Assessing the Relationship Between Cervical Ectopy and <scp>HIV</scp> Susceptibility: Implications for <scp>HIV</scp> Prevention in Women

Venkatesh, Kartik K.; Cu‐Uvin, Susan

doi:10.1111/aji.12029

Cited by 19 publications

(24 citation statements)

References 35 publications

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“…It may be explained by previous in vitro observations that columnar epithelial cells of endocervical origin produce higher levels of proinflammatory mediators than isogenic stratified squamous epithelial cells of ectocervical or vaginal origin (39)(40)(41)). An enhanced proinflammatory environment in the lower FGT could potentially increase susceptibility to HIV acquisition and may account for reported associations (42,43) of cervical ectopy with HIV infection.…”

Section: Discussionmentioning

confidence: 99%

Cross-Sectional Analysis of Selected Genital Tract Immunological Markers and Molecular Vaginal Microbiota in Sub-Saharan African Women, with Relevance to HIV Risk and Prevention

Kyongo

Crucitti

Menten

et al. 2015

Clin. Vaccine Immunol.

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There is a paucity of data on the clinical and epidemiological factors associated with immunological markers and consequently risk of HIV acquisition in various groups of women from SSA. Hormonal variation during the menstrual cycle is accompanied by a transient immune suppression that is necessary to ensure successful fertilization and embryo implantation in the uterus (4). Hormonal differences may result in different mucosal immunological profiles in pregnant women (5, 6) and adolescent girls compared to nonpregnant adult women. Differential exposure to mucosal infections (7) and other behavioral factors that alter HIV acquisition risk such as traditional vaginal practices and having multiple sexual partners might also have an impact on mucosal immunology in the FGT. SSA has the highest prevalence of bacterial vaginosis (BV) (8), which has been associated with greater susceptibility to HIV infection (9) and increased female-to-male HIV-1 transmission (10). All of these factors work in concert and

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Section: Discussionmentioning

confidence: 99%

Cross-Sectional Analysis of Selected Genital Tract Immunological Markers and Molecular Vaginal Microbiota in Sub-Saharan African Women, with Relevance to HIV Risk and Prevention

Kyongo

Crucitti

Menten

et al. 2015

Clin. Vaccine Immunol.

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“…41 'Ectopy' occurs when the columnar epithelium of the endocervical canal extends outwards into the ectocervix. 39 This appears as a single layer of glandular cells that reside in close association with the underlying vascular cervical stroma.…”

Section: Hormonal Changesmentioning

confidence: 99%

Anatomic and Hormonal Changes in the Female Reproductive Tract Immune Environment during the Life Cycle: Implications for HIV/STI Prevention Research

Venkatesh

Cu‐Uvin

2014

American J Rep Immunol

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“…Endocervix was also included in this analysis to model cervical ectopy, a common condition in women during adolescence, pregnancy and contraceptive use that is prone to injury and bleeding7.…”

Section: Resultsmentioning

confidence: 99%

“…A recent meta-analysis of 16 countries showed that Intimate Partner Violence, frequently associated with genital violence, is significantly associated with HIV infection6. In addition to injuries in the lower tract due to sexual intercourse, different causes can induce epithelial disruption in the upper tract, including cervical ectopy7, menstruation or ascending infections. While it is generally assumed that HIV reaches target cells through breaches in the epithelium, little is known about the factors that influence the repair process of the mucosal barrier following disruption.…”

mentioning

confidence: 99%

Tenofovir Inhibits Wound Healing of Epithelial Cells and Fibroblasts from the Upper and Lower Human Female Reproductive Tract

Rodriguez-García

Patel

Shen

et al. 2017

Sci Rep

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Disruption of the epithelium in the female reproductive tract (FRT) is hypothesized to increase HIV infection risk by interfering with barrier protection and facilitating HIV-target cell recruitment. Here we determined whether Tenofovir (TFV), used vaginally in HIV prevention trials, and Tenofovir alafenamide (TAF), an improved prodrug of TFV, interfere with wound healing in the human FRT. TFV treatment of primary epithelial cells and fibroblasts from the endometrium (EM), endocervix (CX) and ectocervix (ECX) significantly delayed wound closure. Reestablishment of tight junctions was compromised in EM and CX epithelial cells even after wound closure occurred. In contrast, TAF had no inhibitory effect on wound closure or tight junction formation following injury. TAF accumulated inside genital epithelial cells as TFV-DP, the active drug form. At elevated levels of TAF treatment to match TFV intracellular TFV-DP concentrations, both equally impaired barrier function, while wound closure was more sensitive to TFV. Furthermore, TFV but not TAF increased elafin and MIP3a secretion following injury, molecules known to be chemotactic for HIV-target cells. Our results highlight the need of evaluating antiretroviral effects on genital wound healing in future clinical trials. A possible link between delayed wound healing and increased risk of HIV acquisition deserves further investigation.

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Assessing the Relationship Between Cervical Ectopy and HIV Susceptibility: Implications for HIV Prevention in Women

Abstract: CitationVenkatesh KK, Cu-Uvin S. Assessing the relationship between cervical ectopy and HIV susceptibility: implications for HIV prevention in women.

Cited by 19 publications

References 35 publications

Cross-Sectional Analysis of Selected Genital Tract Immunological Markers and Molecular Vaginal Microbiota in Sub-Saharan African Women, with Relevance to HIV Risk and Prevention

Cross-Sectional Analysis of Selected Genital Tract Immunological Markers and Molecular Vaginal Microbiota in Sub-Saharan African Women, with Relevance to HIV Risk and Prevention

Anatomic and Hormonal Changes in the Female Reproductive Tract Immune Environment during the Life Cycle: Implications for HIV/STI Prevention Research

Tenofovir Inhibits Wound Healing of Epithelial Cells and Fibroblasts from the Upper and Lower Human Female Reproductive Tract

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