McNally, James M.Zarozinski, Christopher C.Lin, Meei Y.Brehm, Michael A.Chen, Hong D.Welsh, Raymond M.2022-08-232022-08-232001-06-082008-11-21J Virol. 2001 Jul;75(13):5965-76. <a href="http://dx.doi.org/10.1128/JVI.75.13.5965-5976.2001 ">Link to article on publisher's site</a>0022-538X (Print)10.1128/JVI.75.13.5965-5976.200111390598https://hdl.handle.net/20.500.14038/34180Experiments designed to distinguish virus-specific from non-virus-specific T cells showed that bystander T cells underwent apoptosis and substantial attrition in the wake of a strong T-cell response. Memory CD8 T cells (CD8(+) CD44(hi)) were most affected. During acute viral infection, transgenic T cells that were clearly defined as non-virus specific decreased in number and showed an increase in apoptosis. Also, use of lymphocytic choriomeningitis virus (LCMV) carrier mice, which lack LCMV-specific T cells, showed a significant decline in non-virus-specific memory CD8 T cells that correlated to an increase in apoptosis in response to the proliferation of adoptively transferred virus-specific T cells. Attrition of T cells early during infection correlated with the alpha/beta interferon (IFN-alpha/beta) peak, and the IFN inducer poly(I:C) caused apoptosis and attrition of CD8(+) CD44(hi) T cells in normal mice but not in IFN-alpha/beta receptor-deficient mice. Apoptotic attrition of bystander T cells may make room for the antigen-specific expansion of T cells during infection and may, in part, account for the loss of T-cell memory that occurs when the host undergoes subsequent infections.en-USJournal Articlehttps://escholarship.umassmed.edu/gsbs_sp/839670495gsbs_sp/839