4.3 Article

Vaginal transmission causes prolonged Zika virus shedding in the vaginal mucosa and delays systemic dissemination

Journal

IMMUNOLOGY AND CELL BIOLOGY
Volume 100, Issue 6, Pages 468-473

Publisher

WILEY
DOI: 10.1111/imcb.12549

Keywords

inflammation; mucosal immunity; sexually transmitted infection; vaginal mucosa; Zika virus

Funding

  1. Canadian Institutes of Health Research
  2. CIHR Tier 1 Canada Research Chair
  3. Ontario Graduate Scholarship-Doctoral awards

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This study investigated the impact of vaginal infection on Zika virus shedding and dissemination. The findings revealed that vaginal infection led to prolonged virus shedding in the vaginal mucosa and delayed systemic infection. Additionally, heightened vaginal inflammation did not affect virus replication or dissemination, in contrast to mosquito-borne infection.
Zika virus (ZIKV) has emerged as a significant health threat worldwide. Although typically mosquito-borne, recent evidence suggests that ZIKV is also a sexually transmitted virus. While persistent ZIKV infections in male reproductive tissues have been identified, little is understood regarding the outcomes of primary sexual transmission in females. We investigated how the route of infection affects vaginal ZIKV shedding and dissemination. In two mouse models, vaginal infection resulted in prolonged ZIKV shedding in the vaginal mucosa with delayed systemic infection. Furthermore, heightened vaginal inflammation did not influence ZIKV replication or dissemination, in contrast to previous studies of mosquito-borne infection. Thus, vaginal infection significantly alters ZIKV infection kinetics and must be considered when developing novel treatments.

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