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Our results also suggest that i) maturation is not hampered by FIV infection

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Academic year: 2021

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Abstract

During HIV-1 infection, dendritic cells (DCs) can not only prime T cells against the virus but can also transfer HIV to T cells. Feline AIDS is caused by feline immunodeficiency virus (FIV) and it is considereds a model for the human illness because the two diseases have many features in common. Little is known on feline DCs and their interaction with FIV, therefore the present study attempts to shed light on these cells during FIV infection. Infection of monocyte-derived DCs was attempted at ambient gravity and by spinoculation with FIV strains Petaluma and M2. DC infection was particularly evident with FIV Petaluma, which was rapidly released in the supernatants of both DCs and activated PBMCs only after spinoculation. We show that FIV Petaluma was produced by DCs by monitoring viral content in supernatants of infected DCs, by intracellular staining with anti- p25 antibodies, by showing its cytopathic effect. Although activated PBMCs were better substrates for FIV replication, leading to prolonged viral shedding, both immature DCs and DCs matured with lipopolysaccharide supported virus production, mostly during the first two days after infection. At later times, FIV infection induced syncytium formation by DCs. Our results also suggest that i) maturation is not hampered by FIV infection; ii) virus infection per se does not induce DCs to mature. We also show that infected iDCs can efficiently transfer FIV to activated PBMCs. It is concluded that feline DCs can be infected by FIV;

however, infection by FIV does not appear to influence feline DC functionality.

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