improvement of clinical manifestations
A review of the recent literature on immunological changes in CVD, RA, and CMV infection provides strong evidence that expansions of cytotoxic CD4 + CD28−T cells in RA and other chronic inflammatory conditions are limited to CMV-infected patients and driven by CMV infection. They are likely to be responsible for the excess CV mortality observed in these situations. The CD4+CD28− phenotype convincingly links CMV infection to CV
mortality based on a direct cellular-pathological mechanism rather than epidemilogical association.
Pancreatitis after human papillomavirus vaccination: a matter of molecular mimicry