Phylogenetic analysis to define feline immunodeficiency virus subtypes in 31 domestic cats in South Africa

Feline immunodeficiency virus (FIV), a lentivirus, is an important pathogen of domestic cats around the world and has many similarities to human immunodeficiency virus (HIV). A characteristic of these lentiviruses is their extensive genetic diversity which has been an obstacle in the development of successful vaccines. Of the FIV genes, the envelope gene is the most variable and sequence differences in a portion of this gene have been used to define 5 FIV subtypes (A, B, C, D and E). In this study, the proviral DNA sequence of the V3-V5 region of the envelope gene was determined in blood samples from 31 FIV positive cats from 4 different regions of South Africa. Phylogenetic analysis demonstrated the presence of both subtypes A and C, with subtype A predominating. These findings contribute to the understanding of the genetic diversity of FI

Genetic diversity of Brazilian isolates of feline immunodeficiency virus

We isolated Feline immunodeficiency virus (FIV) from three adult domestic cats, originating from two open shelters in Brazil. Viruses were isolated from PBMC following co-cultivation with the feline T-lymphoblastoid cell line MYA-1. All amplified env gene products were cloned directly into pGL8MYA. The nucleic acid sequences of seven clones were determined and then compared with those of previously described isolates. The sequences of all of the Brazilian virus clones were distinct and phylogenetic analysis revealed that all belong to subtype B. Three variants isolated from one cat and two variants were isolated from each of the two other cats, indicating that intrahost diversity has the potential to pose problems for the treatment and diagnosis of FIV infection

Quasispecies and naturally occurring superinfection in feline immunodeficiency virus infection

Analysis of individual clones containing the V1 and V2 domains of the segment of the FIV env gene present in a naturally infected cat (T) was carried out. The polymerase chain reaction (PCR) was used to amplify proviral FIV DNA extracted from peripheral blood mononuclear cells (PBMCs) obtained in October 1994 from this cat. The PCR products were cloned and the DNA sequences determined for 11 clones. Sequences obtained were aligned with sequences corresponding to FIV isolates (T90, T91, T92) previously obtained from the same cat in 1990, 1991 and 1992. Phylogenetic analysis was performed which included consensus sequences of another Australian isolate, N91, as well as UK, US, Swiss and Japanese isolates of FIV. All clones varied from each other, and none of these clones was identical to the consensus sequences of the isolates obtained previously from the same cat (the T-series). However, most of these clones appeared to have originated from the ancestor of the most recent isolate (T92). In addition, 2 of the clones (7 and 11) are closely related to another Australian isolate N91, obtained from a different cat (N) in 1991. Because these two cats (T and N) were housed together for at least 3 years (1990-1993) it is suggested that the first cat (T) has become superinfected with an isolate from a second cat (N) under natural conditions. The identification of clones of differing sequences, which were not identical to each other nor to their ancestors, emphasises the rapid mutation of lentiviruses within the env region, and the difficulty of developing an effective FIV vaccine. More importantly, the possibility of natural superinfection with FIV in cats has implications for the development of a successful lentiviral vaccine

Characterisation of lymphosarcomas in Australian cats using polymerase chain reaction and immunohistochemical examination

Objective: To examine tumour tissue of cats with lymphosarcoma for the presence of feline leukaemia virus and feline immunodeficiency virus and analyse the immunophenotype of the tumours. Design: A retrospective study of feline lymphosarcoma cases. Methods: Formalin-fixed, paraffin-embedded tumour tissue of 14 feline lymphosarcomas was examined for the presence of feline leukaemia virus and feline immunodeficiency virus by polymerase chain reaction and immunohistochemistry. Using polyclonal and monoclonal antibodies against T and B lymphocytes, the phenotypic expression of the tumours was characterised. Results: No feline leukaemia virus antigen or proviral sequences were detected. Feline immunodeficiency virus proviral sequences were detected in two cases by polymerase chain reaction. Immunophenotyping of all 14 cases resulted in seven cases being classified as B-cell phenotype, four as T-cell phenotype, and the remaining three undetermined. Conclusions: In contrast to previous reports overseas, our results suggest that feline leukaemia virus infection appears to be an infrequent cause of lymphosarcoma in the cats that were necropsied. Feline immunodeficiency virus may have a role in lymphomagenesis. The potential role of feline immunodeficiency virus needs to be explored in more depth. Compared with most previous reports, B-cell tumours were more common than T-cell tumours in this series of cats

Feline immunodeficiency virus replicates in salivary gland ductular epithelium during the initial phase of infection

Feline immunodeficiency virus (FIV) antigen was detected by immunochemistry in salivary glands of cats experimentally inoculated with West Australian isolate T91. Six cats were inoculated subcutaneously with 1.0 ml of tissue culture supernatant fluid from a feline T-lymphoblastoid cell line (MYA-1) infected with T91. FIV antigens were detected in the interlobular ducts of the salivary gland of cats infected with FIV 2, 4 and 6 weeks previously. FIV antigen was not detected in the salivary glands of three FIV negative cats and one naturally infected cat. Further, FIV antigen was located only in interlobular duct epithelial cells. The distribution of FIV in the interlobular ducts confirms the important role of salivary glands as a major reservoir of FIV in the early phase of infection and strengthens suggestions that the salivary route is an important mode of transmission of FIV

T-cell-rich B-cell lymphoma in the cat

The clinical and pathological features of eight cases of feline T-cell-rich B-cell lymphoma are described. The disease occurred in older cats (mean age 11.4 ± 3.9 years), which on initial examination generally showed enlargement of a single submandibular or cervical lymph node. After excision, there was no recurrence of the lesions at 6 months in three cats. In one further case, however, the lesion had recurred 6 months later; it was again excised but recurred after an additional 6 months. Microscopically, there was effacement of normal lymph node architecture by a nodular (n = 4) or diffuse (n = 4) proliferation of small to blastic lymphocytes, accompanied by a characteristic population of bizarre giant, or multinucleate, cells. The mitotic rate was low and mitoses were restricted to the atypical population. Immunophenotyping revealed the smaller lymphocytes to be a mixture of CD3 MHC Class II T lymphoctes and BLA36CD79(variable) MHC Class II(variable) B lymphocytes. The atypical cells were of the B-cell lineage (BLA36MHC Class II(variable). Polymerase chain reaction analysis revealed no proviral DNA products of feline leukaemia virus or feline immunodefficiency virus in tissue from any tumour, confirming that these neoplasms were not associated with either virus. The clinical, histological and immunophenotypic findings in these cats were identical with those of 'nodular lymphocyte predominance (lymphocytic and histiocytic/LandH) Hodgkin's disease' in man