Analysis of splicing patterns of human spumaretrovirus by polymerase chain reaction reveals complex RNA structures

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105

The human foamy viruses, or spumaviruses, a distinct subfamily of complex human retroviruses, remain poorly understood both in terms of their pathogenic potential and in terms of the regulatory mechanisms that govern their replication. Here, we demonstrate that the human spumaretrovirus shares with other complex human retroviruses the property of encoding a transcriptional trans activator of the homologous viral long terminal repeat. This regulatory protein is encoded by the viral Bel-l open reading frame and is localized to the nucleus of expressing cells. The Bel-l trans activator is shown to function effectively in cell lines derived from human, simian, murine, and avian sources. The viral target sequence for Bel-l has been mapped 5' to the start of viral transcription and is therefore likely to be recognized as a DNA sequence. Our results further suggest that the mechanism of action of the Bel-l protein may be distinct from those reported for the transcriptional trans activators encoded by members of the other human retroviral subfamilies.

Section: Resultsmentioning

confidence: 99%

Characterization of the transcriptional trans activator of human foamy retrovirus

Keller

Partin

Löchelt

et al. 1991

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105

“…The human foamy virus prototype (HFV) was isolated from nasopharyngeal carcinoma cells (1). In addition to the gag, pol, and env genes, it contains a regulatory region, named bel, in the 3Ј end of its genome which may theoretically encode six different products (24). Among them, only Bel1 has been functionally characterized and shown to transactivate both its HFV promoters (long terminal repeat and an internal promoter in the env gene) (14,18,30,37) and the heterologous long terminal repeat of human immunodeficiency virus (HIV) (13,17).…”

mentioning

confidence: 99%

Expression and maturation of human foamy virus Gag precursor polypeptides

Giron

Colas

Wybier

et al. 1997

In this report, we address the processing of the Gag polypeptides of human foamy virus previously reported to be atypical. In the cytoplasm or the nucleus of infected cells as well as in free virus particles, two Gag precursor polypeptides were identified at approximately 72 and 68 kDa, p72 giving rise to p68 by a maturation process. Efficient maturation of Gag precursors was observed only in two situations: (i) during the early steps of virus adsorption and (ii) under experimental conditions, including treatment with DNase I, known to dissociate actin polymers associated with high ionic strength and ionic detergents. Rather than being a defective viral protease function, an association of Gag precursors with a cytoskeleton network might be responsible for the low rate of Gag protein maturation through inhibition of their cleavage by the protease.

“…The genome of HFV contains gag, pol, and env, as well as several other genes located between env and the 3Ј long terminal repeat (8). These genes, including the bel1, bet, and bel3 genes, are all derived from singly and/or multiply spliced mRNA (18). Among them, only the bel1 gene, which encodes a potent transcriptional transactivator, is required for viral replication (14).…”

mentioning

confidence: 99%

Productive persistent infection of hematopoietic cells by human foamy virus

Stone

Linial

1996

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.