Human retroviruses and AIDS 1996. A compilation and analysis of nucleic acid and amino acid sequences

Myers, Gerald; Foley, Brian; Korber, Bette; Mellors, John W.; Jeang, Kuan Teh; Wain‐Hobson, Simon

doi:10.2172/463607

Cited by 366 publications

(718 citation statements)

References 153 publications

Supporting

Mentioning

680

Contrasting

Unclassified

Order By: Relevance

“…Very few positions can discriminate between transcriptional activation and stimulation of viral DNA replication, (reviewed by McBride and Myers, 1996). We chose to modify two positions of the transactivation domain previously shown to discriminate between transcription and replication in the analogous HPV16 E2 protein (Sakai et al, 1996).…”

Section: Mutations In the Transactivation Domain Of E2 Can Discriminamentioning

confidence: 99%

“…Secondary structures predictions indicate that it might be constituted of two subdomains, the most N-terminal one containing two or three large acidic a-helices, while the domain closest to the hinge may contain a series of small b-sheets. Systematic mutational analysis of the E2TD domain by several groups has not allowed to unambiguously discriminate its functions in transcription and replication (reviewed in McBride and Myers, 1996).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Papillomavirus E2 induces p53-independent apoptosis in HeLa cells

et al. 1999

View full text Add to dashboard Cite

We have previously shown that expression of the papillomavirus E2 protein in HeLa cells induces p53 accumulation and causes both cell cycle arrest and apoptosis. In contrast to growth arrest, onset of apoptosis was not correlated with an increase of p53 transcriptional activity. In the present study, we conducted biochemical and genetic experiments in order to determine whether E2-induced apoptosis was independent of p53 induction. We showed that E2 did not alter the transcription of Bax, a known p53-activated cell death inducer. The time course of apoptotic cell death preceded p53 induction by several hours. Overexpression of the HPV18 E6 oncogene prevented E2-mediated p53 accumulation, but did not alter the rate of cell death. Finally, point mutants of the HPV18 E2 transactivation domain induced apoptosis, although they were unable to induce high p53 accumulation or cell cycle arrest. In addition, the results obtained with these mutants indicated that both transcriptional activation and replication functions of E2 were dispensable for the induction of cell death. These observations show that E2-induced apoptosis is an early event, independent of p53 accumulation and unrelated to downstream p53-dependent transcriptional events.

show abstract

Section: Mutations In the Transactivation Domain Of E2 Can Discriminamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Papillomavirus E2 induces p53-independent apoptosis in HeLa cells

et al. 1999

View full text Add to dashboard Cite

show abstract

“…The HIV-1 SF-2 p24 capsid protein was obtained from the NIH AIDS Research and Reference Reagent Program and differs from HIV-1 LAI p24 at one amino acid position (23). The HIV-1 BH-10 p17 matrix protein was obtained from the MRC AIDS Reagent Project and is identical in sequence to HIV-1 LAI p17 (23). All DNA oligonucleotides were synthesized by Operon, Inc. (Alameda, CA).…”

Section: Reagentsmentioning

confidence: 99%

In vitro selection of RNAs that bind to the human immunodeficiency virus type-1 gag polyprotein

Lochrie

Waugh²,

Pratt³

et al. 1997

Nucleic Acids Research

View full text Add to dashboard Cite

“…All samples carried the wild-type 36 GIV 38 tripeptide sequence. In several samples, polymorphisms were detected at positions of the N helix that have previously been shown to be subject to natural variation in T-20-naive patients (18). None of these polymorphisms was repeatedly found in samples characterized by low or high susceptibility to T-20.…”

mentioning

confidence: 92%

Baseline Susceptibility of Primary Human Immunodeficiency Virus Type 1 to Entry Inhibitors

Labrosse

Labernardière²,

Dam³

et al. 2003

J Virol

View full text Add to dashboard Cite

Human immunodeficiency virus type 1 plasma viruses from 29 entry inhibitor-naive patients were characterized for their susceptibilities to T-20, AMD3100, and RANTES. A strikingly wide range of susceptibilities to T-20 was observed that was influenced by coreceptor usage but not by the susceptibilities of the viruses to inhibitors that target the chemokine receptors or by polymorphisms in the gp41 N helix.The human immunodeficiency virus type 1 (HIV-1) entry process (2,19,27) can be inhibited by several drugs (3,14,22,23), which belong to three groups according to the step they inhibit: (i) inhibitors of the interaction between the viral surface glycoprotein (gp120) and CD4, which target the CD4-binding site on gp120; (ii) inhibitors of the interaction between gp120 and CCR5 or CXCR4 (e.g., chemokines and their derivatives or small organic molecules that antagonize chemokine receptor activity); and (iii) fusion inhibitors, which are peptides derived from the sequence of the viral transmembrane glycoprotein (gp41) that prevent the formation of a hairpin structure required for membrane fusion. One of these peptides, T-20 (enfuvirtide), is currently being evaluated in phase III clinical trials (15,25,26). The optimization of treatment strategies that include entry inhibitors will rely on the availability of methods capable of determining baseline viral susceptibility and acquired resistance to these drugs. In addition, the characterization of the determinants of baseline susceptibility and of acquired resistance to entry inhibitors may provide valuable information on the viral entry process and on the precise mechanism of action of these drugs.We have developed a recombinant virus assay that permits the assessment of viral susceptibility to entry inhibitors. We modified a pNL4-3 molecular clone by deleting the region of the envelope gene encoding gp120 and the ectodomain of gp41 (positions 6480 to 8263) and replacing it with a linker that contains a unique MluI restriction site (vector 43-⌬env). Recombinant virus was produced by cotransfection of 293-T cells with the MluI-linearized 43-⌬env vector and a reverse transcription-PCR product, amplified from patient plasma samples, which encompasses the deleted region and carries short overlaps that allow homologous recombination. Virus-containing supernatants were used to infect subconfluent U373MG-CD4 cells expressing either CCR5 or CXCR4 (17), in the absence or in the presence of increasing concentrations of entry inhibitors. These target cells carry an HIV-1 long terminal repeat-lacZ cassette, which allows the quantification of single cycle infectivity by a colorimetric assay based on HIV-1 Tat-induced expression of ␤-galactosidase (24). The concentrations inhibiting 50% of virus infectivity (IC 50 s) were calculated by using the median-effect equation (6).The recombinant virus assay was first used to determine the baseline susceptibilities of subtype B primary viruses to the fusion inhibitor T-20 (American Peptide Company, Inc., Sunnyvale, Calif.). Plasma samples sel...

show abstract

Human retroviruses and AIDS 1996. A compilation and analysis of nucleic acid and amino acid sequences

Cited by 366 publications

References 153 publications

Papillomavirus E2 induces p53-independent apoptosis in HeLa cells

Papillomavirus E2 induces p53-independent apoptosis in HeLa cells

In vitro selection of RNAs that bind to the human immunodeficiency virus type-1 gag polyprotein

Baseline Susceptibility of Primary Human Immunodeficiency Virus Type 1 to Entry Inhibitors

Contact Info

Product

Resources

About