Dataset Information

Brief Report: HIV-1 Seroconversion Is Not Associated With Prolonged Rectal Mucosal Inflammation.

ABSTRACT:

Objective

Determine the impact of HIV-1 seroconversion on inflammatory cytokines in the rectal mucosa.

Setting

Secondary analysis of data from men who have sex with men and transgender women who participated in a HIV prevention trial Lima, Peru.

Methods

From July to December 2017, 605 men who have sex with men and transgender women were screened for rectal gonorrhea/chlamydia (GC/CT). Fifty GC/CT-positive cases were randomly selected and matched with 52 GC/CT-negative controls by age and number of receptive anal intercourse partners in the last month. All participants were HIV-negative at baseline and those with GC/CT at baseline and/or follow-up received appropriate antibiotic therapy. Participants underwent sponge collection of rectal secretions for the measurement of inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) and were screened for rectal GC/CT and HIV at baseline, 3 months, and 6 months. Wilcoxon rank-sum tests compared inflammatory cytokine levels between participants diagnosed with HIV during follow-up and persons who remained HIV-negative.

Results

Eight participants were diagnosed with HIV at the 3-month (n = 6) or 6-month (n = 2) visit. The median number of receptive anal intercourse partners in the month before HIV diagnosis was the same for those who acquired HIV and those who did not. There were no significant differences in inflammatory cytokine levels in rectal mucosa between participants who did and did not experience HIV seroconversion at any time point.

Conclusions

Despite a surge in viral replication during acute infection, findings from this study suggest that there is no prolonged effect of HIV-1 seroconversion on inflammatory cytokine levels in the rectal mucosa.

SUBMITTER: Blair CS

PROVIDER: S-EPMC7933122 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature

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Publications

Brief Report: HIV-1 Seroconversion Is Not Associated With Prolonged Rectal Mucosal Inflammation.

Blair Cheríe S CS Lake Jordan E JE Passaro Ryan C RC Chavez-Gomez Susan S Segura Eddy R ER Elliott Julie J Fulcher Jennifer A JA Shoptaw Steven S Cabello Robinson R Clark Jesse L JL

Journal of acquired immune deficiency syndromes (1999) 20210401 5

<h4>Objective</h4>Determine the impact of HIV-1 seroconversion on inflammatory cytokines in the rectal mucosa.<h4>Setting</h4>Secondary analysis of data from men who have sex with men and transgender women who participated in a HIV prevention trial Lima, Peru.<h4>Methods</h4>From July to December 2017, 605 men who have sex with men and transgender women were screened for rectal gonorrhea/chlamydia (GC/CT). Fifty GC/CT-positive cases were randomly selected and matched with 52 GC/CT-negative contr ...[more]

PMID: 33351532

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Project description:Regardless of infection route, the intestine is the primary site for HIV-1 infection establishment and results in significant mucosal CD4+ T lymphocyte depletion, induces an inflammatory state that propagates viral dissemination, facilitates microbial translocation, and fosters establishment of one of the largest HIV reservoirs. Here we test the prediction that HIV infection modifies the composition and function of the mucosal commensal microbiota.Rectal mucosal microbiota were collected from human subjects using a sponge-based sampling methodology. Samples were collected from 20 HIV-positive men not receiving combination anti-retroviral therapy (cART), 20 HIV-positive men on cART and 20 healthy, HIV-negative men. Microbial composition of samples was analyzed using barcoded 16S Illumina deep sequencing (85,900 reads per sample after processing). Microbial metagenomic information for the samples was imputed using the bioinformatic tools PICRUST and HUMAnN. Microbial composition and imputed function in HIV-positive individuals not receiving cART was significantly different from HIV-negative individuals. Genera including Roseburia, Coprococcus, Ruminococcus, Eubacterium, Alistipes and Lachnospira were depleted in HIV-infected subjects not receiving cART, while Fusobacteria, Anaerococcus, Peptostreptococcus and Porphyromonas were significantly enriched. HIV-positive subjects receiving cART exhibited similar depletion and enrichment for these genera, but were of intermediate magnitude and did not achieve statistical significance. Imputed metagenomic functions, including amino acid metabolism, vitamin biosynthesis, and siderophore biosynthesis differed significantly between healthy controls and HIV-infected subjects not receiving cART.HIV infection was associated with rectal mucosal changes in microbiota composition and imputed function that cART failed to completely reverse. HIV infection was associated with depletion of some commensal species and enrichment of a few opportunistic pathogens. Many imputed metagenomic functions differed between samples from HIV-negative and HIV-positive subjects not receiving cART, possibly reflecting mucosal metabolic changes associated with HIV infection. Such functional pathways may represent novel interventional targets for HIV therapy if normalizing the microbial composition or functional activity of the microbiota proves therapeutically useful.

Project description:ObjectivesIn the general population, the lower socioeconomic status (SES) associates with greater systemic and arterial inflammation and a greater risk of cardiovascular disease. Because arterial inflammation is heightened in individuals living with HIV, we tested the hypothesis that SES associates with arterial inflammation in this population.SettingsProspective cohort study.MethodsMen living with HIV were recruited. Arterial inflammation and leukopoietic activity (ie, bone marrow activity) were measured using 18F-fluorodeoxyglucose positron emission tomography/computed tomography. Zip code-level SES measures were derived from the US Census Bureau. Linear regression and mediation analyses were used to assess associations between SES, arterial inflammation, leukopoietic activity, C-reactive protein (CRP), and interleukin-6.ResultsThirty-nine virologically suppressed men living with HIV were studied (mean ± SD age 50.5 ± 11.1 years). The median CD4 count was 663 cells/mm3 (interquartile range: 399-922); 82% were receiving antiretroviral therapies. Local median income inversely associated with arterial inflammation [standardized β (95% confidence interval): -0.42 (-0.76 to -0.08)] after adjusting for age, Framingham risk score, statin use, antiretroviral use, and nadir CD4 count. The high-school graduation rate independently associated with arterial inflammation [-0.45 (-0.78 to -0.12)] and CRP [-0.49 (-0.86 to -0.012)]. Mediation analysis demonstrated the impact of SES on arterial inflammation was partially mediated by heightened circulating inflammatory levels: ↓SES (as high school graduation rate) →↑CRP →↑arterial inflammation accounting for 44% of the total effect (P < 0.05).ConclusionIn individuals living with HIV, lower SES independently associated with higher leukopoietic activity, circulating markers of inflammation, and arterial inflammation. Furthermore, the link between SES and arterial inflammation was mediated by increased systemic inflammation.

Dataset Information

Brief Report: HIV-1 Seroconversion Is Not Associated With Prolonged Rectal Mucosal Inflammation.

Objective

Setting

Methods

Results

Conclusions

Publications

Brief Report: HIV-1 Seroconversion Is Not Associated With Prolonged Rectal Mucosal Inflammation.

Similar Datasets

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