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Epididymal epithelium propels early sexual transmission of Zika virus in the absence of interferon signaling

Author

Listed:
  • Alexander G. Pletnev

    (National Institutes of Health)

  • Olga A. Maximova

    (National Institutes of Health)

  • Guangping Liu

    (National Institutes of Health)

  • Heather Kenney

    (National Institutes of Health)

  • Bianca M. Nagata

    (National Institutes of Health)

  • Tatiana Zagorodnyaya

    (Center for Biologics Evaluation and Research, U.S. Food and Drug Administration)

  • Ian Moore

    (National Institutes of Health)

  • Konstantin Chumakov

    (Center for Biologics Evaluation and Research, U.S. Food and Drug Administration)

  • Konstantin A. Tsetsarkin

    (National Institutes of Health)

Abstract

Recognition of Zika virus (ZIKV) sexual transmission (ST) among humans challenges our understanding of the maintenance of mosquito-borne viruses in nature. Here we dissected the relative contributions of the components of male reproductive system (MRS) during early male-to-female ZIKV transmission by utilizing mice with altered antiviral responses, in which ZIKV is provided an equal opportunity to be seeded in the MRS tissues. Using microRNA-targeted ZIKV clones engineered to abolish viral infectivity to different parts of the MRS or a library of ZIKV genomes with unique molecular identifiers, we pinpoint epithelial cells of the epididymis (rather than cells of the testis, vas deferens, prostate, or seminal vesicles) as a most likely source of the sexually transmitted ZIKV genomes during the early (most productive) phase of ZIKV shedding into the semen. Incorporation of this mechanistic knowledge into the development of a live-attenuated ZIKV vaccine restricts its ST potential.

Suggested Citation

  • Alexander G. Pletnev & Olga A. Maximova & Guangping Liu & Heather Kenney & Bianca M. Nagata & Tatiana Zagorodnyaya & Ian Moore & Konstantin Chumakov & Konstantin A. Tsetsarkin, 2021. "Epididymal epithelium propels early sexual transmission of Zika virus in the absence of interferon signaling," Nature Communications, Nature, vol. 12(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22729-5
    DOI: 10.1038/s41467-021-22729-5
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