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Prevention of herpes simplex virus type 1 infection in immunocompetent patients

Robyn S Klein, MD, PhD
Section Editor
Martin S Hirsch, MD
Deputy Editor
Jennifer Mitty, MD, MPH


Herpes simplex virus type 1 (HSV-1) may cause gingivostomatitis, which is characterized by vesiculoulcerative lesions of the oral mucosa. Reactivation of HSV-1 occurs in the trigeminal sensory ganglion and may lead to herpes labialis (eg, "cold sores"), which often occurs along the vermillion border of the lip.

The prevention of HSV-1 infections will be reviewed here. The clinical manifestations and treatment of primary and episodic recurrent HSV infections are discussed elsewhere. (See "Clinical manifestations and diagnosis of herpes simplex virus type 1 infection" and "Treatment of herpes simplex virus type 1 infection in immunocompetent patients".)

The treatment and prophylaxis of HSV-1 infections in the immunocompromised patient are discussed elsewhere. (See "Prevention of infections in hematopoietic cell transplant recipients".)


There is currently no effective vaccine against HSV-1 infection [1].

In recurrent cutaneous HSV-1 infection, there is a sequential infiltrate of CD4+ and then CD8+ T lymphocytes into lesions. CD4 lymphocytes produce intralesional IFN-gamma and recognize the structural proteins of HSV (ie, glycoproteins D and B) when restimulated in vitro. Research on the immunodominant epitopes of these two glycoproteins may help inform future vaccine trials in humans [2,3].

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Literature review current through: Nov 2017. | This topic last updated: Sep 15, 2016.
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