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Increases in Endogenous or Exogenous Progestins Promote Virus-Target Cell Interactions within the Non-human Primate Female Reproductive Tract.

Increases in Endogenous or Exogenous Progestins Promote Virus-Target Cell Interactions within the Non-human Primate Female Reproductive Tract.
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Carias AM, Allen SA, Fought AJ, Kotnik Halavaty K, Anderson MR, Jimenez ML, McRaven MD, Gioia CJ, Henning TR, Kersh EN, Smith JM, Pereira LE, Butler K, McNicholl SJ, Hendry RM, Kiser PF, Veazey RS, Hope TJ,


Carias AM, Allen SA, Fought AJ, Kotnik Halavaty K, Anderson MR, Jimenez ML, McRaven MD, Gioia CJ, Henning TR, Kersh EN, Smith JM, Pereira LE, Butler K, McNicholl SJ, Hendry RM, Kiser PF, Veazey RS, Hope TJ, (click to view)

Carias AM, Allen SA, Fought AJ, Kotnik Halavaty K, Anderson MR, Jimenez ML, McRaven MD, Gioia CJ, Henning TR, Kersh EN, Smith JM, Pereira LE, Butler K, McNicholl SJ, Hendry RM, Kiser PF, Veazey RS, Hope TJ,

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PLoS pathogens 2016 9 2212(9) e1005885 doi 10.1371/journal.ppat.1005885

Abstract

Currently, there are mounting data suggesting that HIV-1 acquisition in women can be affected by the use of certain hormonal contraceptives. However, in non-human primate models, endogenous or exogenous progestin-dominant states are shown to increase acquisition. To gain mechanistic insights into this increased acquisition, we studied how mucosal barrier function and CD4+ T-cell and CD68+ macrophage density and localization changed in the presence of natural progestins or after injection with high-dose DMPA. The presence of natural or injected progestins increased virus penetration of the columnar epithelium and the infiltration of susceptible cells into a thinned squamous epithelium of the vaginal vault, increasing the likelihood of potential virus interactions with target cells. These data suggest that increasing either endogenous or exogenous progestin can alter female reproductive tract barrier properties and provide plausible mechanisms for increased HIV-1 acquisition risk in the presence of increased progestin levels.

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