Pathogenesis of herpes simplex virus type 2 experimental genital infection in pregnant mice

Sanjuán, Norberto; Zimberlin, María Noel

doi:10.1111/j.1574-695x.2001.tb01570.x

Cited by 6 publications

(7 citation statements)

References 21 publications

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“…It is also important to mention that HSV infections can cause constipation, urinary retention and weight loss in animal model of infection [Sanjuan and Zimberlin, ] which was also observed in this experimental study. However, our deeper investigations found no alterations in histological (liver and kidney) analysis in this animal model of HSV‐2 infection (data not shown).…”

Section: Discussionsupporting

confidence: 69%

Diphenyl Diselenide Reduces Oxidative Stress and Toxicity Caused by HSV‐2 Infection in Mice

Sartori

Jardim

Sari

et al. 2017

J of Cellular Biochemistry

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Herpes simplex viruses can cause uncommon systemic complications as acute liver failure (ALT) or urinary tract dysfunctions. Diphenyl diselenide, (PhSe) , a classical studied organic selenium compound, has a novel antiviral action against HSV-2 infection and well-known antioxidant and anti-inflammatory properties. This study aimed to investigate if (PhSe) reduces oxidative stress and systemic toxicity caused by HSV-2 infection in mice. Adult BALB/c mice were pre-treated with (PhSe) (5 mg kg /day, intragastric, i.g.) during 5 days; at day 6 mice were infected with HSV-2 (10 μl-10 PFU/mL ) and post-treated with (PhSe) for more 5 days. At day 11, they were killed and samples of liver and kidney were obtained to determine: reactive species (RS); malondialdehyde (MDA), and non-protein thiols (NPSH) levels; the activities of antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT). The activities of adenosine deaminase (ADA), Na /K -ATPase (liver and kidney); alanine aminotransferase (ALT), aspartate aminotransferase (AST), and the levels of urea (plasma) were determined as markers of hepatic and renal toxicity. The results revealed that (PhSe) treatment was effective against the increase of renal and hepatic oxidative stress in infected mice and also normalized hepatic and renal ADA activity. It recovered the activity of Na /K - and was not effective against the increase in urea levels in infected mice. Different from (PhSe) , acyclovir (positive control), caused an increase in ADA activity and a decrease in hepatic CAT activity. Considering the interest of alternative therapies to treat HSV-2 infections and secondary complications, (PhSe) become a notable candidate. J. Cell. Biochem. 118: 1028-1037, 2017. © 2016 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 69%

Diphenyl Diselenide Reduces Oxidative Stress and Toxicity Caused by HSV‐2 Infection in Mice

Sartori

Jardim

Sari

et al. 2017

J of Cellular Biochemistry

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“…Because sympathetic neurons have their origin in the thoracolumbar cord and parasympathetic neurons arise in the sacral cord, we hypothesized that these findings may be related to viral infection of autonomic ganglia (2). Both HSV-1 and HSV-2 are able to infect autonomic neurons (3,5,7,10,12,(14)(15)(16)(17). HSV-2 infection of autonomic neurons can give rise to transient bladder paralysis in humans, and latently infected murine parasympathetic neurons express the latency-associated transcript (12).…”

mentioning

confidence: 99%

Spread of Herpes Simplex Virus to the Spinal Cord Is Independent of Spread to Dorsal Root Ganglia

Ohashi

Bertke

Patel

et al. 2011

J Virol

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Levels of herpes simplex virus 1 (HSV-1) and HSV-2 DNA in dorsal root ganglia (DRG) and spinal cord (SC) were quantified after inoculation of guinea pig genitals and footpads. In genital infection, viral DNA reached SC and DRG simultaneously (at 2 to 3 days after inoculation) but was more abundant in SC than in DRG. After inoculation of footpads, which lack parasympathetic innervation, the viruses spread more efficiently to DRG than to SC. These results show important differences between genital and footpad infections, including independence of spread to DRG and SC, and imply that autonomic neurons may play an important role in the pathogenesis of viral latency after genital inoculation.The related species herpes simplex virus 1 (HSV-1) and HSV-2 exhibit differences in latency and recurrence patterns. While both viruses establish latency in sensory ganglia and reactivate to cause recurrent disease, HSV-1 reactivates more efficiently from trigeminal ganglia to cause cold sores or keratitis and HSV-2 reactivates more efficiently from lumbosacral dorsal root ganglia (DRG) to cause genital herpes (8). HSV-1 and HSV-2 also display different tropisms for nociceptive sensory neurons, with HSV-1 more likely to be detected during latency in murine neurons displaying the surface marker A5 and HSV-2 in those displaying KH10 (9). Both of these findings are associated with HSV-1 or HSV-2 viral species-specific latency-associated transcript (LAT) sequences (9, 18).Although most studies have focused on viral latency in sensory neurons of either the dorsal root or trigeminal ganglia, we recently showed that levels of virus DNA in spinal cord exceeded those in the corresponding DRG, suggesting that other sites of latency may be important (1). After genital infection of guinea pigs, the quantities of latent HSV-1 DNA are greater in the thoracolumbar spinal cord than in the sacral spinal cord, while latent HSV-2 DNA is more abundant in the sacral spinal cord. Mutations in the LAT did not influence this tropism for different spinal cord levels. Because sympathetic neurons have their origin in the thoracolumbar cord and parasympathetic neurons arise in the sacral cord, we hypothesized that these findings may be related to viral infection of autonomic ganglia (2). Both HSV-1 and HSV-2 are able to infect autonomic neurons (3,5,7,10,12,(14)(15)(16)(17). HSV-2 infection of autonomic neurons can give rise to transient bladder paralysis in humans, and latently infected murine parasympathetic neurons express the latency-associated transcript (12). Viral infection of autonomic ganglia is difficult to study directly in animal models of HSV-2 infection because perigenital ganglia are very small, are located in the perigenital fat, and are difficult to identify. In the present study, we used genital (6) and footpad models of HSV infection to further examine these phenomena that are potentially related to differences in autonomic neuronal infections with HSV-1 and HSV-2.To further investigate the spread of virus to the spinal cord, we examined ...

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“…The peroxidase‐antiperoxidase (PAP) technique was employed as described previously . Briefly, paraffin‐embedded sections were treated with xilene and decreasing concentrations of ethanol and then washed with 0.05 M Tris–HCl pH 7.6.…”

Section: Methodsmentioning

confidence: 99%

Striated muscle involvement in experimental oral infection by herpes simplex virus type 1

González

Sanjuán

2013

J Oral Pathology Medicine

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Herpes simplex virus type 1 is one of the most frequent causes of oral infection in humans, especially during early childhood. Several experimental models have been developed to study the pathogenesis of this virus but all of them employed adult animals. In this work, we developed an experimental model that uses mice younger than 4 days old, to more closely resemble human infection. Mice were infected subcutaneously with the prototype strain McIntyre of Herpes simplex-1, and the progression of infection was studied by immunoperoxidase. All animals died within 24-72 h post-infection, while viral antigens were found in the oral epithelium, nerves and brain. The most striking result was the finding of viral antigens in the nucleus and cytoplasm of cells belonging to striated muscles. Organotypic cultures of striated muscles were performed, and viral replication was observed in them by immunocytochemistry, electron microscopy and viral isolation. We conclude that the infection of striated muscles is present from the onset of oral infection and, eventually, could explain some clinical observations in humans.

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Pathogenesis of herpes simplex virus type 2 experimental genital infection in pregnant mice

Cited by 6 publications

References 21 publications

Diphenyl Diselenide Reduces Oxidative Stress and Toxicity Caused by HSV‐2 Infection in Mice

Diphenyl Diselenide Reduces Oxidative Stress and Toxicity Caused by HSV‐2 Infection in Mice

Spread of Herpes Simplex Virus to the Spinal Cord Is Independent of Spread to Dorsal Root Ganglia

Striated muscle involvement in experimental oral infection by herpes simplex virus type 1

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