Arch Virol (1998) 143: 1839–1845
Cats are protected against feline immunodeﬁciency
virus infection following vaccination with a homologous AP-1
binding site-deleted mutant
, T. Miyazawa
, E. Sato, K. Uetsuka
, Y. Nishimura
G. Inada, K. Doi
, and T. Mikami
Department of Veterinary Microbiology, University of Tokyo, Tokyo, Japan
Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences,
University of Tokyo, Tokyo, Japan
Accepted March 31, 1998
Summary. Following establishment, via the vaginal route, of infection with an
AP-1 binding-site deleted mutant (AP-1) of feline immunodeﬁciency virus
(FIV), cats were challenged with a homologous intact strain (TM2) of FIV. The
cats were observed for 23 weeks to evaluate the efﬁcacy of the AP-1 against
the homologous TM2 strain challenge. These two viruses were differentiated
by Southern blotting after ampliﬁcation of proviral DNA by semi-nested poly-
merase chain reaction in DNAs of peripheral blood mononuclear cells and tissues.
A TM2-speciﬁc band was detected in one cat exposed to but not infected with
AP-1, but not in two AP-1-infected. These results indicate that AP-1 could
protect against subsequent challenge with homologous FIV TM2 strain.
Feline immunodeﬁciency virus (FIV) is a lentivirus which causes persistent infec-
tion and progressive acquired immunodeﬁciency-like disease in cats [7, 18]. The
infection in cats is used as a small animal model for human immunodeﬁciency
virus (HIV) infection in human. In HIV infection, the mucosal surface is a major
route of sexual and vertical transmissions . In FIV infection, virus particles
and FIV-infected cells were detected in genital secretion of infected cats [6, 15].
Recently, experimental vaginal infections in cats with FIV using cell-associated
or cell-free inocula were also reported ([1, 2, 14], Kohmoto et al., submitted).
AP-1 binding site is one of the enhancer/promoter binding sites present in the
long terminal repeat (LTR) of FIV and proved to be important for basal promoter