Stem Cell Therapy and Its Significance in HIV Infection.

Human immunodeficiency virus (HIV) infection is a major global public health issue. Despite this, the only treatment available in mainstay is antiretroviral therapy. This treatment is not curative, it needs to be used lifelong, and there are many issues with compliance and side effects. In recent years, stem cell therapy has shown promising results in HIV management, and it can have a major impact on the future of HIV treatment and prevention. The idea behind anti-HIV hematopoietic stem/progenitor cell (HSPC)-directed gene therapy is to genetically engineer patient-derived (autologous) HSPC to acquire an inherent resistance to HIV infection. Multiple stem-cell-based gene therapy strategies have been suggested that may infer HIV resistance including anti-HIV gene reagents and gene combinatorial strategies giving rise to anti-HIV gene-modified HSPCs. Such stem cells can hamper HIV progression in the body by interrupting key stages of HIV proliferation: viral entry, viral integration, HIV gene expression, etc.Hematopoietic stem cells (HSCs) may also protect leukocytes from being infected. Additionally, genetically engineered HSCs have the ability to continuously produce protected immune cells by prolonged self-renewal that can attack the HIV virus. Therefore, a successful treatment strategy has the potential to control the infection at a steady state and eradicate HIV from patients. This will allow for a potential future benefit with stem cell therapy in HIV treatment.

JAK2 and TET2 Mutation in Polycythemia Vera.

The Ten-Eleven Translocation-2 (TET2) gene, located on chromosome 4q24, has been implicated in hematological malignancies. The TET2 gene shows mutations in variable myeloid malignancies with the involvement of 15% of myeloproliferative neoplasms (MPNs). The inactivation of the TET2 gene in both mice and humans has shown a high degree of deregulation of the hematopoiesis process leading to hematological malignancies. Polycythemia vera (PV), an MPN characterized by increased red blood cell mass, has been associated with the TET2 gene. Furthermore, TET2 genes have been found to facilitate Janus kinase-2 and signal transducer activator of transcription 5, as well as modulate the epigenetic composition of genomic DNA. However, little is known about the role of TET2 mutations in patients with PV. Several studies have been conducted to further assess the significant role of TET2 gene function in various disease processes and prognoses to enhance the management and care of these patients.

Hyperuricemia in Patients With Coronary Artery Disease and Its Association With Disease Severity.

The biochemical background of coronary artery disease (CAD) has been intensively explored in the past several decades. Previous clinical investigations have demonstrated the association of non-traditional risk factors, such as hyperuricemia, with CAD. Studies have shown that increased serum uric acid (SUA) was associated with an increased risk of adverse cardiovascular (CV) outcomes in patients with CAD. While the exact pathophysiological mechanisms leading to increased risk are still unknown, it has been postulated that hyperuricemia leads to endothelial dysfunction, oxidative metabolism, and platelet adhesiveness and aggregation, leading to CAD. Moreover, previous studies have shown that hyperuricemia is an independent risk factor for CAD. However, the correlation between high SUA levels and the severity of CAD remains unclear. The purpose of this review was to elucidate the association of hyperuricemia to CAD severity and to determine the effect of urate-lowering therapy (ULT) on CAD. A search of PubMed up to June 24, 2021, was carried out by the reviewers. From the findings, hyperuricemia stands as an independent risk factor for CAD, and CAD patients treated with ULT had improved CV outcomes and reduced mortality. Therefore, while SUA level is valuable in predicting an augmented risk of CAD and anticipating worse outcomes, ULT has promising cardioprotective effects.

Stem Cell Therapy and Its Significance in Pain Management.

Pain management has always been a challenging issue, which is why it has been a major focus of many rigorous studies. Chronic pain which typically lasts for more than three months is prevalent at an astounding rate of 11% to 19% of the adult population. Pain management techniques have gone through major advances in the last decade with no major improvement in the quality of life in affected populations. Recently there has been growing interest in the utilization of stem cells for pain management. Advancement of stem cell therapy has been noted for the past few years and is now being used in human clinical trials. Stem cell therapy has shown promising results in the management of neuropathic, discogenic back, osteoarthritis, and musculoskeletal pain. In this article, we will discuss the role of stem cells in the pain management of the aforementioned conditions, along with the mechanism, adverse effects, and risks of stem cell therapy.

Chimeric Antigen Receptor T Cell Therapy and Its Significance in Multiple Myeloma.

Multiple myeloma (MM) has a five-year prevalence worldwide of 230,000 people and is known as the second most common hematological malignancy within the United States. Extensive research has been conducted to gain a wide range of treatment strategies, providing hope to these patients. Combination therapy using chemotherapy, monoclonal antibodies, and immunomodulatory drugs are the current management of choice. After the introduction of chimeric antigen receptor (CAR) T cell therapy, promising results have been evidenced. In this therapy, T cells are derived from the patient and modified in-vitro to induce receptors that later target specific antigens when they are injected into patients. CAR T cells use three mechanisms to kill tumor cells: cytolytic pathways, cytokine release, and Fas/FasL axis. In this review, we highlight the different tumor markers targeted for therapy against multiple myeloma (MM). Target antigens for CAR T cell therapy include B-cell maturation antigen (BCMA), signaling lymphocyte activation molecule F7 (SLAMF7), CD38, CD138, CD19, immunoglobulin kappa light chain, orphan G protein-coupled receptor class C group 5 member D (GPRC5D). With the benefit of improving survival and prognosis, this therapy does carry a risk of some adverse events such as cytokine release syndrome, encephalopathy, infections, hypogammaglobulinemia, and tumor lysis syndrome.