A B S T R A C T Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (Ti) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral To disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-'I, followed in 5-7 days by 'I-T4 intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound 'I and protein-bound 'I, and urinary 125I and 'I, together with frequent estimates of serum "'I-T4 (Murphy-Pattee) and free T4 (FT4), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of '"'I-T4 during infection included significant decreases in the fractional disappearance rate for To [(k)], and in the clearance and daily disposal of T4, all of which returned to control values during convalescence. Total serum 'I-T4 increased late in the infected period to become greater during convalescence than either before or during infection, while FT4 did not increase significantly until convalescence. An analysis of serum 'I-T4/I-Ti and 'I-T4/ PB'I ratios confirmed these observations. The slope with time of ratios for urinary 'I/I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum 'I-T, concentration in the convalescent phase mnay reflect in part A preliminary report on this work appeared in abstract form in 1971. Clin. Res. 19: 384.