One day, I observed a precipitin line that did not take up the lipid stain, but stained intensely red when a protein counterstain was applied. Searching the template for that experiment, I found that this novel immune reaction was between the serum of a patient with hemophilia and that of an Australian aborigine, the latter serving as the population du jour on that given day. We initially called this unidentified antigen the “Red Antigen” for its staining properties, but later debated whether to call it the Bethesda

antigen for the place where it was discovered or the Australia antigen for the person Crizotinib mw in whom it was found. Blumberg insisted on the latter, in keeping with evolving nomenclature for newly identified hemoglobins that were being named after the location of the patient. Later, when the Australia antigen was identified as the surface protein of the

hepatitis B virus (HBV), I was frequently asked what it was like to be the first to see this antigen. In truth, it was not the “eureka moment” one would have hoped for because PI3K inhibitor it was an isolated finding that had no clinical relevance at the time. It was not like reaching some long-sought-after endpoint, because neither Blumberg, a geneticist, nor I, a hematologist, were in search of a hepatitis virus. It was not even remotely on our radar, but this isolated finding set the course of my career and ultimately represented the single most important event in hepatitis discovery and prevention. A day I remember much more vividly

than finding the Australia antigen was in November 1963, when I entered the Blumberg lab to find everyone morosely huddled around the radio. President Kennedy had been shot and we were all in disbelief and stunned silence. It click here was the end of an age of innocence that was to be further compounded by the subsequent assassinations of Martin Luther King, Jr., and Bobby Kennedy and the multiple tragedies of the Vietnam War. Scientifically, it was a time of my emergence. Politically, it was a time of despair. I spent 1963 and early 1964 trying to characterize the clinical associations and biophysical properties of the Australia antigen. I found that whereas the antigen was present in 10% of aborigines, it was present in only 0.1% of healthy U.S. blood donors. In testing Clinical Center patient populations, the striking finding was that the antigen was present in 10% of patients with leukemia. Hence, the first publication[1] on this “red antigen” was titled, “The Australia Antigen: A ‘New’ Antigen in Leukemia Sera.” Indeed, we postulated that this antigen might be part of a leukemia-inducing virus and planned to do electron microscopy (EM) to search for a particle, but somehow we delayed doing this. Had EM been performed at that time, the prolific hepatitis B surface antigen (HBsAg) particles would have been seen easily and probably shortened the road to HBV discovery by about 5 years.