Related Experiment Video

Updated: Aug 14, 2026

Recombinant Retroviral Production and Infection of B Cells
09:19

Recombinant Retroviral Production and Infection of B Cells

Published on: February 18, 2011

Current perspectives on cytokines for anti-retroviral therapy in AIDS related B-cell lymphomas

V Sharma1

  • 1Laboratory of Cytokine Research, Department of Biology, 11000 University Parkway, University of West Florida, Pensacola, Florida 32514-5751, USA. vsharma@uwf.edu

Current Drug Targets. Infectious Disorders
|May 29, 2003
PubMed

The development of high-grade B-cell lymphoma in Acquired Immunodeficiency Syndrome (AIDS) patients is a relatively late manifestation induced by Human Immunodeficiency Virus-1 (HIV) infection and is considered to be an AIDS-defining condition. Multiple, ongoing molecular and cytogenetic aberrations appear necessary for the development of AIDS-related lymphoma. Studying a panel of human B-cell lines derived from patients with Burkitt's lymphoma (BL) and AIDS-associated Burkitt's lymphoma (AIDS-BL) we had described constitutive expression and secretion of large amounts of Interleukin-16 (IL-16), Macrophage Inflammatory Protein-1alpha (MIP-1alpha), Macrophage Inflammatory Protein-1beta (MIP-1beta), Interleukin-12 (IL-12), Interleukin-10 (IL-10), and Interleukin-7 (IL-7). Some of these cytokines like IL-16, MIP-1beta, MIP-1alpha and Regulated upon activation normal T expressed and secreted (RANTES) are shown to have inhibitory effect on HIV replication. Interestingly, we identified a novel transcription factor family, Macrophage Inflammatory Protein-1alpha Nuclear Protein (MNP), which is suggested as a potential target for anti-retroviral therapy based on the implication of its role and involvement as a key regulator of MIP-1alpha. It is apparent, that HIV induces the production of a cascade of cytokines and cytokine receptors. Some of these molecules serve to increase the infection and replication of HIV per se, and some others serve to induce a state of B-cell growth, activation, and differentiation. This review attempts to delineate the complex mechanisms of viral, B-cell, oncogene, cytokine/cytokine receptor and transcription factor interactions that are involved in AIDS associated lymphomagenesis. Unfolding the relationship between cytokines and the underlying mechanisms of the disease will not only help in understanding the pathophysiology but also will facilitate focusing on the development of new diagnostic and therapeutic strategies.

More Related Videos

Expanding Cytotoxic T Lymphocytes from Umbilical Cord Blood that Target Cytomegalovirus, Epstein-Barr Virus, and Adenovirus11:18

Expanding Cytotoxic T Lymphocytes from Umbilical Cord Blood that Target Cytomegalovirus, Epstein-Barr Virus, and Adenovirus

Published on: May 7, 2012

Radial Mobility and Cytotoxic Function of Retroviral Replicating Vector Transduced, Non-adherent Alloresponsive T Lymphocytes10:01

Radial Mobility and Cytotoxic Function of Retroviral Replicating Vector Transduced, Non-adherent Alloresponsive T Lymphocytes

Published on: February 11, 2015

Related Concept Videos

Retrovirus Life Cycles01:10

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...