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Updated: Jul 5, 2026

Measuring Endoplasmic Reticulum Stress and Unfolded Protein Response in HIV-1 Infected T-Cells and Analyzing its Role in HIV-1 Replication
Published on: June 14, 2024
Estradiol and progesterone regulate HIV type 1 replication in peripheral blood cells
Susana N Asin1, Alysha M Heimberg, Susan K Eszterhas
1V.A. Medical Center, White River Junction, Vermont 05009, USA. Susana.Asin@Dartmouth.edu
Sex hormones estradiol and progesterone influence human immunodeficiency virus type 1 (HIV-1) replication. Estradiol and progesterone alter viral transcription, affecting HIV-1 replication in peripheral blood mononuclear cells (PBMCs).
Area of Science:
- Immunology
- Virology
- Endocrinology
Background:
- Endogenous estradiol and progesterone levels vary cyclically in premenopausal women.
- Sex hormones may impact human immunodeficiency virus type 1 (HIV-1) replication.
- Peripheral blood mononuclear cells (PBMCs) are key targets for HIV-1 infection.
Purpose of the Study:
- To investigate the effect of estradiol and progesterone on HIV-1 replication in PBMCs.
- To determine how different phases of the reproductive cycle influence HIV-1 replication.
- To elucidate the specific stages of the HIV-1 life cycle affected by sex hormones.
Main Methods:
- HIV-1 replication assays in PBMCs cultured with varying concentrations of estradiol and progesterone.
- Real-time PCR to quantify HIV-1 integration and viral transcription.
- Assessment of HIV-1 Long Terminal Repeat (LTR) activity in the absence of the viral Tat protein.
Main Results:
- Mid-proliferative phase hormone levels (low estradiol/progesterone) increased HIV-1 replication.
- Mid-secretory phase hormone levels (high estradiol/progesterone) decreased HIV-1 replication.
- Sex hormones modulated HIV-1 integration and transcription, but not reverse transcription or CCR5 expression.
- Estradiol and progesterone directly regulated HIV-1 LTR activity.
Conclusions:
- Estradiol and progesterone significantly regulate HIV-1 replication in PBMCs.
- Hormonal regulation primarily occurs at the transcriptional level of the HIV-1 life cycle.
- These findings highlight a potential mechanism for sex-based differences in HIV-1 pathogenesis and suggest therapeutic targets.
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