Virology of Covid Attacks22 Aug 2020 15:12
The following explains in simple terms what happens in a Covid/ HIV attack. When a virus invades the body, it infects and kills cells, as it hijacks the cellular apparatus to replicate itself. Injured and infected cells respond to this attack by releasing cytokines, which are chemical messengers which "call for help", initiating an inflammatory response to fight the infection. A subset of cytokines are chemokines (chemotaxic cytokines), which mobilize infection fighting cells to areas of tissue damage and inflammation.
One of the principal chemokines in the activation of the immune system is CCL5 or RANTES. RANTES is released by a number of cell types, but in Covid infection, it is importantly released by injured epithelial cells in the lungs. White blood cells, including T cells and macrophages respond to the site of infection. Unfortunately in severe Covid disease, the injured cells continue to release RANTES. More inflammatory cells migrate to areas of inflammation, creating a vicious circle, eventually escalating to the "cytokine storm". The excess migration of these cells to the lungs is a large component of the acute respiratory distress syndrome and pulmonary collapse in severe covid. A cascade of other cytokines are released as part of an inflammatory cascade, including interleukin 6 and TNF-alpha, which have been the target of other unsuccessful Covid treatments. The combination of extreme cytokine levels and excess activation and mobilization of inflammatory cells results in a profound immune dysregulation. This is profoundly injurious and eventually deadly.
Excess stimulation of the cytokine storm eventually exhausts the ability of these immune fighting cells to function properly. Macrophages, a type of white blood cell, become polarized and act in an inflammatory fashion, rather than helpfully devouring viruses and infected cells. T cells, rather than producing granzyme-a, an important enzyme to kill infected cells, lie about helplessly.
Leronlimab is a therapeutic monoclonal antibody which is on the cusp of approval, with blockbuster, if not paradigm-shifting potential.
Leronlimab is a monoclonal antibody, which was designed to treat HIV. It blocks the binding site (the doorway) on the CCR5 receptor, the primary site to which CCL5/RANTES binds. Leronlimab is awaiting approval for HIV. The HIV virus enters T cells through CCR5, infecting and killing them and destroying a major part of the immune system. Leronlimab "blocks this door", preventing HIV entry, and returning patients to health. Trial patients have had undetectable levels of HIV virus for six years while taking leronlimab, all without taking any antiviral medication. The immune system, when not damaged, clears the virus by itself.
In covid, administration of leronlimab blocks the same CCR5 receptor. By blocking CCR5, immune cells no longer migrate to areas of inflammation, preventing runaway inflammation and reversing the disproportionate inflammation of the cytokine st