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. 2003 Jan;77(1):460–469. doi: 10.1128/JVI.77.1.460-469.2003

FIG. 4.

FIG. 4.

Influenza vRNPs accumulate in late endosomes in cells lacking PKCβII activity. HeLa cells were transiently transfected with the PKCβII wild-type or T500V plasmids for 16 h before a high-multiplicity infection for 60 min. (A) Indirect immunofluorescence studies were used to analyze the expression pattern of influenza virus and cellular vesicles. Influenza virus localization was determined using a polyclonal NP antibody. EEA1 (a marker for early endosomes), M6PR and CD63/Lamp3 (markers for late endosomes), and the Golgi apparatus were localized using their respective monoclonal antibodies. (B) Confocal microscopy studies were used to analyze the expression pattern of influenza virus and late endocytic vesicles. Influenza localization was determined by the polyclonal NP antibody, and late endosomes were localized with a monoclonal antibody to CD63/Lamp3. Bars = 5 μm.