Regulation of Equine Infectious Anemia Virus Expression

Maury, Wendy

doi:10.1159/000025307

Cited by 2 publications

(2 citation statements)

References 31 publications

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“…For instance, it has been reported that HIV-1 subtype E viruses replicate more efficiently than other subtypes in Langerhans cells, the possible target in heterosexual transmission (54), although follow-up studies could not confirm these results (16,43). The lentivirus equine infectious anemia virus provides an interesting example where the presence of an Ets-1 site in the LTR promoter was found to be essential for productive virus replication in macrophages (10,38). Despite accumulating sequence data on the genomes of HIV-1 strains belonging to the different subtypes (18,41), no subtype-specific differences in virus biology have been described.…”

Section: Fig 12mentioning

confidence: 99%

Evolution of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat Promoter by Conversion of an NF-κB Enhancer Element into a GABP Binding Site

Verhoef

Sanders²,

Fontaine

et al. 1999

J Virol

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Human immunodeficiency virus type 1 (HIV-1) transcription is regulated by the viral Tat protein and cellular factors, of which the concentration and activity may depend on the cell type. Viral long terminal repeat (LTR) promoter sequences are therefore optimized to suit the specific nuclear environment of the target host cell. In long-term cultures of a Tat-defective, poorly replicating HIV-1 mutant, we selected for a faster-replicating virus with a 1-nucleotide deletion in the upstream copy of two highly conserved NF-κB binding sites. The variant enhancer sequence demonstrated a severe loss of NF-κB binding in protein binding assays. Interestingly, we observed a new binding activity that is specific for the variant NF-κB sequence and is present in the nuclear extract of unstimulated cells that lack NF-κB. These results suggest that inactivation of the NF-κB site coincides with binding of another transcription factor. Fine mapping of the sequence requirements for binding of this factor revealed a core sequence similar to that of Ets binding sites, and supershift assays with antibodies demonstrated the involvement of the GABP transcription factor. Transient transfection experiments with LTR-chloramphenicol acetyltransferase constructs indicated that the variant LTR promoter is specifically inhibited by GABP in the absence of Tat, but this promoter was dramatically more responsive to Tat than the wild-type LTR. Introduction of this GABP site into the LAI virus yielded a specific gain of fitness in SupT1 cells, which contain little NF-κB protein. These results suggest that GABP potentiates Tat-mediated activation of LTR transcription and viral replication in some cell types. Conversion of an NF-κB into a GABP binding site is likely to have occurred also during the worldwide spread of HIV-1, as we noticed the same LTR modification in subtype E isolates from Thailand. This typical LTR promoter configuration may provide these viruses with unique biological properties.

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Section: Fig 12mentioning

confidence: 99%

Evolution of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat Promoter by Conversion of an NF-κB Enhancer Element into a GABP Binding Site

Verhoef

Sanders²,

Fontaine

et al. 1999

J Virol

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“…There is substantial variation in the LTR of different lentiviruses (Thompson, Elder, and Neil, 1994;Yamada et al, 1995) and evidence that differences in regulatory regions can affect phenotype. For example, acquisition of a transcription regulatory site can change tissue tropism and affect the level of virus production in a stimulated cell (Carvalho, Kirkland, and Derse, 1993;Maury, 1998;Tsichlis and Lazo, 1991). Further, there is subtype-specific variation in the HIV-1 LTR that affects viral replication in vitro (Jeeninga et al, 2000;Naghavi et al, 1999;van Opijnen et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Evolution of the long terminal repeat and accessory genes of feline immunodeficiency virus genomes from naturally infected cougars

Poss

Ross

2008

Virology

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FIVpco is a member of the feline immunodeficiency virus family that is endemic in wild cougar populations. Virus replication is robust in FIVpco-infected cougars but there are no consequences of infection to cougar survival, fecundity or susceptibility to other infections. Unlike pathogenic lentiviruses, there is no evidence for positive selection on FIVpco gag or env. To better understand how lentivirus genomes evolve in natural infections, we evaluated the regulatory region and accessory genes from fourteen full-length FIVpco genomes, which represent the FIVpco diversity in the Northern Rockies Ecosystem. Our data demonstrate that the two sister groups of FIVpco have each acquired binding sites for different interferon response factors (IRF). The most variable gene in the FIVpco genome encodes OrfA, although there is no indication that it, or any other accessory gene, is under positive selection. There is a single-splice acceptor site for vif expression, which is conserved among all FIVpco genomes. However, there are several putative means to express rev and orfA, which differ between the phylogenetic groups of FIVpco. Our comparative study on divergent FIVpco genomes indicates that variation in potential gene regulation mechanisms, not changes in structural proteins, characterize the evolution of FIVpco in natural infections.

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Regulation of Equine Infectious Anemia Virus Expression

Cited by 2 publications

References 31 publications

Evolution of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat Promoter by Conversion of an NF-κB Enhancer Element into a GABP Binding Site

Evolution of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat Promoter by Conversion of an NF-κB Enhancer Element into a GABP Binding Site

Evolution of the long terminal repeat and accessory genes of feline immunodeficiency virus genomes from naturally infected cougars

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