The characteristic site-specific reactivation phenotypes of HSV-1 and HSV-2 depend upon the latency-associated transcript region

Tetsushi Yoshikawa, James M. Hill, Lawrence R. Stanberry, Nigel Bourne, Jumana F. Kurawadwala, Philip R. Krause

研究成果: Article査読

51 被引用数 (Scopus)

抄録

After replication at sites of initial inoculation, herpes simplex virus type 1 and 2 (HSV-1 and HSV-2) established lifelong latent infections of the sensory and automatic neurons of the ganglia serving those sites. Periodically, the virus reactivates from these neurons, and travels centripetally along the neuronal axon to cause recurrent epithelial infection. The major clinically observed difference between infections with herpes simplex virus type 1 and type 2 is the anatomic site specificity of recurrence. HSV-1 reactivates most efficiently and frequently from trigeminal ganglia, causing recurrent ocular and oral-facial lesions, while HSV-2 reactivates primarily from sacral ganglia causing recurrent genital lesions. An intertypic recombinant virus was constructed and evaluated in animal models of recurrent ocular and genital herpes. Substitution of 1 2.8-kbp region from the HSV-1 latency-associated transcript (LAT) for native HSV-2 sequences caused HSV-2 to reactivate with an HSV-1 phenotype in both animal models. The HSV-2 phenotype was restored by replacing the mutated sequences with wild-type HSV-2 LAT-region sequences. These sequences or their products must act specifically in the cellular environments of trigeminal and sacral neurons to promote the reactivation patterns characteristic of each virus.

本文言語English
ページ(範囲)659-664
ページ数6
ジャーナルJournal of Experimental Medicine
184
2
DOI
出版ステータスPublished - 01-08-1996

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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