Question

David (the bubble boy's) SCID was due to defects in genes encoding for:

A. the IL-2 receptor alpha
B. the IL-2 receptor gamma
C. the CD4 molecule
D. the CD8 molecule

Answer 1

David's SCID was due to defects in genes encoding for the IL-2 receptor gamma, affecting both B cell and T cell immune responses.

Step-by-step explanation:

David, known as the bubble boy, suffered from severe combined immunodeficiency (SCID), which is often caused by an X-linked recessive mutation that interferes with normal B cell and T cell production. In David's case, his SCID was due to defects in genes encoding for the IL-2 receptor gamma.

This mutation affects both the B cell and T cell arms of the adaptive immune response, impairing T-cell dependent antibody responses as well as cell-mediated immune responses and preventing the development of immunological memory.

Answer 2

David (the bubble boy's) SCID was due to defects in genes encoding for the IL-2 receptor gamma, which is essential for T cell function and is a common cause for X-linked SCID.

Step-by-step explanation:

David (the bubble boy's) SCID was due to defects in genes encoding for the IL-2 receptor gamma. Severe combined immunodeficiency (SCID) is a primary immunodeficiency disease, and the most common form is X-linked SCID, which accounts for nearly 50% of all cases. This form primarily affects males and involves genetic defects that impair the functions of B cells and T cells, vital components of the adaptive immune system. One of the mutations that can cause SCID affects the IL-2 receptor gamma chain, which is essential for the development and function of T cells, as well as to some extent B cells.

David Vetter, known as the "Bubble Boy," lived with this condition, preventing him from developing a functioning immune system. As a result, he had to live in a sterile environment to avoid opportunistic infections. Although David received a bone marrow transplant, complications arose due to an undetected Epstein-Barr virus in the donated marrow, leading to his untimely death at the age of 12. Bone marrow transplants and recent advances in gene therapy are among the treatment options for children with SCID to potentially correct lymphocyte development defects.