May 1991
Volume 32, Issue 6
Free
Articles  |   May 1991
Detection of herpes simplex virus thymidine kinase and latency-associated transcript gene sequences in human herpetic corneas by polymerase chain reaction amplification.
Author Affiliations
  • B L Rong
    Molecular Virology Laboratory, Eye Research Institute, Boston, MA 02114.
  • D Pavan-Langston
    Molecular Virology Laboratory, Eye Research Institute, Boston, MA 02114.
  • Q P Weng
    Molecular Virology Laboratory, Eye Research Institute, Boston, MA 02114.
  • R Martinez
    Molecular Virology Laboratory, Eye Research Institute, Boston, MA 02114.
  • J M Cherry
    Molecular Virology Laboratory, Eye Research Institute, Boston, MA 02114.
  • E C Dunkel
    Molecular Virology Laboratory, Eye Research Institute, Boston, MA 02114.
Investigative Ophthalmology & Visual Science May 1991, Vol.32, 1808-1815. doi:
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      B L Rong, D Pavan-Langston, Q P Weng, R Martinez, J M Cherry, E C Dunkel; Detection of herpes simplex virus thymidine kinase and latency-associated transcript gene sequences in human herpetic corneas by polymerase chain reaction amplification.. Invest. Ophthalmol. Vis. Sci. 1991;32(6):1808-1815.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Herpes simplex virus (HSV) latency in sensory ganglion neurons is well documented, but the existence of extraneuronal corneal latency is less well defined. To investigate the possibility of extraneuronal latency during ocular HSV infection, corneal specimens from 18 patients with quiescent herpes simplex keratitis (HSK) were obtained at the time of keratoplasty. Polymerase chain reaction (PCR) amplification followed by southern blot hybridization with a radiolabeled oligonucleotide probe was done to detect the presence of HSV-1 genome in these human corneal samples. Two pairs of oligonucleotides from the region of the HSV thymidine kinase (TK) gene and the latency-associated transcript (LAT) gene were used as primers in the PCR amplification. The DNA sequences from either the TK or the LAT gene were identified in 15 of 18 HSK corneas (83%). These results demonstrate that the HSV genome was retained, at least in part, in human corneas during quiescent HSV infection, giving further support to the concept of corneal extraneuronal latency.

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