Epidemiological analysis of Cassava Mosaic and Brown Streak Diseases, and Bemisia tabaci in the Comoros Islands

first_pagesettingsOrder Article Reprints Open AccessArticle Epidemiological Analysis of Cassava Mosaic and Brown Streak Diseases, and Bemisia tabaci in the Comoros Islands by Rudolph Rufini Shirima 1,*ORCID,Everlyne Nafula Wosula 1ORCID,Abdou Azali Hamza 2,Nobataine Ali Mohammed 2,Hadji Mouigni 2,Salima Nouhou 2,Naima Mmadi Mchinda 2,Gloria Ceasar 1,Massoud Amour 1,Emmanuel Njukwe 3 andJames Peter Legg 1ORCID 1 International Institute of Tropical Agriculture (IITA-Tanzania), P.O. Box 34441, Dar es Salaam 14112, Tanzania 2 Institut National de Recherche pour L’Agriculture, La Pêche et L’Environnement (INRAPE), Moroni BP 1406, Comoros 3 West and Central African Council for Agricultural Research and Development (CORAF), Dakar CP 18523, Senegal * Author to whom correspondence should be addressed. Viruses 2022, 14(10), 2165; https://doi.org/10.3390/v14102165 Received: 2 August 2022 / Revised: 15 September 2022 / Accepted: 28 September 2022 / Published: 30 September 2022 (This article belongs to the Special Issue Plant Virus Surveillance and Metagenomics) Download Browse Figures Review Reports Versions Notes Abstract A comprehensive assessment of cassava brown streak disease (CBSD) and cassava mosaic disease (CMD) was carried out in Comoros where cassava yield (5.7 t/ha) is significantly below the African average (8.6 t/ha) largely due to virus diseases. Observations from 66 sites across the Comoros Islands of Mwali, Ngazidja, and Ndzwani revealed that 83.3% of cassava fields had foliar symptoms of CBSD compared with 95.5% for CMD. Molecular diagnostics confirmed the presence of both cassava brown streak ipomoviruses (CBSIs) and cassava mosaic begomoviruses (CMBs). Although real-time RT-PCR only detected the presence of one CBSI species (Cassava brown streak virus, CBSV) the second species (Ugandan cassava brown streak virus, UCBSV) was identified using next-generation high-throughput sequencing. Both PCR and HTS detected the presence of East African cassava mosaic virus (EACMV). African cassava mosaic virus was not detected in any of the samples. Four whitefly species were identified from a sample of 131 specimens: Bemisia tabaci, B. afer, Aleurodicus dispersus, and Paraleyrodes bondari. Cassava B. tabaci comprised two mitotypes: SSA1-SG2 (89%) and SSA1-SG3 (11%). KASP SNP genotyping categorized 82% of cassava B. tabaci as haplogroup SSA-ESA. This knowledge will provide an important base for developing and deploying effective management strategies for cassava viruses and their vectors

Assessment of PABPN1 nuclear inclusions on a large cohort of patients and in a human xenograft model of oculopharyngeal muscular dystrophy

Oculopharyngeal muscular dystrophy (OPMD) is a rare muscle disease characterized by an onset of weakness in the pharyngeal and eyelid muscles. The disease is caused by the extension of a polyalanine tract in the Poly(A) Binding Protein Nuclear 1 (PABPN1) protein leading to the formation of intranuclear inclusions or aggregates in the muscle of OPMD patients. Despite numerous studies stressing the deleterious role of nuclear inclusions in cellular and animal OPMD models, their exact contribution to human disease is still unclear. In this study, we used a large and unique collection of human muscle biopsy samples to perform an in-depth analysis of PABPN1 aggregates in relation to age, genotype and muscle status with the final aim to improve our understanding of OPMD physiopathology. Here we demonstrate that age and genotype influence PABPN1 aggregates: the percentage of myonuclei containing PABPN1 aggregates increases with age and the chaperone HSP70 co-localize more frequently with PABPN1 aggregates with a larger polyalanine tract. In addition to the previously described PRMT1 and HSP70 co-factors, we identified new components of PABPN1 aggregates including GRP78/BiP, RPL24 and p62. We also observed that myonuclei containing aggregates are larger than myonuclei without. When comparing two muscles from the same patient, a similar amount of aggregates is observed in different muscles, except for the pharyngeal muscle where fewer aggregates are observed. This could be due to the peculiar nature of this muscle which has a low level of PAPBN1 and contains regenerating fibers. To confirm the fate of PABPN1 aggregates in a regenerating muscle, we generated a xenograft model by transplanting human OPMD muscle biopsy samples into the hindlimb of an immunodeficient mouse. Xenografts from subjects with OPMD displayed regeneration of human myofibers and PABPN1 aggregates were rapidly present-although to a lower extent-after muscle fiber regeneration. Our data obtained on human OPMD samples add support to the dual non-exclusive models in OPMD combining toxic PABPN1 intranuclear inclusions together with PABPN1 loss of function which altogether result in this late-onset and muscle selective disease