Cytopathic Effects In Infected Cells Research Articles

Interactions between HIV-infected monocytes and the extracellular matrix: increased capacity of HIV-infected monocytes to adhere to and spread on extracellular matrix associated with changes in extent of virus replication and cytopathic effects in infected cells.

Monocytes express cell surface receptors for extracellular matrix (ECM) proteins of basement membranes. These receptors are engaged during extravasation of cells through capillary endothelium into tissue. The number of human immunodeficiency virus (HIV)-infected monocytes that adhered to ECM over 2 h was threefold higher than that of uninfected control cells. This difference was ECM specific and was not observed with a bovine serum albumin substrate. Enhanced adhesion to ECM was evident in monocytes by 4 days after HIV infection and increased through 10 days. Monocytes exposed to a T cell-tropic HIV strain that binds to but does not replicate in monocytes showed no changes in adherence to ECM. Thus, productive infection of monocytes by HIV induces a significant increase in the capacity of these cells to interact with ECM. Enhanced adhesion of HIV-infected monocytes to ECM was associated with increased spreading: at 12 h, sixfold more HIV-infected monocytes were spread on ECM than were uninfected control cells. Cell processes of HIV-infected monocytes formed a complex network on ECM: many of these cells expressed HIV proteins as detected by indirect immunofluorescence. HIV-associated cytopathic effects and levels of virion-associated reverse transcriptase activity depended on the substrate to which monocytes were attached. Virus replication and cytopathic effects in monocytes adhered to ECM, fibronectin, or plastic alone were comparable. In contrast, HIV-infected monocytes attached to laminin showed a significant increase in virus replication and in extent of cytopathic effects through 2 weeks after infection. The lowest levels of HIV replication and cytopathic effects were in monocytes attached to collagen IV. Interactions between monocytes and ECM profoundly affect the manner in which these cells control HIV infection: HIV infection changes the capacity of infected monocytes to attach and spread on ECM; attachment to ECM alters the extent of virus replication in infected cells.

Human Immunodeficiency Viruses and the Pathogenesis of AIDS

THE ACQUIRED immunodeficiency syndrome (AIDS) is caused by a newly recognized member of the lentivirus family, the human immunodeficiency virus (HIV). 1 This retrovirus family is distinct from the other subfamilies of human retroviruses, the Spumavirinae and Oncovirinae (Table 1). In particular, lentivirus genomes are large and contain several viral genes; the viruses frequently induce cytopathic effects in infected cells, and the disease they cause has a long incubation period resulting in immunologic disorders and neurological disease. 2 Lentiviruses have been identified in several other animal species, including horses, sheep, goats, cows, cats, and monkeys. 1,2 This finding suggests that a progenitor virus entered the animal kingdom in the distant past and various strains evolved over time within each species. This could be the reason that the primate and human lentiviruses (the simian immunodeficiency virus and HIV) resemble each other. 3 Two subtypes of HIV, HIV-1 and HIV-2, have been

Cytological evidence supporting the inclusion of poplar mosaic virus in the carlavirus group of plant viruses.

The filamentous particles of poplar mosaic virus (PopMV) were detected in palisade, mesophyll and parenchyma cells of systemically infected leaves of Nicotiana clevelandii and N. megalosiphon. The particles were sometimes found scattered throughout the cytoplasm, but more often they occurred loosely associated within ovoid aggregates (up to 3.5 x 1.5 mum) adjacent to chloroplasts and/or mitochondria. PopMV did not induce the formation of 'pinwheel' inclusions, nor other conspicuous ultrastructural or cytopathic effects in infected cells. These observations provide additional evidence that PopMV is a Carlavirus and not a Potyvirus nor a mite-borne virus. PopMV particles were also detected occasionally within plasmodesmata.