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Basic science
Short report
Genital HSV-1 DNA detection is associated with a low inflammatory profile in HIV-uninfected South African women
  1. Andile Mtshali1,2,
  2. Sinaye Ngcapu1,2,
  3. Farzana Osman1,
  4. Nigel Garrett1,3,
  5. Ravesh Singh2,4,
  6. Anne Rompalo5,
  7. Adrian Mindel1,6,
  8. Lenine J P Liebenberg1,2
  1. 1 Centre for the AIDS Programme of Research in South Africa, Durban, KwaZulu-Natal, South Africa
  2. 2 School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, KwaZulu-Natal, South Africa
  3. 3 Discipline of Public Health, University of KwaZulu-Natal, Durban, KwaZulu-Natal, South Africa
  4. 4 Department of Microbiology, National Health Laboratory Services, KwaZulu-Natal Academic Complex, Inkosi Albert Luthuli Central Hospital, Durban, South Africa
  5. 5 Johns Hopkins School of Medicine, Baltimore, Maryland, USA
  6. 6 Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia
  1. Correspondence to Dr Lenine J P Liebenberg, Centre for the Aids Programme of Research in South Africa, Durban 4013, South Africa; lenine.liebenberg{at}caprisa.org

Abstract

Objectives Genital herpes simplex virus (HSV) infections are common in South Africa and worldwide. While HSV-2 is known to cause genital lesions, HSV-1 is better known to cause oral infections. Due to the global rise in genital HSV-1 infections, we aimed to compare the genital cytokine environment associated with HSV-1 and HSV-2 infections and their relation to the proinflammatory genital immune environment associated with HIV risk in African women.

Methods HSV-1 and HSV-2 DNA were detected by quantitative real-time PCR in menstrual cup specimens collected from 251 HIV-negative women participating in the CAPRISA 083 study in Durban, South Africa. HSV shedding was defined as detection at >150 copies/mL. Forty-eight cytokines were measured in genital fluid by multiplexed ELISA, and multivariable regression models determined associations between genital cytokines and HSV DNA detection.

Results HSV-1 DNA detection (24/251 (9.6%)) and shedding (13/24 (54.2%)) was more common than HSV-2 (detection in 14/251 (5.6%), shedding in 0/14). None of the women with detectable HSV had evidence of genital lesions. HSV-2 DNA detection was associated with increased interleukin (IL)−18 and decreased cutaneous T-cell attracting chemokine concentrations, but only in univariable analysis. By contrast, in both univariable and multivariable analyses, the detection of HSV-1 DNA was associated with reduced concentrations of granulocyte-colony stimulating factor, IL-7, IL-4, platelet-derived growth factor-ββ and five proinflammatory cytokines associated with HIV risk: IL-6, IL-1β, macrophage inflammatory protein (MIP)−1α, MIP-1β and tumour necrosis factor-α.

Conclusions That HSV-1 DNA was more commonly detected and shed than HSV-2 emphasises the need for clinical screening of both viruses, not just HSV-2 in young women. Efforts to reduce genital inflammation may need to consider implementing additional strategies to mitigate a rise in HSV replication.

  • genital herpes
  • immunology
  • sexual health
http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/sextrans-2020-054458

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    Footnotes

    • Handling editor Anna Maria Geretti

    • Twitter @nigegarrett

    • Contributors AnM and LJPL conceptualised and designed the project; FO, LJPL and AnM contributed to data analysis and interpretation; AdM, LJPL, NG and SN reviewed the manuscript; RS and AnM performed the experiments. All authors contributed to the preparation of the manuscript.

    • Funding The CAPRISA 083 study was funded by a United States–South African Program for Collaborative Biomedical Research grant through the South African Medical Research Council and the National Institute of Health (AI116759). This research was conducted as part of the DSI-NRF Centre of Excellence in HIV Prevention, which is supported by the Department of Science and Innovation, and the National Research Foundation. AnM received support from the CAPRISA Research Administration and Management Training Program (grant no. G11 TW010555-01). LJPL is funded by a SANTHE Path to Independence award, and by a FLAIR Fellowship supported by the African Academy of Sciences and the Royal Society.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Ethics approval This study was approved by the Biomedical Research Ethics Committee of the University of KwaZulu-Natal (Ref: BE403/16).

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data availability statement Data are available upon request (https://www.caprisa.org/Pages/CAPRISAStudies).