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Herpes simplex virus specific T cell response in a cohort with primary genital infection correlates inversely with frequency of subsequent recurrences

Artikel i vetenskaplig tidskrift
Författare E. Franzen-Rohl
D. Schepis
F. Atterfelt
K. Franck
A. Wikstrom
Jan-Åke Liljeqvist
Tomas Bergström
E. Aurelius
K. Karre
L. Berg
H. Gaines
Publicerad i Sexually Transmitted Infections
Volym 93
Nummer/häfte 3
ISSN 1368-4973
Publiceringsår 2017
Publicerad vid Institutionen för biomedicin, avdelningen för infektionssjukdomar
Språk en
Länkar dx.doi.org/10.1136/sextrans-2016-05...
Ämnesord VARICELLA-ZOSTER-VIRUS, GLYCOPROTEIN G, TYPE-1, REACTIVATION, IDENTIFICATION, ANTIBODIES, EPITOPES, IMMUNITY, IL-10, HSV-2
Ämneskategorier Infektionsmedicin

Sammanfattning

Objectives During the last decades, a changing epidemiological pattern of genital herpes simplex virus (HSV) infection has emerged. Primary infection is now caused as often by HSV-1 as by HSV-2. Once established, HSV can be reactivated leading to recurrent mucocutaneous lesions as well as meningitis. Why some otherwise immune-competent individuals experience severe and frequent recurrences is not known, and the immunological mechanism underlying recurrent symptomatic HSV infection is not fully understood. In this study, we investigate and characterise the immune response of patients with first episode of HSV genital infection and its relation to the frequency of symptomatic recurrences. Methods In this cohort study, clinical and immunological data were collected from 29 patients who were followed 1 year after presenting with a first episode of genital or meningeal HSV infection. They were classified by PCR and serology as those with primary HSV-1, primary HSV-2 and non-primary HSV-2 infection. Results HSV-specific interleukin(Il)-4 and II-10 responses at first visit were higher in primary infected HSV-2 infected patients experiencing lower numbers of recurrences during subsequent year. Conclusions The median number of recurrences following primary HSV-2 genital infection may partly be predicted by the strength of an early HSV-specific IL-4 and IL-10 response.

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