Influenza viruses are single-stranded RNA viruses that are classified into three major serotypes of A, B, and C. Influenza A virus is the most significant as it causes a more severe disease compared to B and C and it also has a greater tendency to undergo significant antigenic changes. Disease initially consists of fever, myalgia, headache, and shaking chills. After 6-12 hours, a nonproductive cough develops. These acute symptoms persist for a week, however, resolution of all the symptoms may not occur until 2-3 weeks later. Occasionally, the patient develops a progressive infection that involves the tracheobronchial tree and lungs, which may lead to pneumonia. In some cases, a bacterial superinfection may occur significantly worsening the patient’s condition.

 

The Influenza virus outer glycoproteins are hemagglutinin (HA) and neuraminidase (NA). Hemagglutinin serves as the receptor binding protein and interacts with host N-acetylneuraminic acid-containing glycoprotein or glycolipid receptor sites on human respiratory target cells. Neuraminidase acts on HA receptors by cleaving terminal neuraminic acid destroying receptor activity. Influenza virus contain a wide variety of subtypes due to its ability to mutate and recombine its RNA genome via a processs of antigenic drifts and shifts especially with its HA and NA genes. Because of this, limited to no protection is conferred with immunity to one type or subtype to another type or subtype, which is major limitation to current vaccine or therapeutic antibody strategies. Since HA and NA are essential for viral attachement and entry, they are the targets of BMI’s Immune Dampening and Refocusing Technology such that broadly reactive immune responses and therapeutic antibodies can be made.