The effect of repeated infestations of BALB/c mice with Ixodes ricinus (L.) nymphs on tick borne encephalitis (TBE) virus infection was studied. Enhancement of nymphal feeding, occurring in noninfected mice during the quaternary infestations, was less apparent or absent in female nymphs engorged on TBE virus infected mice. The mice infected with TBE virus during quaternary tick infestation survived significantly longer (P < 0.01) than mice infected with TBE virus during the primary tick infestation. The mean titre of virus in murine blood (determined by plaque assay) was significantly lower (P < 0.01) and the number of nymphs acquiring virus was reduced (P < 0.05) when feeding on hosts infected during the quaternary infestation. The results indicate that repeated infestations of I. ricinus nymphs on BALB/c mice, although enhancing tick feeding, reduced infection with TBE virus when inoculated intraperitoneally.
Body fat content is controlled, at least in part, by energy charge of adipocytes. In vitro studies indicated that lipogenesis as well as lipolysis depend on cellular ATP levels. Respiratory uncoupling may, through the depression of ATP synthesis, control lipid metabolism of adipose cells. Expression of some uncoupling proteins (UCP2 and UCP5) as well as other protonophoric transporters can be detected in the adipose tissue. Expression of other UCPs (UCP1 and UCP3) can be induced by pharmacological treat
ments that reduce adiposity. A negative correlation between the accumulation of fat and the expression of UCP2 in adipocytes was also found. Ectopic expression of UCP1 in the white fat of aP2-Ucp1 transgenic mice mitigated obesity induced by genetic or dietary factors. In these mice, changes in lipid metabolism of adipocytes were associated with the depression of intracellular energy charge. Recent data show that
AMP-activated protein kinase may be involved in the complex changes elicited by respiratory uncoupling in adipocytes. Changes in energy metabolism of adipose tissue may mediate effects of treatments directed against adiposity, dyslipidemia, and insulin resistance.