48 research outputs found
FUSION OF PHOSPHOLIPID VESICLES INDUCED BY DIVALENT CATIONS, MONITORED BY MIXING OF AQUEOUS CONTENTS
Differential effects of free and liposome encapsulated amikacin on the survival of Mycobacterium avium complex in mouse peritoneal macrophages
Direct Fusion between Poly(ethylene oxide)-lipid Modified Liposomes and Murine Mitotic B16 Melanoma Cells
A common mechanism for influenza virus fusion activity and inactivation
The fusion of influenza virus (A/PR/8/34 strain) with PC- 12 cells was monitored by a fluorescence
assay, and the results were analyzed with a mass-action model which could explain and predict the kinetics
of fusion. The model accounted explicitly for the reduction in the fusion rate constant upon exposure of
the virus to low pH, either for the virus alone in suspension or for the virus bound to the cells. When the
pH was lowered without previous viral attachment to cells, an optimal fusion activity was detected at pH
5.2. When the virus was prebound to the cells, however, reduction of pH below 5.2 resulted in enhanced
fusion activity at the initial stages. These results were explained by the fact that the rate constants of both
fusion and inactivation increased severalfold at pH 4.5 or 4, compared to those at pH 5.2. At pH 5.2,
lowering the temperature from 37 to 20 or 4 "C resulted in a decrease in the fusion rate constant by more
than 30- or 1000-fold, respectively. Inactivation of the virus when preincubated in the absence of target
membranes at pH 5 was found to be rapid and extensive at 37 OC, but was also detected at 0 OC. Our
results indicate a strong correlation between fusion and inactivation rate constants, suggesting that the
rate-limiting step in viral hemagglutinin (HA)-mediated fusion, that is, rearrangement of viral glycoproteins
at the contact points with the target membrane, is similar to that involved in fusion inactivation