Citrus leprosis complex is an emerging disease in the Americas, associated with two unrelated taxa of viruses distributed in South, Central, and North America. The cytoplasmic viruses are Citrus leprosis virus C (CiLV-C), Citrus leprosis virus C2 (CiLV-C2), and Hibiscus green spot virus 2, and the nuclear viruses are Citrus leprosis virus N (CiLV-N) and Citrus necrotic spot virus. These viruses cause local lesion infections in all known hosts, with no natural systemic host identified to date. All leprosis viruses were believed to be transmitted by one species of mite, Brevipalpus phoenicis. However, mites collected from CiLV-C and CiLV-N infected citrus groves in Mexico were identified as B. yothersi and B. californicus sensu lato, respectively, and only B. yothersi was detected from CiLV-C2 and CiLV-N mixed infections in the Orinoco regions of Colombia. Phylogenetic analysis of the helicase, RNA-dependent RNA polymerase 2 domains and p24 gene amino acid sequences of cytoplasmic leprosis viruses showed a close relationship with recently deposited mosquito-borne negevirus sequences. Here, we present evidence that both cytoplasmic and nuclear viruses seem to replicate in viruliferous Brevipalpus species. The possible replication in the mite vector and the close relationship with mosquito borne negeviruses are consistent with the concept that members of the genus Cilevirus and Higrevirus originated in mites and citrus may play the role of mite virus vector.

Clinical findings seem to confirm an apparent predilection of astroblastomas for younger children (median age of onset, 5 years) and the existence of two prognostically different types of tumor-well differentiated (low grade) and anaplastic (high grade). Microscopic findings suggest a closer resemblance of tumor cells to astroblasts rather than to "tanycytes" or ependymal cells. It seems, however, that anaplastic astroblasts have a tendency to evolve toward, or be associated with, less differentiated cells, either neuroepithelial or sarcomatous.

The neuropathologic findings in a 17-year-old boy with ataxia-telangiectasia are described. In agreement with previous reports, pathologic changes were present in the cerebellum, spinal cord, dorsal root ganglia, and straited muscle. The lesions in the spinal cord and dorsal root ganglia were more severe than previously described. Abnormalities were also seen in several brain stem nuclei, including the mesencephalic nucleus of the trigeminus and the substantia nigra. In addition, a small hamartomatous tumor was found in that thalamus.