Ornithoros tick salivary, an intrinsic component of vector competence in transmission of African swine fever virus to pigs. [O30]

African swine fever (ASF) is a lethal haemorrhagic swine disease with disastrous consequences for pig production. Ornithodoros ticks such as O. erraticus in Spain and Portugal, and O. moubata sensu lato in eastern and southern Africa are able to maintain and transmit the virus, and are competent vectors and reservoirs for ASFV (1). These ticks can maintain ASFV for years and transmit the virus through different routes such as transovarial and/or sexual transmission from tick to tick, as well as horizontal transmission to suids via contaminated saliva or coxal fluid. Vector competence in virus transmission can be related to extrinsic or intrinsic factors. Here we present the intrinsic effect of O. porcinus tick salivary gland extract on the African swine fever virus infection in domestic pig. During the early stage of pig infection with ASFV, mononuclear phagocytic cells are the main targets for viral replication (2). Tick saliva has been shown to modulate the host physiological and immunological responses during feeding on skin, thus affecting viral infection. To better understand the interaction between soft tick, ASFV and pig at the bite location and the possible influence of tick saliva on pig infection by ASFV, salivary gland extract (SGE) of Ornithodoros porcinus, co-inoculated or not with ASFV, was used for intradermal auricular inoculation. Our observations focused both on the pig systemic immune response and on pig skin inflammation and cellular modulation (especially LCs and macrophages) at the tick bite location. Unlike previous studies, the assessment of such immune modulations was conducted on the natural host, domestic pigs, and a highly adapted tick-virus association with O. porcinus ticks collected from Madagascar and a Madagascan ASF virus strain. Our results showed that, after the virus triggered the disease, pigs inoculated with virus and SGE presented greater hyperthermia than pigs inoculated with virus alone. The density of Langerhans cells was modulated at the tick bite or inoculation site, either through recruitment by ASFV or inhibition by SGE. Additionally, SGE and virus induced macrophage recruitment each. This effect was enhanced when they were co-inoculated. Finally, the co-inoculation of SGE and virus delayed the early local spread of virus to the first lymph node after the inoculation site. This study has shown that the effect of SGE was powerful enough to be quantified in pig, both on the systemic and local immune response (3). We believe this model should be developed with infected tick and could improve knowledge of both tick vector competence and tick saliva immunomodulation. (Résumé d'auteur)