Systematic review and meta-analysis of the global prevalence of sexually transmitted infections in people living with HIV and associated risk factors.

People living with HIV (PLWH) constitute a vulnerable population for acquiring additional sexually transmitted infections (STIs). This study was conducted to provide a summary of the evidence on the global prevalence of STIs in PLWH with an emphasis on infectious agents, diagnostic methods, and related risk factors. PubMed, Scopus, and Web of Science were systematically searched to include records published from January 01, 1990, to January 31, 2022, and the Google Scholar search engine was used to check the search strategy. In total, 132 eligible studies reporting STIs in PLWH were included, enrolling subjects from 35 countries across five continents. The pooled proportion of STIs was estimated to be 30.23% (95% CI, 26.1-34.45%) in PLWH and 20.01% (95% CI, 17.17-23.01%) in HIV-negative patients. Our meta-analysis indicated that in PLWH, the pooled OR of STIs compared to HIV-negatives was 1.77 (95% CI: 1.58-1.98) (p < 0.0001). The pooled OR of STIs by viral infectious agents was highest in PLWH (52.19% [95% CI: 43.88-60.43]) compared with fungal (22.19% [95% CI: 15.64-29.53]), bacterial (19.07% [95% CI: 13.59-26.63]), and parasitic (14.05% [95% CI: 11.88-16.38]) infections. Our findings show that there is a rather significant frequency of STIs among PLWH. This study highlights the need for new programs for the detection, treatment, and prevention of STIs in this at-risk population.

Amylose resistant starch (HAM-RS2) supplementation increases the proportion of Faecalibacterium bacteria in end-stage renal disease patients: Microbial analysis from a randomized placebo-controlled trial.

INTRODUCTION: Many of the deleterious effects associated with chronic kidney disease (CKD) are secondary to the resultant systemic inflammation. The gut microbial changes caused by CKD are thought to perpetuate systemic inflammation. Therefore, strategies aimed at modulating the gut microbiota may be helpful in reducing complications associated with CKD. We hypothesized that supplementation with high-amylose maize resistant starch type 2 (HAM-RS2) would beneficially alter the gut microbiome and lead to lower levels of systemic inflammation. METHODS: A double-blind, parallel, randomized, placebo-controlled trial was performed comparing dietary supplementation of HAM-RS2 with placebo in patients with end-stage CKD. Fecal microbial data were obtained from a subset of patients after DNA extraction and 16s sequencing. FINDINGS: Supplementation of HAM-RS2 led to a decrease in serum urea, IL-6, TNFα, and malondialdehyde (P < 0.05). The Faecalibacterium genus was significantly increased in relative abundance following HAM-RS2 supplementation (HAM-RS2-Day 0: 0.40 ± 0.50 vs. HAM-RS2-Day 56: 3.21 ± 4.97 P = 0.03) and was unchanged by placebo (Control-Day 0: 0.72 ± 0.72 vs. Control-Day 56: 0.83 ± 1.57 P = 0.5). DISCUSSION: Supplementation of amylose resistant starch, HAM-RS2, in patients with CKD led to an elevation in Faecalibacterium and decrease in systemic inflammation. Microbial manipulation in CKD patients by using the prebiotic fiber may exert an anti-inflammatory effect through an elevation in the bacterial genera Faecalibacterium.

Microbes involving in carcinogenesis; growing state of the art.

Lateral gene transfer (LGT) has been demonstrated as a transfer process of novel genes between different species. LGT proceedings are occurring between microbes and plants, as well as between microbes and animals. New evidence demonstrates that bacterial insertional mutagenesis may occur in cancer cells. Due to the important role of genetic changes in the increase of cell proliferation and cancer development, we reviewed the effects of microbial-animal LGT in human oncogenesis. In addition, viral DNA can induce cancer development by random insertion into cancer-related genes or by inducing translocations. In conclusion, growing evidence shows the contribution of the microbial genome in cancer and autoimmune disease.