bafilomycin-a1 and Feline-Infectious-Peritonitis

Infection of the monocyte/macrophage lineage with feline infectious peritonitis virus (FIPV) is enhanced in the presence of anti-FIPV antibodies (antibody-dependent enhancement or ADE). We investigated the following unclear points concerning ADE of FIPV infection: (i) involvement of the virus receptor, feline aminopeptidase N (fAPN), in ADE activity in FIPV infection; (ii) necessity of acidification of the endosome in cellular invasion of FIPV. Virus receptor-blocking experiments using anti-fAPN antibodies at 4 or 37 degrees C and experiments using fAPN-negative U937 cells revealed that fAPN is not involved in ADE of FIPV infection. Experiments using lysosomotropic agents clarified that acidification of the endosome is necessary for cellular invasion by FIPV, regardless of the presence or absence of antibodies. These findings may be very important for understanding the mechanism of ADE of FIPV infection.

Topics: Ammonium Chloride; Animals; Antibodies, Viral; Antibody-Dependent Enhancement; Cats; CD13 Antigens; Coronavirus, Feline; Dose-Response Relationship, Drug; Endosomes; Feline Infectious Peritonitis; Macrolides; Macrophages, Alveolar; Receptors, Virus; Virus Replication