scholarly journals Experimental Mucosal Infection with Molecularly Cloned Feline Immunodeficiency Viruses

2003 ◽  
Vol 10 (1) ◽  
pp. 185-188 ◽  
Author(s):  
Mariko Kohmoto ◽  
Yasuhiro Ikeda ◽  
Eiji Sato ◽  
Yorihiro Nishimura ◽  
Yasuo Inoshima ◽  
...  
Keyword(s):  
Virus Strain ◽  
Feline Immunodeficiency Virus ◽  
Deletion Mutant ◽  
Cell Tropism ◽  
Specific Pathogen Free ◽  
Mucosal Epithelium ◽  
Immunodeficiency Virus ◽  
Mucosal Infection ◽  
Specific Pathogen

ABSTRACT Four of six specific pathogen-free cats were infected after intravaginal exposure to molecularly cloned lymphotropic but non-Crandell feline kidney (CRFK)-tropic feline immunodeficiency virus strain TM2 and its AP-1 deletion mutant. The sequences of the env V3-to-V5 region which defines the CRFK tropism were unchanged in the infected cats through the infection. These data suggest that the strain was transmitted across the mucosal epithelium without a broadening of cell tropism.

scholarly journals Molecularly cloned feline immunodeficiency virus NCSU1 JSY3 induces immunodeficiency in specific-pathogen-free cats.

1996 ◽  
Vol 70 (5) ◽  
pp. 3011-3017 ◽  
Author(s):  
J S Yang ◽  
R V English ◽  
J W Ritchey ◽  
M G Davidson ◽  
T Wasmoen ◽  
...  
Keyword(s):  
Feline Immunodeficiency Virus ◽  
Specific Pathogen Free ◽  
Immunodeficiency Virus ◽  
Specific Pathogen

scholarly journals A feline immunodeficiency virus vif-deletion mutant remains attenuated upon infection of newborn kittens

2007 ◽  
Vol 88 (10) ◽  
pp. 2793-2799 ◽  
Author(s):  
Xiaoying Shen ◽  
Christian M. Leutenegger ◽  
Kelly Stefano Cole ◽  
Niels C. Pedersen ◽  
Ellen E. Sparger
Keyword(s):  
T Cell ◽  
Feline Immunodeficiency Virus ◽  
Peripheral Blood ◽  
Deletion Mutant ◽  
Cell Subset ◽  
Cd4 T Cell ◽  
Wild Type ◽  
Immunodeficiency Virus ◽  
Antiviral Antibody ◽  
Cd4 T Cell Count

This report characterizes lentivirus attenuation associated with a vif mutation by inoculation of newborn kittens with a vif-deleted feline immunodeficiency virus provirus plasmid (FIV-pPPRΔvif). Virus in peripheral blood, antiviral antibody or CD4 T-cell count alterations were not detected in kittens inoculated with FIV-pPPRΔvif plasmid, with the exception of one kitten that demonstrated FIV Gag antibody production at 42 weeks after inoculation. In contrast, wild-type FIV-pPPR-infected kittens were viraemic, seropositive and exhibited a decrease in the CD4 T-cell subset in peripheral blood. Interestingly, FIV-specific T-cell proliferative responses detected at 32 and 36 weeks after infection were comparable for both FIV-pPPRΔvif- and wild-type FIV-pPPR-inoculated kittens and suggested the possibility of a discreet tissue reservoir supporting sustained FIV-pPPRΔvif expression or replication. Overall, these findings confirmed that the severe virus attenuation for both replication and pathogenicity exhibited by a vif-deleted FIV mutant is similar for both neonatal and adult hosts.

Mucosal infection and vaccination against feline immunodeficiency virus

1999 ◽  
Vol 73 (2-3) ◽  
pp. 213-221 ◽  
Author(s):  
C.R Stokes ◽  
S Finerty ◽  
T.J Gruffydd-Jones ◽  
C.P Sturgess ◽  
D.A Harbour
Keyword(s):  
Feline Immunodeficiency Virus ◽  
Immunodeficiency Virus ◽  
Mucosal Infection

scholarly journals AIDS Vaccination Studies Using an Ex Vivo Feline Immunodeficiency Virus Model: Homologous Erythrocytes as a Delivery System for Preferential Immunization with Putative Protective Antigens

1998 ◽  
Vol 5 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Laura Chiarantini ◽  
Donatella Matteucci ◽  
Mauro Pistello ◽  
Umberto Mancini ◽  
Paola Mazzetti ◽  
...  
Keyword(s):  
Feline Immunodeficiency Virus ◽  
Vaccine Development ◽  
Ex Vivo ◽  
Degree Of Protection ◽  
Aids Vaccine ◽  
Protective Antigens ◽  
Homologous Virus ◽  
Immunodeficiency Virus ◽  
Specific Pathogen

ABSTRACT Feline immunodeficiency virus (FIV) is a useful model for testing of criteria for AIDS vaccine development. In the protocol we adopted, we used a primary isolate of FIV as a source of antigen and, for challenge, plasma from cats infected with the homologous virus never passaged in vitro. Cat erythrocytes (RBC) were coated with the surface components of freshly harvested and purified FIV by means of biotin-avidin-biotin bridges and used to immunize specific-pathogen-free cats (four doses at monthly intervals; total amount of FIV antigen administered per cat, approximately 14 μg). Immunized cats developed moderate levels of antibodies directed mainly to surface components of the virion and clearly evident lymphoproliferative responses. Four months after the last dose of immunogen, FIV-immunized cats and control cats immunized with bovine serum albumin-coated RBC were challenged. Judged from the results of the subsequent 12-month follow-up, FIV-immunized cats exhibited at least some degree of protection. However, following rechallenge, most of the FIV-immunized animals became virus positive in spite of a booster immunogen dose given 2 months before the second challenge.

scholarly journals Differential Cell Tropism of Feline Immunodeficiency Virus Molecular Clones In Vivo

1999 ◽  
Vol 73 (4) ◽  
pp. 2596-2603 ◽  
Author(s):  
Gregg A. Dean ◽  
Sunee Himathongkham ◽  
Ellen E. Sparger
Keyword(s):  
Feline Immunodeficiency Virus ◽  
Mononuclear Cells ◽  
Lymphocyte Subsets ◽  
Cell Tropism ◽  
Replication Efficiency ◽  
Proviral Dna ◽  
Immunodeficiency Virus ◽  
Differential Cell

ABSTRACT Independent studies have demonstrated different cell tropisms for molecular clones of feline immunodeficiency virus (FIV). In this report, we examined three clones, FIV-pF34, FIV-14, and FIV-pPPR, for replication in Crandell feline kidney (CrFK) cells, feline peripheral blood mononuclear cells (PBMC), and feline macrophage cultures. Importantly, cell tropism for these three clones was also examined in vivo. FIV-pF34 replication was efficient in CrFK cells but severely restricted in PBMC, whereas replication of FIV-pPPR was vigorous in PBMC but severely restricted in CrFK cells. FIV-14 replication was productive in both CrFK cells and PBMC. Interestingly, all three molecular clones replicated with similar efficiencies in primary feline monocyte-derived macrophages. In vivo, FIV-pF34 proved least efficient for establishing persistent infection, and proviral DNA when detectable, was localized predominately to nonlymphoid cell populations (macrophages). FIV-pPPR proved most efficient for induction of a persistent viremia in vivo, and proviral DNA was localized predominately in CD4+ and CD8+ lymphocyte subsets. FIV-14 inoculation of cats resulted in an infection characterized by seroconversion and localization of proviral DNA in CD4+ lymphocytes only. Results of this study on diverse FIV molecular clones revealed that in vitro replication efficiency of an FIV isolate in PBMC directly correlated with replication efficiency in vivo, whereas proficiency for replication in macrophages in vitro was not predictive for replication potential in vivo. Also, infection of both CD4+ and CD8+ lymphocyte subsets was associated with higher virus load in vivo. Results of the studies on these three FIV clones, which exhibited differential cell tropism, indicated a correlation between in vitro and in vivo cell tropism and virus replication.

scholarly journals Lentivirus Infection in the Brain Induces Matrix Metalloproteinase Expression: Role of Envelope Diversity

2000 ◽  
Vol 74 (16) ◽  
pp. 7211-7220 ◽  
Author(s):  
J. B. Johnston ◽  
Y. Jiang ◽  
G. van Marle ◽  
M. B. Mayne ◽  
W. Ni ◽  
...  
Keyword(s):  
Feline Immunodeficiency Virus ◽  
Sequence Diversity ◽  
Conditioned Media ◽  
Envelope Gene ◽  
Cell Tropism ◽  
Protein Levels ◽  
Immunodeficiency Virus ◽  
Envelope Sequence ◽  
The Brain

ABSTRACT Infection of the brain by lentiviruses, including human immunodeficiency virus (HIV) and feline immunodeficiency virus (FIV), causes inflammation and results in neurodegeneration. Molecular diversity within the lentivirus envelope gene has been implicated in the regulation of cell tropism and the host response to infection. Here, we examine the hypothesis that envelope sequence diversity modulates the expression of host molecules implicated in lentivirus-induced brain disease, including matrix metalloproteinases (MMP) and related transcription factors. Infection of primary macrophages by chimeric HIV clones containing brain-derived envelope fragments from patients with HIV-associated dementia (HAD) or nondemented AIDS patients (HIV-ND) showed that MMP-2 and -9 levels in conditioned media were significantly higher for the HAD clones. Similarly, STAT-1 and JAK-1 levels were higher in macrophages infected by HAD clones. Infections of primary feline macrophages by the neurovirulent FIV strain (V1CSF), the less neurovirulent strain (Petaluma), and a chimera containing the V1CSF envelope in a Petaluma background (FIV-Ch) revealed that MMP-2 and -9 levels were significantly higher in conditioned media from V1CSF- and FIV-Ch-infected macrophages, which was associated with increased intracellular STAT-1 and JAK-1 levels. The STAT-1 inhibitor fludarabine significantly reduced MMP-2 expression, but not MMP-9 expression, in FIV-infected macrophages. Analysis of MMP mRNA and protein levels in brain samples from HIV-infected persons or FIV-infected cats showed that MMP-2 and -9 levels were significantly increased in lentivirus-infected brains compared to those of uninfected controls. Elevated MMP expression was accompanied by significant increases in STAT-1 and JAK-1 mRNA and protein levels in the same brain samples. The present findings indicate that two lentiviruses, HIV and FIV, have common mechanisms of MMP-2 and -9 induction, which is modulated in part by envelope sequence diversity and the STAT-1/JAK-1 signaling pathway.

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