In Bruton’s agammaglobulinemia, which feature explains reduced EBV infection?

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Multiple Choice

In Bruton’s agammaglobulinemia, which feature explains reduced EBV infection?

Bruton’s agammaglobulinemia blocks B cell development, so there are no mature B cells and essentially no immunoglobulins. Epstein-Barr virus relies on infecting B lymphocytes (via receptors like CD21) and establishing latency there. If B cells are absent, EBV has no primary target to infect or immortalize, so EBV infection occurs much less or not at all. The other features (normal T cells and NK cells, or defective phagocytosis) don’t explain why EBV infection would be reduced, since EBV’s main early target is B cells. Therefore, absence of B cells best explains the observed reduction in EBV infection.

Bruton’s agammaglobulinemia blocks B cell development, so there are no mature B cells and essentially no immunoglobulins. Epstein-Barr virus relies on infecting B lymphocytes (via receptors like CD21) and establishing latency there. If B cells are absent, EBV has no primary target to infect or immortalize, so EBV infection occurs much less or not at all. The other features (normal T cells and NK cells, or defective phagocytosis) don’t explain why EBV infection would be reduced, since EBV’s main early target is B cells. Therefore, absence of B cells best explains the observed reduction in EBV infection.

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