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【Objective】Since 2017, an anthracnose was extensively occurred on P. cyrtonema in the Hunan province of China. The present paper aimed to clarify the pathogen and the sensitivity of the pathogen to fungicides.【Method】The pathogen fungal stains were isolated from symptomatic leaves and identified by both morphological and molecular tools using both the ITS, ACT, CHS-1 and GPDH gene regions. Pathogenicity was confirmed with inoculation experiments that fulfilled the Koch's postulates. On this basis, the indoor toxicity of 5 fungicides to the pathogen was determined by mycelial growth rate method.【Result】By tissue isolation, 16 morphologically identical strains were isolated from the diseased diseased leaves of four plantation in Hunan province, and the colony morphology and culture characteristics of the strains were observed to confirm that they were Colletotrichum sp.. Molecular identification of CLHJY4-3 determined that the pathogen was C. spaethianum. The pathogenicity was confirmed by inoculation and the Koch's postulates was verified. The average growth rate of the hyphae of this pathogen was 1.1 cm/day. Conidia were 18.4 to 25.0 μm long and 3.9 to 5.3 μm wide. The seta were dark brown, with 2-3 septs, 79-107 μm long. The results of indoor toxicity determination showed that among the five agents, prochloraz had the strongest inhibitory effect on hyphal growth, EC50 was 0.031 μg/mL, followed by pyraclostrobin and tebuconazole, with the EC50 of 0.049 and 0.252 μg/mL, respectively. The inhibitory effects of thiophanate-methyl and carbendazim were relatively poor, with the EC50 of 2.911 and 1.763 μg/mL, respectively. 【Conclusion】C. spaethianum was the pathogen of leaf spot of P. cyrtonema in Hunan province. Moreover, prochloraz and pyraclostrobin were screened as better fungicides against the pathogen fungus. [ABSTRACT FROM AUTHOR]

The Nobel Prize in Physiology or Medicine 2020 was awarded jointly to Harvey J. Alter, Michael Houghton, and Charles M. Rice for their contributions in the discovery of hepatitis C virus (HCV). However, eight years lapsed between Houghton hunting down the virus in 1989 and Rice proving HCV alone could cause hepatitis in 1997. How did this seemingly low-hanging fruit turn out to take so long? We reviewed literature to piece together studies during those years, and determined contributions by different groups (Rice's group included). Through a close look into its performance at two milestones (determining the 3'-terminal sequence of HCV genome RNA and constructing an infectious molecular clone), we analyzed, from dimensions of technology stack, path dependence, and goal setting, why Rice's group leapfrogged its competitive peers. [ABSTRACT FROM AUTHOR]