The etiologic agent of the acquired immune deficiency syndrome, human T-cell lymphotropic virus type m (HTLV-III), has recently been shown to morphologically resemble and share sequence homology with visna virus, a pathogenic lentivirus. Molecular hybridization, heteroduplex mapping, and DNA sequence analyses were used to compare HTLV-Ill to other lentiviruses of domestic animals, including visna, caprine arthritis encephalitis, and equine infectious anemia viruses. Hybridization results showed that a substantial amount of sequence homology exists between each of these viruses and HTLV-Ill. In addition, a closer relationship was found between visna and caprine arthritis encephalitis viruses than for any of the other lentiviruses studied. These results, along with nucleotide and amino acid sequence comparisons, have been used in a comprehensive effort to derive a systematic relationship for lentiviruses and to provide further evidence for classifying HTLV-III with the LUntivirinae subfamily of retroviruses. This relationship predicts that similarities in biology and disease process can be expected between HTLV-III and other Lentivirinae members. Gonda et al. (1) recently showed that human T-cell lymphotropic virus type III (HTLV-III) morphologically resembles and shares nucleotide sequence homology with visna virus, a pathogenic, neurotropic lentivirus of sheep. Visna virus also shares other biological similarities with HTLV-III. For example, HTLV-III exhibits a strong tropism for cells of the immune system, in particular, helper T-lymphocytes upon which it exerts its biologic effects. In culture, HTLV-III induces syncytia and is cytolytic (2). Moreover, HTLV-IIIinduced acquired immune deficiency syndrome (AIDS) is characterized by T-cell depletion, immunosuppression, and opportunistic infections, and the propensity for HTLV-III to infect brain cells suggests a possible neuropathic role for HTLV-III in AIDS-related encephalopathy and dementia (2, 3). Visna virus also infects cells of the immune system (monocytes) and is cytolytic in cell culture, and it produces a slowly progressive inflammatory condition of the central nervous system, often leading to total paralysis and death from inanition (4-7).Lentiviruses (subfamily Lentivirinae in the family Retroviridae) are exogenous, nononcogenic retroviruses (8) that cause persistent but debilitating infections, replicate at a slow but progressive rate, and have been shown to have pathogenic potential in vitro. Lentiviruses have been isolated from a variety of domestic ungulates including ovine (4-7), caprine (9-12), equine (13), and bovine (14) species.The morphologic, genetic, and biologic similarities with visna virus provide strong evidence for a close evolutionary relationship between HTLV-III and the Lentivirinae subfamily of retroviruses (1). Further analysis of the evolutionary and systematic relationship between HTLV-III and other lentiviruses has awaited the molecular cloning of representative species (15-18). As a sequel to the initial findings of G...

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Borna disease virus (BDV) is a neurotropic nonsegmented negative-strand RNA virus with limited homology to rhabdoviruses and paramyxoviruses. A distinguishing feature of BDV is that it replicates in the nucleus of infected cells. Strand-specific probes used for in situ hybridization of infected rat brain showed that there was differential localization of positive- and negative-strand RNAs within the nucleus of neurons. Within nuclei, sense-strand RNAs were preferentially localized within nucleolar regions while genomic-sense RNAs were found in both nucleolar and nonnucleolar regions. These results suggested a role for the nucleolus in BDV replication. Nucleoli isolated from persistently infected neuroblastoma cells contained both genomic and antigenomic BDV RNA species as well as an enrichment of the 39/38-kDa and gp18 BDV proteins. Since the nucleolus is the site of rRNA transcription, we examined BDV transcription in the presence of inhibitors of RNA polymerase I. Inhibition of RNA polymerase I did not affect levels of BDV transcription.