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Lasiodiplodia hormozganensis, initially recognized as a fungal plant pathogen, is recognized now acknowledged as a potential threat to humans. However, our understanding of the pathogenesis mechanisms of Lasiodiplodia species remains limited, and the impact of temperature on its pathogenicity is unclear. This study aims to elucidate the effects of temperature on the biology of L. hormozganensis, focusing on the expression of pathogenesis-related molecules and its ability to function as a cross-kingdom pathogen. We conducted experiments at two different temperatures, 25 and 37 °C, analyzing the proteome and transcriptome of L. hormozganensis. Using strain CBS339.90, initially identified as L. theobromae but confirmed through ITS and tef1-α sequence analysis to be L. hormozganensis, we aimed to understand the fungus's protein expression under varying temperature conditions. Results from the functional analysis of the secretome at 25 °C showed a noteworthy presence of proteins related to carbohydrate metabolism, catabolism, plant cell wall degradation, and pathogenesis. However, when grown at 37 °C, the fungus exhibited an increased production of stress response and pathogenesis-related proteins. Our findings identified various pathways crucial for pathogenesis in both plants and humans, suggesting that L. hormozganensis possesses the genetic foundation to infect both hosts. Specific pathogenesis-related proteins, including the phytotoxin snodprot1, aspartic protease aspergillopepsin, and virulence protein SSD1, were also identified. Concluding, we propose a possible mechanism of how L. hormozganensis adapts to different temperatures. The shift in temperature results in the expression of genes that favor human related pathogenesis molecules., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

The trypanocidal effect of five benzimidazole derivatives (1-5) was determined in vitro and in vivo assays against two strains of Trypanosoma cruzi (NINOA and INC5). The in vitro trypanocidal activity was evaluated by measuring the percentage of lysis of bloodstream trypomastigotes of T. cruzi. Results point to 5-chloro-1H-benzimidazole-2-thiol (1) as the best activity profile compound with a 50% lytic concentration (LC(50)) of 0.014 mM (NINOA strain) and 0.32 mM (INC5 strain). Reference drugs were nifurtimox (Nfx) and benznidazole (Bnz), which on NINOA strain displayed a LC(50)=0.60 mM and LC(50)=0.78 mM, respectively; while on INC5 strain they exhibited LC(50) values of 0.31 mM and 0.69 mM, respectively. The in vivo trypanocidal activity of 1-5 on parasitemia in a murine model acute Chagas' disease indicated that 1 and Nfx showed similar activity on INC5 strain, while 5-chloro-1-methyl-1H-benzimidazole-2-thiol (2) and its regioisomer, 6-chloro-1-methyl-1H-benzimidazole-2-thiol (3), displayed better activity than Nfx and Bnz on NINOA strain. All compounds showed low cytotoxicity against Vero cells, with selective index 38-3000 times higher to the parasite., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Fifty-one adults with HIV infection, including 20 chronic hemodialysis patients with superimposed HIV infection and 31 patients with HIV-associated nephropathy requiring chronic maintenance hemodialysis were followed to evaluate survival on outpatient dialysis in relation to the clinical stage of the HIV infection. Regardless of when they contracted the infection, AIDS patients who required maintenance hemodialysis had a poor prognosis. All 17 patients who developed AIDS died after a mean of 93 +/- 32 days on hemodialysis (median 30 days; range 2 to 540 days). On the other hand, 12 asymptomatic HIV carriers were alive after a mean follow-up on chronic hemodialysis of 488 +/- 75 days (median 420 days; range 142 to 850 days); and five hemodialyzed patients with ARC were alive after 564 +/- 191 days (median 420 days; range 150 to 1230 days). The data confirm the lack of effectiveness of maintenance hemodialysis for prolonging life in patients with AIDS. This dismal prognosis was evident whether renal failure antedated HIV infection or whether it was HIV-associated. In asymptomatic HIV carriers and in patients with ARC, however, maintenance hemodialysis provides meaningful, long-term life support.

The histopathology and incidence of AIDS-related glomerulopathy was evaluated by renal biopsy (N = 24) or at autopsy in 159 patients, including 131 adults and 28 infants and children with AIDS. Thirty-five patients had overt clinical manifestations of renal disease characterized by a nephrotic syndrome with focal and segmental glomerular sclerosis (FSS). Fifteen patients had diffuse glomerular mesangial hyperplasia (MH) without or with minimal clinical renal disease and 109 had intact or minimally involved glomeruli. Whereas 15 of 30 (50%) i.v. drug users with AIDS had evidence of renal disease, only one of 53 (2%) homosexuals had clinical renal disease and only 6 (11%) had histologic evidence of glomerular pathology. The study confirms the important risk of i.v. drug use as a pathogenic factor of renal disease and shows a rarity of renal disease in homosexual or bisexual men with AIDS. On the other hand, 30% of adult Haitians with AIDS had FSS or diffuse MH, although i.v. drug use is not an important risk factor in this population. Moreover, eight of 28 (29%) children with perinatal AIDS had evidence of renal involvement, including four with a nephrotic syndrome and FSS. The data provide strong evidence for the existence of an AIDS-related glomerulopathy independent of i.v. drug use, but suggest that unrecognized co-factors may be important in the development of renal disease.