Abstract:
Asparagus samples were examined from growing areas of Germany and selected European as well as North, Central and South American countries. Overall, 474 samples were analyzed for Asparagus virus 1 (AV1) using DAS-ELISA. In our survey, 19 AV1 isolates were further characterized. Experimental transmission to 11 species belonging to Aizoaceae, Amarantaceae, Asparagaceae, and Solanaceae succeeded. The ultrastructure of AV1 infection in asparagus has been revealed and has been compared with the one in indicator plants. The cylindrical inclusion (CI) protein, a core factor in viral replication, localized within the cytoplasm and in systemic infections adjacent to the plasmodesmata. The majority of isolates referred to pathotype I (PI). These triggered a hypersensitive resistance in inoculated leaves of Chenopodium spp. and were incapable of infecting Nicotiana spp. Only pathotype II (PII) and pathotype III (PIII) infected Nicotiana benthamiana systemically but differed in their virulence when transmitted to Chenopodium spp. The newly identified PIII generated amorphous inclusion bodies and degraded chloroplasts during systemic infection but not in local lesions of infected Chenopodium spp. PIII probably evolved via recombination in asparagus carrying a mixed infection by PI and PII. Phylogeny of the coat protein region recognized two clusters, which did not overlap with the CI-associated grouping of pathotypes. These results provide evidence for ongoing modular evolution of AV1.
摘要:
对德国种植地区的芦笋样品进行了检查,并选择了欧洲和北方,中美洲和南美洲国家。总的来说,使用DAS-ELISA分析474个样品的芦笋病毒1(AV1)。在我们的调查中,进一步表征了19个AV1分离株。实验传播给11种属于菊科的物种,Amarantaceae,天门冬科,茄科成功了.已揭示了芦笋中AV1感染的超微结构,并将其与指示植物中的超微结构进行了比较。圆柱形包涵(CI)蛋白,病毒复制的核心因素,定位于细胞质内和邻近胞浆的全身性感染中。大多数分离株称为病理型I(PI)。这些在接种的藜属植物叶片中引发了超敏抗性。无法感染烟草.只有病理型II(PII)和病理型III(PIII)系统感染了本氏烟草,但在传播到Chenopodiumspp时,其毒力有所不同。新鉴定的PIII在全身感染期间产生无定形包涵体并降解叶绿体,但在受感染的Chenopodiumspp的局部病变中未产生。PIII可能是通过在携带PI和PII混合感染的芦笋中重组而进化的。外壳蛋白区域的系统发育识别两个簇,与CI相关的病理类型分组不重叠。这些结果为AV1正在进行的模块化进化提供了证据。