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Assessment of Immunologically Relevant Dynamic Tertiary Structural Features of the HIV-1 V3 Loop Crown R2 Sequence by ab initio Folding
Published on: September 15, 2010
Interferon induction by HIV glycoprotein 120: role of the V3 loop
H Ankel1, M R Capobianchi, C Castilletti
1Department of Biochemistry, Medical College of Wisconsin, Milwaukee 53226.
Virology
|November 15, 1994
Summary
HIV-1
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Human Immunodeficiency Virus type 1 (HIV-1) infection can trigger immune responses.
- Interferon (IFN) induction is a key component of the innate immune system.
- Peripheral blood mononuclear cells (PBMC) are crucial in immune responses to viral infections.
Purpose of the Study:
- To elucidate the mechanism by which HIV-1 induces IFN in PBMC.
- To identify the viral and cellular components involved in IFN induction by HIV-1.
Main Methods:
- Utilized recombinant HIV-1 gp120 glycoproteins from different strains (HIVIIIB and MN) as potential inducers.
- Employed monoclonal antibodies (mABs) targeting specific domains of gp120 and CD4.
- Investigated the inhibitory effects of mABs and V3-homologous peptides on IFN induction.
Main Results:
- HIVIIIB-derived gp120 induced IFN in PBMC, while MN-derived gp120 did not.
- Antibodies blocking gp120-CD4 binding or targeting the CD4 hinge region abolished IFN induction.
- Antibodies against the HIV-1 V3 loop and V3-homologous peptides also inhibited IFN induction.
Conclusions:
- HIV-1 gp120 binding to CD4 initiates a conformational change, positioning the V3 loop.
- Interaction of the V3 loop with a putative secondary receptor on PBMC triggers IFN induction.
- This mechanism highlights a novel pathway for viral-mediated immune activation by HIV-1.
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