Herpes Simplex Virus Type 1 Infection via the Bloodstream with Apolipoprotein E Dependence in the Gonads Is Influenced by Gender
- Burgos, Javier S. 12
- Ramirez, Carlos 12
- Sastre, Isabel 12
- Alfaro, Juan M. 12
- Valdivieso, Fernando 12
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1
Universidad Autónoma de Madrid
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2
Centro de Biología Molecular Severo Ochoa
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ISSN: 0022-538X, 1098-5514
Año de publicación: 2005
Volumen: 79
Número: 3
Páginas: 1605-1612
Tipo: Artículo
Otras publicaciones en: Journal of Virology
Resumen
Herpes simplex virus type 1 (HSV-1) causes disease in humans and animals. Infection usually occurs via the neural route and possibly occurs via the hematogenous route. The latter, however, is the main route by which immunosuppressed individuals and neonates are infected. Gender-dependent differences in the incidence and severity of some viral infections have been reported. To detect differences between the sexes with respect to HSV-1 colonization and disease, the characteristics of both acute and latent infections in hematogenously infected male and female mice were compared. In acute infection, the female mice had a poorer outcome: HSV-1 colonization was more effective, especially in the gonads and brain. In the encephalon, the midbrain had the highest viral load. In latent infection, brain viral loads were not significantly different with respect to sex. Significant differences were seen, however, in the blood and trigeminal ganglia: HSV-1 seroprevalence was observed in females, with no virus detected in males. In brain dissections, only the cerebral cortex of the females had viral loads statistically higher than those observed in the males. The spread of the virus to several organs of interest during acute infection was examined immunohistochemically. Female mice showed greater viral immunostaining, especially in the adrenal cortex, gonads, and midbrain. In male mice, HSV-1 was detected predominantly in the adrenal cortex. It was also found that apolipoprotein E promotes virus colonization of the ovaries, the APOE gene dose being directly related to viral invasiveness.
Información de financiación
We thank the Asociación de Familiares de Enfermos de Alzheimer (AFAL), the Fundación Areces, the Obra Social Caja Madrid, the Universidad Autónoma de Madrid, and the Comunidad de Madrid for supporting our research. We thank F. Mayor for continuous encouragement and help and L. Carrasco for providing HSV-1 strain KOS.Financiadores
- Asociación de Familiares de Enfermos de Alzheimer (AFAL) Spain
- Fundación Areces Spain
- Obra Social Caja Madrid Spain
- Universidad Autónoma de Madrid Spain
- Comunidad de Madrid Spain
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