Hematogenous Vertical Transmission of Herpes Simplex Virus Type 1 in Mice

  1. Burgos, Javier S. 1
  2. Ramirez, Carlos 1
  3. Guzman-Sanchez, Fernando 1
  4. Alfaro, Juan M. 1
  5. Sastre, Isabel 1
  6. Valdivieso, Fernando 1
  1. 1 Centro de Biología Molecular Severo Ochoa
    info

    Centro de Biología Molecular Severo Ochoa

    Madrid, España

    ROR https://ror.org/03v9e8t09

Revista:
Journal of Virology

ISSN: 0022-538X 1098-5514

Año de publicación: 2006

Volumen: 80

Número: 6

Páginas: 2823-2831

Tipo: Artículo

DOI: 10.1128/JVI.80.6.2823-2831.2006 GOOGLE SCHOLAR lock_openAcceso abierto editor

Otras publicaciones en: Journal of Virology

Objetivos de desarrollo sostenible

Resumen

Herpes simplex virus type 1 (HSV-1) is a neurotropic virus that causes severe disease and death in newborn humans but, to date, it remains unclear how neonatal infection occurs. We show here that the vertical transmission of HSV-1 in mice is mainly hematogenous and involves the colonization of the neonate central nervous system (CNS). HSV-1 DNA was mainly detected in the blood and CNS of the offspring born to latently infected mothers; no significant differences were seen between the viral DNA concentrations in the blood of these mothers and their female progeny (either neonate or adult). The administration of acyclovir during gestation reduced or eliminated both the maternal and the neonatal viral DNA in the blood. Embryo transfer was performed to ensure (as far as possible) that only vertical hematogenous infection took place. Immunohistochemical analysis detected viral proteins in the encephalon of the offspring. Immunofluorescence studies provided immunoreactive evidence of HSV-1 proteins in the neurons of the hippocampus and showed that these viruses can molecularly reactivate after hyperthermia. Neonatal HSV-1 infection therefore appears to be mainly caused by hematogenous vertical transmission, and the viruses that colonize the offspring CNS are capable of molecular reactivation after a period of latency.

Información de financiación

This study was supported by a grant from the Obra Social Caja Madrid to the Asociación de Familiares de Enfermos de Alzheimer and by an institutional grant by the Fundación Areces to the Centro de Biología Molecular Severo Ochoa. J.S.B. and C.R. were, respectively, supported by a contract with and a grant from the Universidad Autónoma de Madrid. We thank F. Mayor for his continuous encouragement and help and L. Carrasco for providing the HSV-1 KOS strain. We are grateful to J. Ripoll for excellent technical assistance.

Financiadores

  • Obra Social Caja Madrid Spain
  • Asociación de Familiares de Enfermos de Alzheimer Spain
  • Fundación Areces Spain
  • Centro de Biología Molecular Severo Ochoa Spain

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