Recombinant HIV type 2 gp36 [GST]

Name: Recombinant HIV type 2 gp36 [GST]
SKU: DAG4739
Rating: 5 (1 reviews)

Recombinant HIV type 2 gp36 from E. coli [GST]

COA

SDS

Datasheet

Summary

Product Overview

Recombinant HIV-II coat protein gp36, GST-tagged

Specificity

Immunoreactive with sera of HIV2-infected individuals.

Nature

Recombinant

Tag/Conjugate

GST

Alternative Names

Human Immunodeficiency Virus; HIV gp36; HIV; HIV-2 gp36; HIV-2; HIV type 2 gp36

Purity

> 95%, as determined by SDS-PAGE.

Format

Lyophilized from 50mM TRIS HCL 8M urea, pH-9.0.

Preservative

None

Storage

This product can be stored in working aliquots at4° C for one month, or at -20° C for six months, with a carrier protein without detectable loss of activity. Avoid repeated freeze/thaw cycles.

Introduction

HIV-1 and HIV-2 appear to package their RNA differently. HIV-1 binds to any appropriate RNA whereas HIV-2 preferentially binds to mRNA which creates the Gag protein itself. This means that HIV-1 is better able to mutate. HIV-2 is transmitted in the same ways as HIV-1: Through exposure to bodily fluids such as blood, semen, tears and vaginal fluids. Immunodeficiency develops more slowly with HIV-2.HIV-2 is less infectious in the early stages of the virus than with HIV-1.The infectiousness of HIV-2 increases as the virus progresses.Major differences include reduced pathogenicity of HIV-2 relative to HIV-1, enhanced immune control of HIV-2 infection and often some degree of CD4-independence. Despite considerable sequence and phenotypic differences between HIV-1 and 2 envelopes, structurally they are quite similar. Both membrane-anchored proteins eventually form the 6-helix bundles from the N-terminal and C-terminal regions of the ectodomain, which is common to many viral and cellular fusion proteins and which seems to drive fusion. HIV-1 gp41 helical regions can form more stable 6-helix bundles than HIV-2 gp41 helical regions however HIV-2 fusion occurs at a lower threshold temperature (25°C), does not require Ca2+ in the medium, is insensitive to treatment of target cells with cytochalasin B, and is not affected by target membrane glycosphingolipid composition.

Keywords

Human Immunodeficiency Virus; HIV gp36; HIV; HIV-2 gp36; HIV-2; HIV type 2 gp36

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References

HIV-1 gp41 selectively inhibits spontaneous cell proliferation of human cell lines and mitogen- and recall antigen-induced lymphocyte proliferation

IMMUNOLOGY LETTERS

Authors: Chen, YH; Christiansen, A; Dierich, MP

Abstract

Human immunodeficiency virus type 1 (HIV-1) transmembrane glycoprotein 41 (gp41) contains an immunosuppressive domain (Env amino acids 583-599). Previous studies by us and others using recombinant soluble gp41 (rsgp41; amino acids 539-684) and immunosuppressive peptide (1SP; a gp41 peptide, amino acids 583-599) have shown that HIV-1 gp41 by the immunosuppressive domain could bind to several proteins on human T, B and monocyte cell lines, and also to normal human peripheral blood mononuclear cells. In this study we demonstrated that HIV-1 rsgp41 could inhibit spontaneous cell proliferation of human T cell lines H9 and Jurkat, B cell lines Raji and Daudi, monocyte cell line U937, but could not inhibit cell proliferation of human fibroblast cell line HEF and green monkey kidney cell line Cos-1. HIV-1 rsgp41 could inhibit also concanavalin A (Con A)-, phytohaemagglutinin (PHA)- and tetanus toroid (TT)-induced cell proliferation of normal human peripheral blood lymphocytes, with 50% inhibition at a concentration of 8 mu M, but could not inhibit pokeweed mitogen (PWM)-induced lymphocyte proliferation. Furthermore, recombinant soluble gp36 of HIV-2 like HIV-1 rsgp41 could inhibit Con A-, but not PWM-induced lymphocyte proliferation. These results indicate that HIV-1 gp41-induced inhibition of proliferation is selective in so far as the effect of PWM is not altered while the effects of several other stimuli are.

Frequency of human immunodeficiency virus type-2 in hiv infected patients in Maputo City, Mozambique

VIROLOGY JOURNAL

Authors: Maueia, Cremildo; Costa, Deise; Meggi, Bindiya; Ismael, Nalia; Walle, Carla; Curvo, Raphael; Abreu, Celina; Bhatt, Nilesh; Tanuri, Amilcar; Jani, Ilesh V.; Ferreira, Orlando C., Jr.

Abstract

The HIV/AIDS pandemic is primarily caused by HIV-1. Another virus type, HIV-2, is found mainly in West African countries. We hypothesized that population migration and mobility in Africa may have facilitated the introduction and spreading of HIV-2 in Mozambique. The presence of HIV-2 has important implications for diagnosis and choice of treatment of HIV infection. Hence, the aim of this study was to estimate the prevalence of HIV-2 infection and its genotype in Maputo, Mozambique. HIV-infected individuals (N = 1,200) were consecutively enrolled and screened for IgG antibodies against HIV-1 gp41 and HIV-2 gp36 using peptide-based enzyme immunoassays (pepEIA). Specimens showing reactivity on the HIV-2 pepEIA were further tested using the INNO-LIA immunoblot assay and HIV-2 PCR targeting RT and PR genes. Subtype analysis of HIV-2 was based on the protease gene. After screening with HIV-2 pepEIA 1,168 were non-reactive and 32 were reactive to HIV-2 gp36 peptide. Of this total, 30 specimens were simultaneously reactive to gp41 and gp36 pepEIA while two samples reacted solely to gp36 peptide. Only three specimens containing antibodies against gp36 and gp105 on the INNO-LIA immunoblot assay were found to be positive by PCR to HIV-2 subtype A. The proportion of HIV-2 in Maputo City was 0.25% (90%CI 0.01-0.49). The HIV epidemic in Southern Mozambique is driven by HIV-1, with HIV-2 also circulating at a marginal rate. Surveillance program need to improve HIV-2 diagnosis and consider periodical survey aiming to monitor HIV-2 prevalence in the country.