Accelerated viraemia in cats vaccinated with fixed autologous FIV-infected cells

• Published in: Veterinary immunology and immunopathology 1998-10, Vol.65 (2), p.353-365
• Main Authors: Karlas, Jos A, Siebelink, Kees H.J, v. Peer, Maartje A, Huisman, Willem, Rimmelzwaan, Guus F, D.M.E. Osterhaus, Albert
• Format: Article
• Language: English
• Subjects: AIDS/HIV; Animals; Antibodies, Viral - analysis; Autologous vaccination; Blood Component Transfusion; Blood Transfusion, Autologous; Cats; DNA Primers - chemistry; DNA, Viral - analysis; Enhancement of infection; Feline Acquired Immunodeficiency Syndrome - immunology; Feline Acquired Immunodeficiency Syndrome - prevention & control; Feline immunodeficiency virus; FIV; Immunodeficiency Virus, Feline - genetics; Immunodeficiency Virus, Feline - immunology; Polymerase Chain Reaction - veterinary; T-Lymphocytes - immunology; T-Lymphocytes - virology; Vaccination - veterinary; Vaccines; Viral Load; Viral Vaccines - administration & dosage; Viremia - etiology; Viremia - immunology
• ISSN: 0165-2427; 1873-2534
• DOI: 10.1016/S0165-2427(98)00166-4

We have vaccinated cats with fixed autologous FIV infected PBMC to determine whether autologous presentation of antigen is capable of inducing a protective immune response against homologous challenge. To this end autologous PBMC were infected with a FIV molecular clone (19k1). When infection was established, cells were inactivated by dialysis against paraformaldehyde. Upon vaccination, cats developed a virus specific immune response as measured by ELISA against the Gag protein of FIV. No antibodies against the envelope protein were detected with a peptide ELISA. Virus neutralizing antibodies however could be detected with a neutralization assay based on infection of CrFK cells, but not in an assay based on infection of primary T-cells. Although vaccination led to the induction of these virus-specific immune responses, vaccinated cats were not protected against homologous challenge but showed an accelerated viraemia upon infection. This was shown both by PCR and cell-associated viral load. The possible mechanisms underlying this observation are discussed in this paper.