The CAEV tat Gene Trans-activates the Viral LTR and Is Necessary for Efficient Viral Replication

Saltarelli, Mary; Schoborg, Robert V.; Gdovin, Susan L.; Clements, Janice E.

doi:10.1006/viro.1993.1564

Cited by 23 publications

(18 citation statements)

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“…The crosstransactivation by JDV Tat of the HIV LTR suggested a close evolutionary relationship between JDV and other primate lentiviruses. To analyze the evolutionary genetic relationship between JDV and other lentiviruses, a neighbor-joining phylogenetic tree based on the published sequences of lentiviral Tat peptides which are competent in transactivation was constructed (3,11,17,20,21,36,41,51,52,55) (Fig. 7A).…”

Section: Jdv Tat Can Complement Hiv Tat(؊) Provirus Expressionmentioning

confidence: 99%

Jembrana Disease Virus Tat Can Regulate Human Immunodeficiency Virus (HIV) Long Terminal Repeat-Directed Gene Expression and Can Substitute for HIV Tat in Viral Replication

Chen

Fong

et al. 2000

J Virol

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Section: Jdv Tat Can Complement Hiv Tat(؊) Provirus Expressionmentioning

confidence: 99%

Jembrana Disease Virus Tat Can Regulate Human Immunodeficiency Virus (HIV) Long Terminal Repeat-Directed Gene Expression and Can Substitute for HIV Tat in Viral Replication

Chen

Fong

et al. 2000

J Virol

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“…Lentiviruses are complex retroviruses carrying genes encoding regulatory functions involved in their replication cycle. One such gene is tat, which has been reported to mediate upregulation of gene transcription from the VMV (Carruth et al, 1994) and CAEV (Saltarelli et al, 1993) long terminal repeat (LTR) promoters, although these are not predicted to form stem-loop structures clearly analogous to the transactivatorresponse elements of primate or bovine lentiviruses. The basal level of transcription, particularly from the CAEV LTR, is elevated even in the absence of tat, however, and a clone of CAEV lacking functional tat has been shown to be capable of maintaining infection and causing disease in experimentally infected goats (Harmache et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Conserved sequence motifs involving the tat reading frame of Brazilian caprine lentiviruses indicate affiliations to both caprine arthritis-encephalitis virus and visna-maedi virus.

Castro

Greenland

Leite

et al. 1999

Journal of General Virology

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The sequence variation in small ruminant lentiviruses from Brazilian herds of milking goats was sampled in a representative region of the pol gene and in a region including the entire tat open reading frame. Clones were amplified from cDNA derived from virus produced in vitro using primers targetting conserved sequences of the pol gene. Iterative sequencing of clones indicated that animals from two herds in the Minas Gerais area were infected by a caprine arthritis-encephalitis virus (CAEV)-like virus and that individual animals carried variant virus populations. Sequences derived from an infected goat from a herd in Pernambuco showed no nucleic acid variation and were distant from the CAEV-type sequence but marginally closer to ovine visna-maedi virus (VMV) sequences. Sequences amplified from a region including the tat gene, amplified with a common upstream primer within the vif coding region and different downstream primers because of the local divergence between CAEV-and VMV-type sequences, confirmed the affiliation of the Minas Gerais sequences to CAEV and indicated that the Pernambuco isolate was indeed related to VMV, which had not previously been reported to cause natural caprine infection. The overlap between the vif and tat open reading frames clearly distinguished between CAEV-like small ruminant lentiviruses, which shared eight common nucleotides, and the VMV group, where the overlap was reduced to a single base ; the final adenine of the vif terminator (TAA) is the initial adenine of the presumptive tat initiator codon. This may be useful for epizoological tracing of the origin of outbreaks.

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“…The functional domains characteristic of type 1 Tat include a basic region for nuclear localization and binding to TAR (38), an N-terminal acidic region, a conserved core region, and a cysteine-rich region; the latter two are important for transactivation activity (18). Unlike the potent type 1 transcriptional transactivators, type 2 Tat proteins are weak transactivators (25,35,41,44). Moreover, lentiviruses that express a type 2 Tat do not have LTRs containing a hairpin RNA loop structure characteristic of the HIV TAR region; instead, they include LTR promoters capable of high basal levels of transcription (25,35,41,44).…”

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confidence: 99%

Feline Immunodeficiency Virus Orf-A Is Required for Virus Particle Formation and Virus Infectivity

Gemeniano¹,

Sawai

Leutenegger³

et al. 2003

J Virol

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The orf-A (orf-2) gene of feline immunodeficiency virus (FIV) is a small open reading frame predicted to encode a 77-amino-acid protein that contains putative domains similar to those of the ungulate lentiviral Tat protein. Orf-A is reported to be critical for efficient viral replication in vitro and in vivo. A series of FIVpPPR-derived proviruses with in-frame deletions and point mutations within orf-A were constructed and tested for replication in feline lymphoid cells. Orf-A mutant proviruses were also tested for viral gene and protein expression, viral particle formation, and virion infectivity. Deletions within orf-A severely restricted FIV replication in feline peripheral blood mononuclear cells (PBMC) and interleukin-2-dependent T-cell lines. In addition, substitutions of alanines for leucines in the putative leucine-rich domain, for cysteines in the putative cysteine-rich domain, and for a tryptophan at position 43 in Orf-A restricted the replication of FIV mutants. Deletions and point mutations in orf-A imposed a small effect or no effect on FIV long-terminal-repeat-driven viral gene expression and had no effect on viral protein expression. However, release of cell-free, virionassociated viral RNA in supernatants from cells transfected with orf-A mutant proviruses was severely restricted but was rescued by cotransfection with a wild-type Orf-A expression vector. In addition, virions derived from orf-A mutant proviruses expressed reduced infectivity for feline PBMC. Our findings suggest that Orf-A functions involve multiple steps of the FIV life cycle including both virion formation and infectivity. Furthermore, these observations suggest that Orf-A represents an FIV-encoded analog more similar to the accessory gene vpr, vpu, or nef than to the regulatory gene tat encoded by the primate lentiviruses.

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The CAEV tat Gene Trans-activates the Viral LTR and Is Necessary for Efficient Viral Replication

Cited by 23 publications

References 0 publications

Jembrana Disease Virus Tat Can Regulate Human Immunodeficiency Virus (HIV) Long Terminal Repeat-Directed Gene Expression and Can Substitute for HIV Tat in Viral Replication

Jembrana Disease Virus Tat Can Regulate Human Immunodeficiency Virus (HIV) Long Terminal Repeat-Directed Gene Expression and Can Substitute for HIV Tat in Viral Replication

Conserved sequence motifs involving the tat reading frame of Brazilian caprine lentiviruses indicate affiliations to both caprine arthritis-encephalitis virus and visna-maedi virus.

Feline Immunodeficiency Virus Orf-A Is Required for Virus Particle Formation and Virus Infectivity

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