In December 2019, a new and highly contagious infectious disease emerged in Wuhan, China. The etiologic agent was identified as a novel coronavirus, now known as Severe Acute Syndrome Coronavirus-2 (SARS-CoV-2). Recent research has revealed that virus entry takes place upon the union of the virus S surface protein with the type I transmembrane metallo-carboxypeptidase, angiotensin converting enzyme 2 (ACE-2) identified on epithelial cells of the host respiratory tract. Virus triggers the synthesis and release of pro-inflammatory cytokines, including IL-6 and TNF-α and also promotes downregulation of ACE-2, which promotes a concomitant increase in levels of angiotensin II (AT-II). Both TNF-α and AT-II have been implicated in promoting overexpression of tissue factor (TF) in platelets and macrophages. Additionally, the generation of antiphospholipid antibodies associated with COVID-19 may also promote an increase in TF. TF may be a critical mediator associated with the development of thrombotic phenomena in COVID-19, and should be a target for future study.

Venoms are products of specialized glands and serve many living organisms to immobilize and kill prey, start digestive processes and act as a defense mechanism. Venoms affect different cells, cellular structures and tissues, such as skin, nervous, hematological, digestive, excretory and immune systems, as well as the heart, among other structures. Components of both the innate and adaptive immune systems can be stimulated or suppressed. Studying the effects on the cells and molecules produced by the immune system has been useful in many biomedical fields. The effects of venoms can be the basis for research and development of therapeutic protocols useful in the modulation of the immunological system, including different autoimmune diseases. This review focuses on the understanding of biological effects of diverse venom on the human immune system and how some of their components can be useful for the study and development of immunomodulatory drugs.

Genomic incorporation of viruses as human endogenous retroviruses (HERVs) are components of our genome that possibly originated by incorporating ancestral of exogenous viruses. Their roles in the evolution of the human genome, gene expression, and the pathogenesis of autoimmune diseases (ADs) and neoplastic phenomena are the subject of intense research. This review analyzes the evolutionary and virological aspects of HERVs and other viruses that incorporate their genome into the human genome and have known role in the genesis of ADs. These insights are helpful to understand further the possible role in autoimmunity genesis of HERVs, other ancestral viruses no HERVs and modern viruses with the ability to incorporate into the human genome or interact with HERVs.

There are more than 100 autoimmune diseases (AD), which have a high prevalence that ranges between 5% and 8% of the general population. Type I diabetes mellitus, multiple sclerosis, systemic lupus erythematosus and rheumatoid arthritis remain the health problem of highest concern among people worldwide due to its high morbidity and mortality. The development of new treatment strategies has become a research hotspot. In recent years, the study of the ion channels presents in the cells of the immune system, regarding their functional role, the consequences of mutations in their genes and the different ways of blocking them are the subject of intense research. Pharmacological blockade of KV1.3 channel inhibits Ca2+ signaling, T cell proliferation, and pro-inflammatory interleukins production in human CD4⁺ effector memory T cells. These cells mediated most of the AD and their inhibition is a promising therapeutic target. In this review, we will highlight the biological function of KV1.3 channel in T cells, consequence of the pharmacological inhibition (through anemone and scorpion toxins, synthetic peptides, nanoparticles, or monoclonal antibodies) as well as the possible therapeutical application in AD.