Thrombocytopenia is a common symptom and one of the warning signs of dengue virus (DENV) infection. Platelet depletion is critical as it may lead to other severe dengue symptoms. Understanding the molecular events of this condition during dengue infection is challenging because of the multifaceted factors involved in DENV infection and the dynamics of the disease progression. Platelet levels depend on the balance between platelet production and platelet consumption or clearance. Megakaryopoiesis and thrombopoiesis, two interdependent processes in platelet production, are hampered during dengue infection. Conversely, platelet elimination via platelet activation, apoptosis and clearance processes are elevated. Together, these anomalies contribute to thrombocytopenia in dengue patients. Targeting the molecular events of dengue-mediated thrombocytopenia shows great potential but still requires further investigation. Nonetheless, the application of new knowledge in this field, such as immature platelet fraction analysis, may facilitate physicians in monitoring the progression of the disease.

The ability to externally regulate the expression or function of a gene product has proven to be a powerful tool in the study of proteins and disease in vitro, and more recently in transgenic animal models. The transfer of these technologies to regulate a therapeutic, adoptively transferred gene product in a clinical setting may provide a means to exert additional control over a large variety of therapies for many diseases, leading to increased safety and effectiveness. This could be applied to any biological therapy, including gene therapy, viral therapies, cellular therapies (such as immune cell therapies, stem cell therapies and bone marrow transplant), some vaccines and even organ transplant. A variety of systems have been used in a basic research setting to conditionally regulate the function of a protein, including control of transcription and mRNA stability, and the use of protein inhibitors. However, most of these have disadvantages for medical use, where a simple, specific, tunable, reversible and broadly applicable means to regulate protein function is needed. Recent advances in controlling the stability or function of proteins through the interaction of small-molecule effectors and fusion domains on the protein have raised the possibility that direct and highly specific external control of therapeutic protein function in humans will be feasible.

Human herpesvirus 7 (HHV-7) is a recently described T-lymphotropic herpesvirus, which infects almost all children by the age of three years and persists lifelong, with the shedding of infectious virus in saliva. HHV-7 is similar to human herpesvirus 6 (HHV-6) in its genetic content and in many of its biological properties, which include the ability to cause at least some cases of exanthem subitum (roseola). Despite these similarities, important differences between HHV-7 and HHV-6 exist, including the fact that HHV-7 binds to the cellular CD4 molecule and uses this protein as a necessary component of its receptor, while HHV-6 binds to a different (and unknown) receptor. Furthermore, the pathogenesis and sequelae of HHV-7 infection remain very poorly understood. This review provides a critical summary of research on HHV-7.

Autoimmune diseases are pathological autoimmune reactions in the body caused by various factors, which can lead to tissue damage and organ dysfunction. They can be divided into organ-specific and systemic autoimmune diseases. These diseases usually involve various body systems, including the blood, muscles, bones, joints and soft tissues. The transient receptor potential (TRP) and PIEZO receptors, which resulted in David Julius and Ardem Patapoutian winning the Nobel Prize in Physiology or Medicine in 2021, attracted people's attention. Most current studies on TRP and PIEZO receptors in autoimmune diseases have been carried out on animal model, only few clinical studies have been conducted. Therefore, this study aimed to review existing studies on TRP and PIEZO to understand the roles of these receptors in autoimmune diseases, which may help elucidate novel treatment strategies.