Characterization of the influence of semen-derived enhancer of virus infection on the interaction of HIV-1 with female reproductive tract tissues

Shannon A. Allen, Ann M. Carias, Meegan R. Anderson, Eneniziaogochukwu A. Okocha, Lorie Benning, Michael D. McRaven, Z. L. Kelley, John Lurain, Ronald S. Veazey, Thomas J. Hope*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

The majority of human immunodeficiency virus type 1 (HIV-1) transmission events occur in women when semen harboring infectious virus is deposited onto the mucosal barriers of the vaginal, ectocervical, and endocervical epithelia. Seminal factors such as semen-derived enhancer of virus infection (SEVI) fibrils were previously shown to greatly enhance the infectivity of HIV-1 in cell culture systems. However, when SEVI is intravaginally applied to living animals, there is no effect on vaginal transmission. To define how SEVI might function in the context of sexual transmission, we applied HIV-1 and SEVI to intact human and rhesus macaque reproductive tract tissues to determine how it influences virus interactions with these barriers. We show that SEVI binds HIV-1 and sequesters most virions to the luminal surface of the stratified squamous epithelium, significantly reducing the number of virions that penetrated the tissue. In the simple columnar epithelium, SEVI was no longer fibrillar in structure and was detached from virions but allowed significantly deeper epithelial virus penetration. These observations reveal that the action of SEVI in intact tissues is very different in the anatomical context of sexual transmission and begin to explain the lack of stimulation of infection observed in the highly relevant mucosal transmission model.

Original languageEnglish (US)
Pages (from-to)5569-5580
Number of pages12
JournalJournal of virology
Volume89
Issue number10
DOIs
StatePublished - 2015

Funding

ASJC Scopus subject areas

  • Insect Science
  • Virology
  • Microbiology
  • Immunology

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