So, a common issue now is that we’re getting all these wonderful new ways of controlling B-cell malignancies, whether it’s BTK inhibitors, BCL2 inhibitors, CAR-T cell therapies, bispecific T-cell engagers, and all of these are very effective, but they also deplete our normal B cell population. COVID-19 has really brought that to the forefront where we’ve seen patients fail to respond to vaccination, be at higher risk of getting severe outcomes with infections such as COVID-19...
So, a common issue now is that we’re getting all these wonderful new ways of controlling B-cell malignancies, whether it’s BTK inhibitors, BCL2 inhibitors, CAR-T cell therapies, bispecific T-cell engagers, and all of these are very effective, but they also deplete our normal B cell population. COVID-19 has really brought that to the forefront where we’ve seen patients fail to respond to vaccination, be at higher risk of getting severe outcomes with infections such as COVID-19. I think it’s a key and growing question for us as hematologists to address where we may well reach the stage fairly soon, if not already for some diseases such as CLL, where the highest risk might actually be the risk of infection and not the risk of the disease itself. So, I’m involved in a platform study which is operating in Australia and across to New Zealand where we’re actually beginning to look with a variety of randomizations at how we can best prevent infections among people who have long term B-cell aplasia, including CAR-T cell recipients. We aim to look at things such as immunoglobulin replacement therapy, who requires it, how long to use it for, when we can stop, what dose to use. We’re looking at antibiotic prophylaxis and particularly whether this carries other risks such as resistant organism outgrowth. And we’re also going to be looking at vaccinations, hopefully with additional randomizations in that platform in the future. So, it’s a very exciting time, lots of new and emerging questions to answer.