Distribution of herpes simplex virus types 1 and 2 genomes in human spinal ganglia studied by PCR and in situ hybridization.

Obara, Yoshitaka; Furata, Y; Takasu, Toshiyuki; Suzuki, Shin; Suzuki, Hiroshi; Matsukawa, Satoshi; Fujioka, Yuuichiro; Takahashi, Hitomi; Kurata, T; Nagashima, Kyo

doi:10.1016/s0002-9394(14)70887-6

Cited by 5 publications

(6 citation statements)

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“…Bernstein and Stanberry performed a detailed analysis of primary vaginal HSV-2 infection in the guinea pig and found that HSV-2 was detected from ipsilateral dorsal root ganglia on days 2 and 3 postinfection and from contralateral dorsal root ganglia on days 4 and 5 and that the majority (9/12) of animals shed virus on the contralateral genital skin from the initially infected ganglion (28), suggesting that HSV-2 infection can spread throughout neuronal tissues. Although data on the distribution of HSV-2 in human sacral ganglia are limited, Obara et al described PCR and in situ hybridization evidence of widespread sacral ganglion infection in three persons coinfected with HSV-1 and HSV-2, with HSV-2 detected in 21 of 23 sacral ganglia and HSV-1 in 22 of 23 ganglia (29), and concluded that both HSV-1 infection and HSV-2 infection are latent bilaterally throughout the sacral ganglia. Croen et al also detected evidence of HSV-2 infection in the sacral ganglia of 5 persons at autopsy using in situ hybridization; HSV-2 was detected in two or more sacral ganglia in 3 of 5 persons (30).…”

Section: Discussionmentioning

confidence: 99%

Virologic and Immunologic Evidence of Multifocal Genital Herpes Simplex Virus 2 Infection

Johnston

Zhu

Jing

et al. 2014

J Virol

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Genital herpes simplex virus (HSV) reactivation is thought to be anatomically and temporally localized, coincident with limited ganglionic infection. Short, subclinical shedding episodes are the most common form of HSV-2 reactivation, with host clearance mechanisms leading to rapid containment. The anatomic distribution of shedding episodes has not been characterized. To precisely define patterns of anatomic reactivation, we divided the genital tract into a 22-region grid and obtained daily swabs for 20 days from each region in 28 immunocompetent, HSV-2-seropositive persons. HSV was detected via PCR, and sites of asymptomatic HSV shedding were subjected to a biopsy procedure within 24 h. CD4؉ and CD8 ؉ T cells were quantified by immunofluorescence, and HSV-specific CD4 ؉ T cells were identified by intracellular cytokine cytometry. HSV was detected in 868 (7%) of 11,603 genital swabs at a median of 12 sites per person (range, 0 to 22). Bilateral HSV detection occurred on 83 (67%) days with shedding, and the median quantity of virus detected/day was associated with the number of sites positive (P < 0.001). In biopsy specimens of asymptomatic shedding sites, we found increased numbers of CD8 ؉ T cells compared to control tissue (27 versus 13 cells/mm 2 , P ‫؍‬ 0.03) and identified HSV-specific CD4 ؉ T cells. HSV reactivations emanate from widely separated anatomic regions of the genital tract and are associated with a localized cellular infiltrate that was demonstrated to be HSV specific in 3 cases. These data provide evidence that asymptomatic HSV-2 shedding contributes to chronic inflammation throughout the genital tract. IMPORTANCEThis detailed report of the anatomic patterns of genital HSV-2 shedding demonstrates that HSV-2 reactivation can be detected at multiple bilateral sites in the genital tract, suggesting that HSV establishes latency throughout the sacral ganglia. In addition, genital biopsy specimens from sites of asymptomatic HSV shedding have increased numbers of CD8 ؉ T cells compared to control tissue, and HSV-specific CD4 ؉ T cells are found at sites of asymptomatic shedding. These findings suggest that widespread asymptomatic genital HSV-2 shedding is associated with a targeted host immune response and contributes to chronic inflammation throughout the genital tract. H erpes simplex virus 2 (HSV-2) infects over 500 million people worldwide (1) and is the leading cause of genital ulcer disease (2) and increases the risk of HIV acquisition (3). Herpetic genital ulcers in the immunocompetent person are localized with respect to time and anatomic site (4), consistent with reactivation of virus from the ganglion innervating this region. However, most HSV genital shedding is subclinical, with rapid onset and clearance (5, 6). Such subclinical reactivation may be more widespread in the genital area (7), consistent with frequent leakage of virus into the genital skin and mucosa with localized host containment (8, 9). Mathematical models suggest that observed shedding patterns are the result of ove...

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Section: Discussionmentioning

confidence: 99%

Virologic and Immunologic Evidence of Multifocal Genital Herpes Simplex Virus 2 Infection

Johnston

Zhu

Jing

et al. 2014

J Virol

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“…Bustos and Atherton [2002] also reported that HSV-1 DNA was detected in 31 (66%) of 47 trigeminal ganglia by PCR. HSV-1 DNA was also detected in human ciliary, cervical, thoracic, lumber, and sacral ganglia by PCR or by in situ hybridization (ISH) [Obara et al, 1997;Bustos et al, 2002]. However, previous studies have never attempted to detect HSV-1 DNA from a larger number of human trigeminal ganglia samples or to examine the distribution of HSV-1 DNA in terms of laterality, age, and gender.…”

Section: Introductionmentioning

confidence: 99%

Detection of herpes simplex virus type 1 DNA in bilateral human trigeminal ganglia and optic nerves by polymerase chain reaction

et al. 2006

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Herpes simplex virus type 1 (HSV-1) DNA was extracted from human trigeminal ganglia of 121 cadavers aged between 3 months and 94 years, and its PCR amplification was performed for the RL2 HSV-1 sequence using two pairs of primers. The HSV-1 DNA was detected in 74 of 121 patients (61%); 70/74 bilaterally, 3/74 only on the left side, and 1/74 only on the right side. Although the PCR-positive rate was significantly higher in advanced age, the correlation between the PCR-positive rate and gender was unclear. Additionally, HSV-1 DNA was not detected in any of the 50 optic nerve samples.

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“…38,39 Presence of immunity to HSV-1 usually attenuates the symptoms of HSV-2 infection compared with no immunity. Obara et al 40 have shown the coexistence of both HSV-1 and HSV-2 genomes in the wide range of dorsal root ganglia by PCR and in situ hybridization, and HSV-1 and HSV-2 infect and become latent in the same sensory ganglia. Our results are consistent with these observations in humans.…”

Section: Discussionmentioning

confidence: 99%

Effect of immunity on gene delivery into anterior horn motor neurons by live attenuated herpes simplex virus vector

et al. 2001

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Distribution of herpes simplex virus types 1 and 2 genomes in human spinal ganglia studied by PCR and in situ hybridization.

Cited by 5 publications

References 0 publications

Virologic and Immunologic Evidence of Multifocal Genital Herpes Simplex Virus 2 Infection

Virologic and Immunologic Evidence of Multifocal Genital Herpes Simplex Virus 2 Infection

Detection of herpes simplex virus type 1 DNA in bilateral human trigeminal ganglia and optic nerves by polymerase chain reaction

Effect of immunity on gene delivery into anterior horn motor neurons by live attenuated herpes simplex virus vector

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