6][7][8][9]. Decades later, as cell-mediated immunity to VZV declines with advancing age or when humans are immunosuppressed by disease or drug therapy, VZV reactivates to cause herpes zoster (Bshingles^), a painful dermatomally distributed vesicular eruption [1][2][3]. VZV reactivation also produces an increasingly recognized number of acute, subacute, and chronic neurological conditions, often without rash.…”

Section: Introductionmentioning

confidence: 99%

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

Kennedy

2016

Neurotherapeutics

View full text Add to dashboard Cite

Varicella zoster virus (VZV) is a ubiquitous neurotropic human herpesvirus. Primary infection usually causes varicella (chicken pox), after which virus becomes latent in ganglia along the entire neuraxis. Decades later, virus reactivates to produce herpes zoster (shingles), a painful dermatomally distributed vesicular eruption. Zoster may be further complicated by postherpetic neuralgia, VZV vasculopathy, myelitis, and segmental motor weakness. VZV reactivation has also been associated with giant cell arteritis. This overview discusses treatment of various conditions that often require both corticosteroids and antiviral drugs. Treatment for VZV-associated disease is often based on case reports and small studies rather than largescale clinical trials. Issues that require resolution include the optimal duration of such combined therapy, more effective treatment for postherpetic neuralgia, whether some treatments should be given orally or intravenously, the widening spectrum of zoster sine herpete, and the role of antiviral therapy in giant cell arteritis.

show abstract

Cultured vestibular ganglion neurons demonstrate latent HSV1 reactivation

et al. 2011

View full text Add to dashboard Cite

Objectives/Hypothesis Vestibular neuritis is a common cause of both acute and chronic vestibular dysfunction. Multiple pathologies have been hypothesized to be the causative agent of vestibular neuritis; however, whether herpes simplex type I (HSV1) reactivation occurs within the vestibular ganglion has not been demonstrated previously by experimental evidence. We developed an in vitro system to study HSV1 infection of vestibular ganglion neurons (VGNs) using a cell culture model system. Study design basic science study. Results Lytic infection of cultured rat VGNs was observed following low viral multiplicity of infection (MOI). Inclusion of acyclovir suppressed lytic replication and allowed latency to be established. Upon removal of acyclovir, latent infection was confirmed with reverse-transcription polymerase chain reaction and by RNA fluorescent in situ hybridization for the latency-associated transcript (LAT). 29% cells in latently infected cultures were LAT positive. The lytic IPC27 transcript was not detected by reverse-transcription polymerase chain reaction (RT-PCR). Reactivation of HSV1 occurred at a high frequency in latently infected cultures following treatment with trichostatin A (TSA), a histone deactylase inhibitor. Conclusions VGNs can be both lytically and latently infected with HSV1. Furthermore, latently infected VGNs can be induced to reactivate using TSA. This demonstrates that reactivation of latent HSV1 infection in the vestibular ganglion can occur in a cell culture model, and suggests that reactivation of HSV1 infection a plausible etiologic mechanism of vestibular neuritis.

show abstract

Herpes Simplex Virus-1 and Varicella-Zoster Virus Latency in Ganglia

Cited by 27 publications

References 0 publications

Anatomical mapping of human herpesvirus reservoirs of infection

Anatomical mapping of human herpesvirus reservoirs of infection

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

Cultured vestibular ganglion neurons demonstrate latent HSV1 reactivation

Contact Info

Product

Resources

About