Platelets, or thrombocytes, are specialized cellular fragments that form blood clots when we get scrapes and traumatic injuries. Conditions such as viral infections, autoimmune diseases, and others can lead to a decline in platelet count in the body, a condition known as thrombocytopenia.
Through an extensive clinical and research partnership, Dr. Stephan Moll and Dr. Jacquelyn Baskin-Miller, both from the UNC School of Medicine, have identified a connection between adenovirus infections and a rare blood clotting disorder. This discovery marks the first time the widespread respiratory
Their new observation, which was published in the New England Journal of Medicine, sheds new light on the virus and its role in causing an anti-platelet factor 4 disorder. Additionally, the discovery opens a whole new door for research, as many questions remain as to how and why this condition occurs – and who is most likely to develop the disorder.
HIT, VITT, and “Spontaneous HIT”
Antibodies are large Y-shaped proteins that can stick to the surface of bacteria and other “foreign” substances, flagging them for destruction by the immune system or neutralizing the threat directly.
In anti-PF4 disorders, the person’s immune system makes antibodies against platelet factor-4 (PF4), a protein that is released by platelets. When an antibody forms against PF4 and binds to it, this can trigger the activation and rapid removal of platelets in the bloodstream, leading to blood clotting and low platelets, respectively.
Sometimes, the formation of anti-PF4 antibodies is triggered by a patient’s exposure to heparin, called heparin-induced thrombocytopenia (HIT), and sometimes it occurs as an autoimmune condition without heparin exposure, which is referred to as “spontaneous HIT.”
In the last three years, thrombocytopenia has been shown to rarely occur after injection with