Serological, sequence, and in vitro host range analyses of feline parvovirus (FPV) isolates in Vietnam and Taiwan revealed that more than 80% of the isolates were of the canine parvovirus (CPV) type, rather than feline panleukopenia virus (FPLV). Although parvovirus isolates from three Vietnamese leopard cats were genetically related to CPV type 2a or 2b, they had a natural mutation of VP2 residue 300 Gly to an Asp, resulting in remarkable changes in their antigenic properties. These results indicated the possibility that CPV-2a/2b-type viruses can spread in cats more efficiently than conventional FPLV under natural conditions and that CPV-2a/2b viruses are further evolving in cats.

Feline immunodeficiency virus (FIV) induces a disease similar to acquired immunodeficiency syndrome (AIDS) in cats, yet in contrast to human immunodeficiency virus (HIV), CD4 is not the viral receptor. We identified a primary receptor for FIV as CD134 (OX40), a T cell activation antigen and costimulatory molecule. CD134 expression promotes viral binding and renders cells permissive for viral entry, productive infection, and syncytium formation. Infection is CXCR4-dependent, analogous to infection with X4 strains of HIV. Thus, despite the evolutionary divergence of the feline and human lentiviruses, both viruses use receptors that target the virus to a subset of cells that are pivotal to the acquired immune response.

Nine isolates of Canine parvovirus (CPV) were obtained from Vietnamese dogs and cats. One canine isolate showed a unique antigenic property which indicates a novel antigenic variant of CPV-2b when examined with hemagglutination inhibition tests using our monoclonal antibodies, 21C3 and 19D7, which were recently developed. This isolate had an amino acid substitution of residue 426, Asp to Glu, and the same substitution has recently been found in CPV from Italian dogs. This study first showed that such substitution caused an antigenic difference demonstrable by monoclonal antibodies and that a similar evolution may have occurred in CPV in Vietnam.

Xenotransplantation of porcine tissues has the potential to treat a wide variety of major health problems including organ failure and diabetes. Balanced against the potential benefits of xenotransplantation, however, is the risk of human infection with a porcine microorganism. In particular, the transmission of porcine endogenous retrovirus (

The life cycle of calicivirus is not fully understood because most of the viruses cannot be propagated in tissue culture cells. We studied the mechanism of calicivirus entry into cells using feline calicivirus (FCV) The family Caliciviridae comprises a diversity of pathogens in humans and animals. Studies of the life cycle of the virus have been quite limited because of the lack of cell culture methods for most caliciviruses (13). Porcine enteric calicivirus in the genus Sapovirus is known to propagate in vitro with the addition of an intestinal content fluid filtrate, and Chang et al. (6) recently identified bile acids as molecules responsible for culture in cells. Studies with virus-like particles showed that ABH histo-blood group antigens are ligands of noroviruses belonging to the genus Norovirus (24). Studies in vivo also showed that these antigens are critical for human susceptibility to norovirus infection (17,22). Because noroviruses are not cultivable in cell culture (9), it has not been established whether ABH histo-blood antigens function as receptors for them.,Feline calicivirus (FCV) is a member of the genus Vesivirus and causes upper respiratory tract disease and acute mouth ulceration, occasionally associated with chronic stomatitis and acute arthritis in cats (15,21). It is comparatively easy to study the life cycle of FCV, because the virus replicates efficiently in cell culture without specific supplementation. Kreutz et al. (20) investigated the binding of FCV to feline and nonfeline cells.They reported that FCV bound to feline cells but also showed poor binding ability to nonfeline cells. It was also demonstrated that when nonfeline cells were transfected with genomic RNA of FCV, infectious virus could be recovered from the cells (20). These data suggest that FCV host specificity is restricted in the early stage of FCV infection in cells.In this study, to elucidate the cellular determinant(s) of FCV host specificity, we applied an improved expression cloning method (28,29) to identify cell surface molecules that interact with FCV. As a result, feline junctional adhesion molecule 1 (JAM-1) was identified as a binding receptor for FCV. JAM-1 is a member of the immunoglobulin (Ig) superfamily expressed by various cells and is involved in regulation of cell-cell interactions in the immune system and apical tight junction formation (10, 23). We here demonstrate that feline JAM-1 (fJAM-1) possesses the characteristics required of a functional receptor for FCV. MATERIALS AND METHODS Cells.Crandell-Rees feline kidney (CRFK) cells and human embryonic kidney 293T cells were cultured in Dulbecco's modified Eagle's medium (DMEM; Sigma, St. Louis, MO) supplemented with 10% fetal calf serum (FCS). Nonpermissive hamster lung (HmLu-1) cells and African green monkey kidney (Vero) cells were cultured in DMEM with 5% FCS. Murine myeloma P3X63Ag8U.1 (P3U1) cells were grown in RPMI 1640 medium (Sigma) with 10% FCS. Plat-E cells, a 293T-derived murine leukemia virus-based packaging cell line (25), were kindly pr...

We identified a new subgroup of koala retrovirus (KoRV), named KoRV-J, which utilizes thiamine transport protein 1 as a receptor instead of the Pit-1 receptor used by KoRV (KoRV-A). By subgroup-specific PCR, KoRV-J and KoRV-A were detected in 67.5 and 100% of koalas originating from koalas from northern Australia, respectively. Altogether, our results indicate that the invasion of the koala population by KoRV-J may have occurred more recently than invasion by KoRV-A.

During pilot studies to investigate the presence of viral RNA of xenotropic murine leukemia virus (MLV)-related virus (XMRV) infection in sera from chronic fatigue syndrome (CFS) patients in Japan, a positive band was frequently detected at the expected product size in negative control samples when detecting a partial gag region of XMRV using a one-step RT-PCR kit. We suspected that the kit itself might have been contaminated with small traces of endogenous MLV genome or XMRV and attempted to evaluate the quality of the kit in two independent laboratories. We purchased four one-step RT-PCR kits from Invitrogen, TaKaRa, Promega and QIAGEN in Japan. To amplify the partial gag gene of XMRV or other MLV-related viruses, primer sets (419F and 1154R, and GAG-I-F and GAG-I-R) which have been widely used in XMRV studies were employed. The nucleotide sequences of the amplicons were determined and compared with deposited sequences of a polytropic endogenous MLV (PmERV), XMRV and endogenous MLV-related viruses derived from CFS patients. We found that the enzyme mixtures of the one-step RT-PCR kit from Invitrogen were contaminated with RNA derived from PmERV. The nucleotide sequence of a partial gag region of the contaminant amplified by RT-PCR was nearly identical (99.4% identity) to a PmERV on chromosome 7 and highly similar (96.9 to 97.6%) to recently identified MLV-like viruses derived from CFS patients. We also determined the nucleotide sequence of a partial env region of the contaminant and found that it was almost identical (99.6%) to the PmERV. In the investigation of XMRV infection in patients of CFS and prostate cancer, researchers should prudently evaluate the test kits for the presence of endogenous MLV as well as XMRV genomes prior to PCR and RT-PCR tests.

Feline morbillivirus (FmoPV) is an emerging virus in domestic cats and considered to be associated with tubulointerstitial nephritis. Although FmoPV was first described in China in 2012, there has been no report of the isolation of this virus in other countries. In this report, we describe the isolation and characterization of FmoPV from domestic cats in Japan. By using reverse transcription (RT)-PCR, we found that three of 13 urine samples from cats brought to veterinary hospitals were positive for FmoPV. FmoPV strains SS1 to SS3 were isolated from the RT-PCRpositive urine samples. Crandell-Rees feline kidney (CRFK) cells exposed to FmoPV showed cytopathic effects with syncytia formation, and FmoPV N protein was detected by indirect immunofluorescence assays. In addition, pleomorphic virus particles with apparent glycoprotein envelope spikes were observed by electron microscopy. By sequence analysis of FmoPV H and L genes, we found that FmoPVs showed genetic diversity; however, signatures of positive selection were not identified.