Abstract
Mutation of the human immunodeficiency virus by host cells inhibits viral dissemination by creating nonfunctional variants. However, viral mutation does not always eliminate the ability of the virus to disseminate and, in fact, is thought to promote persistence by generating functional mutants that evade immunity or drugs. How and where HIV mutates is not known. Accordingly, where and to what extent variants emerge may be determined by the cell type with optimal mutation apparatus as well as by the properties of the viral genomic sequence itself. Here we considered that HIV, which can infect B cells, may co-opt the Ig somatic hypermutation machinery to generate functional variants and asked whether the HIV envelope coding sequence can diversify in B cells. We show that an HIV envelope coding sequence transfected into B cells mutates in a manner consistent with somatic hypermutation, causing the production of viral protein variants. This result demonstrates that B cells can express and diversify HIV proteins. Thus, B cells may contribute to viral evasion and to the development of multi-drug resistance.
Keywords: B cells, HIV, quasi-species
Current HIV Research
Title: HIV Genes Diversify in B Cells
Volume: 6 Issue: 1
Author(s): Marilia Cascalho, Samuel J. Balin, Ted M. Ross and Jeffrey L. Platt
Affiliation:
Keywords: B cells, HIV, quasi-species
Abstract: Mutation of the human immunodeficiency virus by host cells inhibits viral dissemination by creating nonfunctional variants. However, viral mutation does not always eliminate the ability of the virus to disseminate and, in fact, is thought to promote persistence by generating functional mutants that evade immunity or drugs. How and where HIV mutates is not known. Accordingly, where and to what extent variants emerge may be determined by the cell type with optimal mutation apparatus as well as by the properties of the viral genomic sequence itself. Here we considered that HIV, which can infect B cells, may co-opt the Ig somatic hypermutation machinery to generate functional variants and asked whether the HIV envelope coding sequence can diversify in B cells. We show that an HIV envelope coding sequence transfected into B cells mutates in a manner consistent with somatic hypermutation, causing the production of viral protein variants. This result demonstrates that B cells can express and diversify HIV proteins. Thus, B cells may contribute to viral evasion and to the development of multi-drug resistance.
Export Options
About this article
Cite this article as:
Cascalho Marilia, Balin J. Samuel, Ross M. Ted and Platt L. Jeffrey, HIV Genes Diversify in B Cells, Current HIV Research 2008; 6 (1) . https://dx.doi.org/10.2174/157016208783571919
DOI https://dx.doi.org/10.2174/157016208783571919 |
Print ISSN 1570-162X |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4251 |
Call for Papers in Thematic Issues
HIV vaccine development
The development of a safe and effective vaccine that impedes HIV-1 transmission and/or limits the severity of infection remains a public health priority. The HIV-1/AIDS pandemic continues to have a disproportionate impact on vulnerable and under-served communities in the USA and globally. In the USA, minority communities that have relatively ...read more
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Lentiviral Vector-Based Models of Amyloid Pathology: From Cells to Animals
Current Alzheimer Research Cerebrovascular Complications of Diabetes: SGLT-2 Inhibitors as a Promising Future Therapeutics
Current Drug Targets Role of Opioid Antagonists in the Treatment of Women with Glucoregulation Abnormalities
Current Pharmaceutical Design Synaptic Aging is Associated with Mitochondrial Dysfunction, Reduced Antioxidant Contents and Increased Vulnerability to Amyloid-β Toxicity
Current Alzheimer Research Histone Post-translational Modifications in Huntington’s and Parkinson’s Diseases
Current Pharmaceutical Design The Use of Dexmedetomidine in Anesthesia and Intensive Care: A Review
Current Pharmaceutical Design Genetic Risk Factors for Depression in Alzheimer´s Disease Patients
Current Alzheimer Research Nutrigenomics and Its Approaches for Control of Chronic Diseases
Current Biotechnology Heme Oxygenase-1 Dysregulation in the Brain: Implications for HIVAssociated Neurocognitive Disorders
Current HIV Research Conditional Tat Protein Brain Expression in the GT-tg Bigenic Mouse Induces Cerebral Fractional Anisotropy Abnormalities
Current HIV Research Proinflammatory Cytokines and Chemokines in Neonatal Brain Damage
Current Pediatric Reviews Synthesis, Molecular Docking and Antiamnesic Activity of Selected 2- Naphthyloxy Derivatives
Medicinal Chemistry Novel Therapeutic Targets in Neuropsychiatric Disorders: The Neuroepigenome
Current Pharmaceutical Design Vitamin D: A Regulator of Metabolism and Inflammation
Current Nutrition & Food Science Neuroprotection Abilities of Cytosolic Phospholipase A2 Inhibitors in Kainic acid-induced Neurodegeneration
Current Drug Targets - Cardiovascular & Hematological Disorders Functional Role of Lipoprotein Receptors in Alzheimers Disease
Current Alzheimer Research Structural Analysis of Relevant Drug Targets for Alzheimer's Disease: Novel Approaches to Drug Development
Current Bioactive Compounds Exploitation of Some Natural Products for the Prevention and/or Nutritional Treatment of SARS-CoV2 Infection
Endocrine, Metabolic & Immune Disorders - Drug Targets T Cell-based Therapies for Atherosclerosis
Current Pharmaceutical Design Role of Ischemic Blood-Brain Barrier on Amyloid Plaques Development in Alzheimers Disease Brain
Current Neurovascular Research