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Leishmaniasis is one of the most neglected tropical diseases caused by protozoan parasites belonging to the genus Leishmania. There is much evidence regarding prevalence of Leishmania RNAvirus (LRV) causing Old World leishmaniasis (OWL) and New World leishmaniasis (NWL); however, a combined evidence‐based knowledge on this topic is not still available. The purpose of this systematic review and meta‐analysis was to address the global status of synchronizing LRV in Leishmania in the available literature. The data were systematically collected from the English electronic databases up to May 2018. Then, the studies were screened based on the inclusion and exclusion criteria. The random‐effect model was used by forest plot with 95% confidence interval (CI). Overall, 877 samples from 17 articles were included in this study. Given species of Leishmania, the highest prevalence of LRV belonged to Leishmania (L.) Viannia (V.) guyanensis and L. V. braziliensis. Additionally, the virus was detected also in L. V. amazonensis, L. V. panamanensis, L. V. lainsoni, L. aethiopica, L. major and L. infantum. By random‐effect model, the global prevalence of LRV was estimated to be 26.2% (95% CI: 14.4% ‐ 40.1%). The high prevalence of LRV among causative agents of NWLisolated from the metastatic clinical forms suggests potential association of LRV with metastatic clinical forms in New World endemic regions. A comprehensive investigation on experimental and clinical aspects of LRV is needed to fully appraise the role of these viruses in pathogenicity of Leishmania parasites and their drug resistance.

Aspergillus clavatus is a common environmental species known to cause occupational allergic disease in grain handlers. We have recently observed azole-resistant isolates of this fungus as a cause of onychomycosis. To further characterize the cause of resistance, the genes encoding 14 a-sterol demethylase enzyme (cyp51A and cyp51B) were characterized and analyzed in 9 ITC-susceptible isolates and 6 isolates with high minimum inhibitory concentrations (MICs) of clinical (nail and sputum) and environmental A. clavatus strains. We found that six isolates with itraconazole MIC >16 mg/L demonstrated nonsynonymous mutations, including V51I, L378P, E483K, and E506G, and synonymous mutations, including F53F, A186A, Q276Q, and H359H. Moreover, P486S was detected in five strains with ITR MIC >16 mg/L. One mutation, F324S, was detected in an isolate with posaconazole MIC >16 mg/L. The effect of E483K and P486S mutations of CYP51A on azole resistance was further investigated using homology modeling and molecular dynamics. We found that E483K and P486S mutations were located near the ligand access channel of CYP51A that could partly lead to narrowing the entry of the ligand access channels. Therefore, we concluded that E483K and P486S mutations may potentially contribute to the limited access of inhibitors to the binding pocket and therefore confer resistance to azole agents.

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