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Objectives: The 'treat-all' strategy was implemented in Shenzhen, China in 2016. The effect of this extensive treatment on transmitted drug resistance (TDR) of HIV is unclear.
Methods: TDR analysis was performed, based on the partial HIV-1 pol gene obtained from the newly reported HIV-1 positive cases from 2011 to 2019 in Shenzhen, China. The HIV-1 molecular transmission networks were inferred to analyse the spread of TDR. Logistic regression was used to identify the potential risk factors with TDR mutations (TDRMs) to cluster.
Results: A total of 12 320 partial pol sequences were included in this study. The prevalence of TDR was 2.95% (363/12 320), which increased from 2.57% to 3.52% after 'treat-all'. The TDR prevalence was increased in populations with the characteristics of CRF07_BC, being single, educated to junior college level and above, MSM and male. The sensitivities of viruses to six antiretroviral drugs were decreased. The clustering rate of TDRMs remained stable, and the sequences in the three drug resistance transmission clusters (DRTCs) were mainly found during 2011-16. CRF07_BC and CRF55_01B were the factors associated with TDRMs clustering in the networks.
Conclusions: The 'treat-all' strategy might have contributed to a small increase in TDR, while most of the TDRMs were distributed sporadically, which implies that the 'treat-all' strategy is helpful for the control of TDR in high-risk populations.
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http://dx.doi.org/10.1093/jac/dkad175 | DOI Listing |
BMC Microbiol
September 2025
Botany and Microbiology Department, Faculty of Science, Helwan University, Cairo, 11421, Egypt.
Background: The emergence of drug-resistant pathogens has stimulated the need for the development of new antimicrobial agents. Epigenetic modulation by suppressing epigenetic inhibitors, such as 5-azacytidine (5-aza), has been shown to activate silent biosynthetic gene clusters within a fungus and causes the production of novel secondary metabolites. This research examined this epigenetic modification strategy in the poorly studied filamentous fungus, Ceratorhiza hydrophila, which may help induce the additional production of bioactive compounds.
View Article and Find Full Text PDFWorld J Microbiol Biotechnol
September 2025
School of Life Sciences, Jawaharlal Nehru University, New Mehrauli Road, New Delhi, 110067, India.
We identified, isolated, and functionally characterized a cyclin-dependent kinase (CDK), PiPho85, from Piriformospora indica. The identified PiPho85 contains TY, PSTAIRE, protein kinase domain, and an ATP binding site which is highly conserved among the Pho85/CDK5 family protein specific for Saccharomyces cerevisiae. In a S.
View Article and Find Full Text PDFBull Math Biol
September 2025
Wolfson Centre for Mathematical Biology, Mathematical Institute, Oxford, UK.
Adaptive therapy (AT) protocols have been introduced to combat drug resistance in cancer, and are characterized by breaks from maximum tolerated dose treatment (the current standard of care in most clinical settings). These breaks are scheduled to maintain tolerably high levels of tumor burden, employing competitive suppression of treatment-resistant sub-populations by treatment-sensitive sub-populations. AT has been integrated into several ongoing or planned clinical trials, including treatment of metastatic castrate-resistant prostate cancer, ovarian cancer, and BRAF-mutant melanoma, with initial clinical results suggesting that it can offer significant extensions in the time to progression over the standard of care.
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September 2025
Department of Gastroenterological Surgery, The University of Osaka Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Background: The tyrosine kinase inhibitor (TKI) imatinib targets KIT and PDGFRA, offering significant therapeutic benefits in advanced gastrointestinal stromal tumors (GISTs). However, the high rate of recurrence following treatment discontinuation suggests that drug-tolerant persister cells (DTPs) may contribute to therapy resistance. Elucidating the mechanisms underlying DTP survival is critical for the development of curative strategies.
View Article and Find Full Text PDFEMBO J
September 2025
Department of Surgery & Cancer, Imperial, London, UK.
CDK7 has emerged as a cancer target because of its pivotal roles in cell cycle progression and transcription. Several CDK7 inhibitors (CDK7i) are now in clinical evaluation. Identifying patients most likely to respond to treatment and early detection of tumour evolution towards resistance are necessary for optimal implementation of cancer therapies.
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