Recombinant HIV type 1 (Clade A) Glycoprotein 140 (a.a. 24-680) [His]

Name: Recombinant HIV type 1 (Clade A) Glycoprotein 140 (a.a. 24-680) [His]
SKU: DAG2129
Rating: 5 (1 reviews)

HIV type 1 Glycoprotein 140 (aa 24 - 680) [His], recombinant protein from HEK 293 cells

COA

SDS

Datasheet

Summary

Product Overview

6xHis tagged HIV-1 gp140(Clade A) protein (a.a.24-680)

Nature

Recombinant

Tag/Conjugate

His

Purity

≥ 95%

Format

Each vial contains 100 μg purified protein in PBS containing 0.1% BSA and 25% glycerol.

Concentration

1 mg/ml

Preservative

None

Storage

2-8°C short term, -20°C long term

Introduction

The human immunodeficiency virus (HIV) is a lentivirus (slowly replicating retrovirus) that causes the acquired immunodeficiency syndrome (AIDS), a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.

Antigen Description

Human Immunodeficiency Virus (HIV) can be divided into two major types, HIV type 1 (HIV-1) and HIV type 2 (HIV-2). HIV-1 is related to viruses found in chimpanzees and gorillas living in western Africa. HIV-2 is related to viruses found in sooty mangabeys. HIV-1 viruses may be further divided into groups. The HIV-1 group M viruses predominate and are responsible for the AIDS pandemic. Some of the HIV-1 group M subtypes are known to be more virulent or are resistant to different medications. HIV-2 viruses are thought to be less virulent and transmissible than HIV-1 M group viruses.The HIV-1 envelope glycoprotein gp160, also known as Glycoprotein 160, is cleaved into two chains: the surface protein gp120 and the transmembrane protein gp41. The mature envelope protein (Env) consists of a homotrimer of non-covalently associated gp120-gp41 heterodimers. The surface protein gp120 attaches the virus to the host lymphoid cell by binding to the primary receptor CD4. This interaction induces a structural rearrangement creating a high affinity binding site for a chemokine coreceptor like CXCR4 and/or CCR5. Surface protein gp120 is a ligand for CD209 / DC-SIGN and CLEC4M / DC-SIGNR. It may target the virus to gut-associated lymphoid tissue (GALT) by binding host ITGA4/ITGB7 (alpha-4/beta-7 integrins), a complex that mediates T-cell migration to the GALT. The transmembrane protein gp41 (TM) acts as a class I viral fusion protein, and membranes fusion leads to delivery of the nucleocapsid into the cytoplasm. The external domains of the HIV-1 envelope glycoprotein (gp120 and the gp41 ectodomain, collectively known as gp140) contain all known viral neutralization epitopes.

Keywords

HIV-1 gp140; HIV1 gp140; Envelope surface glycoprotein gp140; Glycoprotein 140; gp140; gp140 glycoprotein; Human Immunodeficiency Virus 1; SU; Surface protein; Retroviridae; Lentivirus; human immunodeficiency virus; HIV1 gp140; human immunodeficiency viru

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References

Brief Report: Toll-like Receptor 9-1635A/G Polymorphism Is Associated With HIV-1 Rebound After Four Weeks of Interruption of Antiretroviral Therapy

JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES

Authors: Vallejo, Alejandro; Molina-Pinelo, Sonia; de Felipe, Beatriz; Abad-Fernandez, Maria; Gonzalez-Escribano, Maria Francisca; Leal, Manuel; Soriano-Sarabia, Natalia

Abstract

Objectives: This study aims to analyze the association of the presence of common polymorphisms [single nucleotide polymorphisms (SNPs)] on Toll-like receptors (TLRs), such as TLR9-1635A/G, TLR2-1892A/C, TLR2-2258G/A, TLR4-899A/G, and TLR4-1196C/T, with the viral rebound after stopping antiretroviral treatment (ART). CCR5-Delta 32 deletion and HLA-A/HLA-B alleles were also analyzed. Design: Interruption of ART may be required to investigate the outcome of strategies aimed to achieve drug-free HIV remission or cure. However, interruption of ART is currently not indicated. This was a retrospective longitudinal study that included 57 long-term suppressed HIV-1-infected individuals. Methods: TLR SNPs were detected by real-time polymerase chain reaction (PCR). CCR5-Delta 32 was analyzed by conventional PCR and HLA-A and HLA-B alleles by PCR-SSOP Luminex. Results: HIV-1 RNA rebound at week 4 after treatment interruption positively correlated with pre-ART HIV-1 load (P= 0.025). The TLR9-1635AA genotype was independently associated with a higher HIV-1 rebound compared with those with AG + GG genotype (multivariate stepwise regression analysis,P= 0.004). Women had lower HIV-1 RNA load both at rebound and during the 72 weeks of follow-up compared with men (P< 0.05 at all time-points), whereas CD4 nadir and CD4 count set-point were similar according to sex. The pre-ART viral load was independently associated with the viral set-point (P= 0.001), whereas the presence of the HLA-A01 allele (P= 0.027) and the CD4 nadir (P= 0.001) were associated with the CD4 count set-point. Conclusions: The association of the TLR9-1635AA genotype with a higher HIV-1 rebound suggests that this SNP may affect the results from strategies requiring interruption of ART aimed to cure HIV-1 infection.

Programmatic evaluation of feasibility and efficiency of at birth and 6-week, point of care HIV testing in Kenyan infant

PLOS ONE

Authors: Wexler, Catherine; Nazir, Niaman; Maloba, May; Brown, Melinda; Goggin, Kathy; Gautney, Brad; Maosa, Nicodemus; Babu, Shadrack; Muchoki, Elizabeth; Mabachi, Natabhona; Lwembe, Raphael; Finocchario-Kessler, Sarah

Abstract

Background Testing infants at birth and with more efficient point of care (POC) HIV diagnostic can streamline EID and expedite infant ART initiation. We evaluated the implementation of at birth and 6-week POC testing to assess the effectiveness and feasibility when implemented by existing hospital staff in Kenya. Methods Four government hospitals were randomly assigned to receive a GeneXpert HIV-1 Qual (n = 2) or Alere m-PIMA (n = 2) machine for POC testing. All HIV-exposed infants enrolled were eligible to receive POC testing at birth and 6-weeks of age. The primary outcome was repeat POC testing, defined as testing both at birth and 6-weeks of age. Secondary outcomes included predictors of repeat POC testing, POC efficiency (turnaround times of key services), and operations (failed POC results, missed opportunities). Results Of 626 enrolled infants, 309 (49.4%) received repeat POC testing, 115 (18.4%) were lost to follow up after an at-birth test, 120 (19.2%) received POC testing at 6-weeks only, 80 (12.8%) received no POC testing, and 2 (0.3%) received delayed POC testing (>12 weeks of age). Three (0.4%) were identified as HIV-positive. Of the total 853 POC tests run at birth (n = 424) or 6-weeks (n = 429), 806 (94.5%) had a valid result documented and 792 (98.3%) results had documented maternal notification. Mean time from sample collection to notification was 1.08 days, with 751 (94.8%) notifications on the same day as sample collection. Machine error rates at birth and 6-weeks were 8.5% and 2.5%, respectively. A total of 198 infants presented for care (48 at birth; 150 at 6-weeks) without receiving a POC test, representing missed opportunities for testing. Discussion At birth POC testing can streamline infant HIV diagnosis, expedite ART initiation and can be implemented by existing hospital staff. However, maternal disengagement and missed opportunities for testing must be addressed to realize the full benefits of at birth POC testing.