Treatment of human immunodeficiency virus (HIV) is currently complicated by increased prevalence of co-infection with Mycobacterium tuberculosis. The development of drug candidates that offer the simultaneous management of HIV and tuberculosis (TB) would be of great benefit in the holistic treatment of HIV/AIDS, especially in sub-Saharan Africa which has the highest global prevalence of HIV-TB coinfection. Bis(diphenylphosphino)-2-pyridylpalladium(II) chloride (1), bis(diphenylphosphino)-2-pyridylplatinum(II) chloride (2), bis(diphenylphosphino)-2-ethylpyridylpalladium(II) chloride (3) and bis(diphenylphosphino)-2-ethylpyridylplatinum(II) (4) were investigated for the inhibition of HIV-1 through interactions with the viral protease. The complexes were subsequently assessed for biological potency against Mycobacterium tuberculosis H37Rv by determining the minimal inhibitory concentration (MIC) using broth microdilution. Complex (3) showed the most significant and competitive inhibition of HIV-1 protease (p = 0.014 at 100 µM). Further studies on its in vitro effects on whole virus showed reduced viral infectivity by over 80 % at 63 µM (p < 0.05). In addition, the complex inhibited the growth of Mycobacterium tuberculosis at an MIC of 5 µM and was non-toxic to host cells at all active concentrations (assessed by tetrazolium dye and real time cell electronic sensing). In vitro evidence is provided here for the possibility of utilizing a single metal-based compound for the treatment of HIV/AIDS and TB.
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http://dx.doi.org/10.1007/s10534-016-9940-6 | DOI Listing |
J Immunol
March 2025
Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, Amherst, MA, United States.
Alveolar macrophages (AMs) are lung-resident myeloid cells and airway sentinels for inhaled pathogens and environmental particles. While AMs can be highly inflammatory in response to respiratory viruses, they do not mount proinflammatory responses to all airborne pathogens. For example, we previously showed that AMs fail to mount a robust proinflammatory response to Mycobacterium tuberculosis.
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February 2025
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Shaqra University, Shaqra, Saudi Arabia.
Introduction: Tuberculosis (TB), caused by the (M.tb), remains a serious medical concern globally. Resistant M.
View Article and Find Full Text PDFChem Biodivers
March 2025
Birla Institute of Technology and Science - Pilani Campus: Birla Institute of Technology & Science Pilani, Pharmacy, Vidya Vihar campus, Pilani, INDIA.
We designed and synthesized pyrazolyl pyrimidine containing derivatives and screened for anti-mycobacterial activity. Different spectral techniques like HRMS, 1H, and 13C NMR are deployed for the structural confirmation of the final derivatives. Final compounds were screened against the Mycobacterium tuberculosis (Mtb) H37Rv strain.
View Article and Find Full Text PDFInt J Infect Dis
March 2025
Centre for Inflammation Research and Translational Medicine, Department of Biosciences, Brunel University of London, United Kingdom. Electronic address:
Host-directed therapy could potentially revolutionise tuberculosis control, as adjunct to traditional antibiotics for the treatment of tuberculosis disease, and as a strategy to prevent disease progression following Mycobacterium tuberculosis infection. The growing type 2 diabetes pandemic is hampering tuberculosis control worldwide, as people with diabetes have an increased risk of developing tuberculosis disease as well as worse treatment outcomes. Pulmonary tuberculosis is characterised by an inflammatory response which can cause alveolar tissue destruction and cavitation, and this inflammation is exacerbated in people with tuberculosis-diabetes comorbidity.
View Article and Find Full Text PDFSTAR Protoc
March 2025
Department of Microbiology, Pediatrics, Radiology and Public Health, University of Zaragoza, Zaragoza, Spain; CIBER Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain. Electronic address:
Here, we present a protocol to perform a time-kill assay (TKA) to quantify bacterial burden at multiple time points using colony-forming units and most probable number readouts simultaneously. We describe steps for preparing inoculum, experimental conditions, and sampling bacterial counts. We then detail procedures for quantification and analysis.
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