Productive persistent infection of hematopoietic cells by human foamy virus

Abstract

Human foamy virus can establish persistent infections in human hematopoietic cell lines, such as H92.1.7 (erythroblastoid cells), Jurkat (CD4 ؉ T cells), and U937 (myeloid-monocytic cells). The infection is characterized by constant production of infectious viruses (for >2 1/2 years) with no cytopathic effects on the host cells. Electron microscopy of the infected cells showed a viral morphology similar to that observed for particles produced after acute infection. We have detected, in addition to the full-length form of bel1, a previously described deletion in the bel1 gene of the proviral DNA in these cells. RNA containing this 301-bp deletion, which mapped to the splice donor and acceptor sites of the intron of the bet gene, was also found in encapsidated virion RNA. However, the presence of this defective provirus harboring the deletion in bel1 does not prevent productive persistence in these chronically infected cells, since the virus titer does not decrease during cultivation.

Foamy Virus Capsid Assembly Occurs at a Pericentriolar Region Through a Cytoplasmic Targeting/Retention Signal in Gag

“…Enveloped particles are then transported to the cell surface and can exit from cells by exocytosis or after cell lysis, while in other instances remain attached to the cell surface or membrane structures and can only be spread by cell‐to‐cell contacts. In the case of PFV, viral exit from cells is inefficient and approximately 90% of infectious virus remains cell associated (51).…”

“…The pellet was then resuspended in 1 mL fixative and incubated overnight at 4 °C. The fixed cells were dehydrated, embedded, and stained using standard techniques (51). Thin‐sectioned samples were examined using a JEOL 1010 transmission electron microscope.…”

Origin, evolution and innate immune control of simian foamy viruses in humans

“…Once productively infected, cells usually form syncitia with a 'foam-like' cytopathic effect, before cell death occurs (Figure 3, A to D). However, some cell lines as well as primary cells of the myeloid or lymphoid lineage can remain chronically infected [20,21]. In NHPs, SFV is latent in blood cells and replicates in the superficial epithelial layer of the oral mucosa [4 ,22], which explains the mode of transmission of SFV to humans, mainly through bites [12 ].…”

HTLV-3/4 and simian foamy retroviruses in humans: Discovery, epidemiology, cross-species transmission and molecular virology

“…4A to D). However, some cell lines as well as primary cells of the myeloid or lymphoid lineage can also remain chronically infected (Mikovits et al, 1996;Yu et al, 1996c). The cellular and viral factors involved in persistence versus lytic infection are not well understood, but might involve the regulatory proteins Tas and Bet, with a switch from Tas expression driving virus particle formation to Tas deletion with a maintained Bet expression (Saib et al, 1995).…”