Anti-Feline Immunodeficiency Virus (FIV) Soluble Factor(s) Produced from Antigen-Stimulated Feline CD8<sup>+</sup>T Lymphocytes Suppresses FIV Replication

Choi, In‐Soo; Hokanson, R; Collisson, Ellen W.

doi:10.1128/jvi.74.2.676-683.2000

Cited by 30 publications

(17 citation statements)

References 47 publications

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“…on May 10, 2018 by guest http://jvi.asm.org/ responses were not measured in these studies, earlier reports imply that cell-mediated responses may be responsible for the observed survival of this one offspring (5,7,13,14). The finding that the dams became infected in both experiments where they nursed infected offspring is surprising and of great interest.…”

Section: Vol 78 2004 Highly Pathogenic Molecular Clone Of Fiv-c 8979contrasting

confidence: 44%

Characterization of a Highly Pathogenic Molecular Clone of Feline Immunodeficiency Virus Clade C

Rozieres

Mathiason

Rolston

et al. 2004

J Virol

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We have derived and characterized a highly pathogenic molecular isolate of feline immunodeficiency virus subtype C (FIV-C) CABCpady00C. Clone FIV-C36 was obtained by lambda cloning from cats that developed severe immunodeficiency disease when infected with CABCpady00C (Abbotsford, British Columbia, Canada). Clone FIV-C36 Env is 96% identical to the noninfectious FIV-C isolate sequence deposited in GenBank (FIV-Cgb; GenBank accession number AF474246) (A. Harmache et al.) but is much more divergent in Env when compared to the subgroup A clones Petaluma (34TF10) and FIV-PPR (76 and 78% divergence, respectively). Clone FIV-C36 was able to infect freshly isolated feline peripheral blood mononuclear cells and primary T-cell lines but failed to productively infect CrFK cells, as is typical of FIV field isolates. Two-week-old specific-pathogen-free cats infected with FIV-C36 tissue culture supernatant became PCR positive and developed severe acute immunodeficiency disease similar to that caused by the uncloned CABCpady00C parent. At 4 to 5 weeks postinfection (PI), 3 of 4 animals developed CD4+-T-cell depletion, fever, weight loss, diarrhea, and opportunistic infections, including ulcerative stomatitis and tonsillitis associated with abundant bacterial growth, pneumonia, and pyelonephritis, requiring euthanasia. Histopathology confirmed severe thymic and systemic lymphoid depletion. Interestingly, the dam also became infected with a high viral load at 5 weeks PI of the kittens and developed a similar disease syndrome, requiring euthanasia at 11 weeks PI of the kittens. This constitutes the first report of a replication-competent, infectious, and pathogenic molecular clone of FIV-C. Clone FIV-C36 will facilitate dissection of the pathogenic determinants of FIV

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Section: Vol 78 2004 Highly Pathogenic Molecular Clone Of Fiv-c 8979contrasting

confidence: 44%

Characterization of a Highly Pathogenic Molecular Clone of Feline Immunodeficiency Virus Clade C

Rozieres

Mathiason

Rolston

et al. 2004

J Virol

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“…Studies on the Petaluma isolate of FIV (FIV PET ) have shown that the human b-chemokines RANTES, MIP-1a, MIP-1b, and MCP-1 could not prevent infection of CrFK cells or T lymphocytes, whilst human SDF-1a could inhibit FIV PET infection of CrFK cells but not T cell lines, depending on the incubation conditions . In contrast, studies on another American isolate of FIV (FIV PPR ), which has 91% homology with FIV PET at the amino acid level, have revealed that human MIP-1a did suppress FIV replication in PBMC at a concentration of 500 ng/ml, whereas human SDF-1a used at the same concentration actually caused increased expression of FIV rather than suppression (Choi et al, 2000). Clari®ca-tion on the role of feline b-chemokines in CD8 T cell-mediated suppression of FIV replication will be reliant upon the availability of these recombinant feline proteins in the future.…”

Section: Discussionmentioning

confidence: 90%

“…Following infection with FIV the host mounts a vigorous virus-speci®c cytotoxic T cell (CTL) response which precedes the development of virus-speci®c humoral immunity (Song et al, 1992;Beatty et al, 1996). In addition, non-cytolytic CD8 T cells, which suppress virus replication in a non-MHC-restricted manner by the secretion of soluble factors, have been described during acute and asymptomatic stages of FIV infection (Jeng et al, 1996;Hohdatsu et al, 1998;Veterinary Immunology and Immunopathology 85 (2002) 159±170 Flynn et al, 1999;Choi et al, 2000). Studies aimed at elucidating the immune correlates of vaccinal immunity have revealed that virus neutralising antibodies, virus-speci®c CTLs, and CD8 T cells capable of suppressing FIV replication, are all involved, either acting alone or in concert (Flynn et al, , 1999Hosie and Flynn, 1996).…”

Section: Introductionmentioning

confidence: 99%

Involvement of cytolytic and non-cytolytic T cells in the control of feline immunodeficiency virus infection

Flynn

Dunham

Mueller

et al. 2002

Veterinary Immunology and Immunopathology

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The appearance of non-cytolytic T cells that suppressed feline immunode®ciency virus (FIV) replication in vitro, and FIV-speci®c cytotoxic T cell (CTL) responses was compared in a group of seven, speci®c pathogen free (SPF) domestic cats following primary infection with the Glasgow 8 isolate of FIV (FIV ). FIV proviral burdens were quanti®ed in the blood and lymphoid tissues by real-time PCR. Non-cytolytic T cell suppression of FIV replication was measured by co-cultivating lymphoblasts prepared from the cats at different time-points during infection with FIV-infected MYA-1 cells in vitro. Non-cytolytic suppressor activity was detected as early as 1 week after infection, and was evident in all the lymphoid tissues examined. Further, this activity was present in subpopulations of T cells in the blood with normal (CD8 hi ) or reduced (CD8 lo ) expression of the CD8 molecule, and temporal modulations in non-cytolytic suppressor activity were unrelated to the circulating CD8 T cell numbers. Virus-speci®c CTL responses, measured by 51 Cr release assays, were not detected until 4 weeks after infection, with the emergence of FIV-speci®c effector CTLs in the blood. Throughout infection the response was predominantly directed towards FIV Gag-expressing target cells, and by 47 weeks after infection CTL responses had become localised in the lymph nodes and spleen. The results suggest that both non-cytolytic T cell suppression of FIV replication and FIV-speci®c CTL responses are important cellular immune mechanisms in the control of FIV replication in infected asymptomatic cats. #

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“…In either case, the absence of this correlation suggests that other mechanisms could be used to resolve viral infection in the absence of a cytotoxic T-lymphoctye response, such as the noncytolytic mechanisms reported in the resolution of hepatitis B virus infection (28). In addition, both cytolytic and noncytolytic T cells are involved in the control of feline immunodeficiency virus infection (15,23). Interestingly, natural killer (NK) cell cytotoxic activity increased from 15 to 35% of specific lysis in T cells cultured from PRRSV-infected pigs and restimulated with PRRSV for 3 weeks (37).…”

Section: Vol 78 2004 Prrsv Load Is Independent Of T-cell Response Imentioning

confidence: 97%

The Level of Virus-Specific T-Cell and Macrophage Recruitment in Porcine Reproductive and Respiratory Syndrome Virus Infection in Pigs Is Independent of Virus Load

Xiao¹,

Batista

Dee

et al. 2004

J Virol

162

126

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Porcine reproductive and respiratory syndrome virus (PRRSV) is the most important infectious disease agent of pigs worldwide, causing reproductive failure in pregnant sows and respiratory problems in nursing and growing pigs. PRRSV infection is characterized by a prolonged viremia of 30 or more days and an extended persistent infection of lymphoid tissues. To better understand the immunological basis for prolonged acute and persistent PRRSV infection, we have examined the cell-mediated immune (CMI) response throughout the course of infection and compared the results to the local distribution and abundance of PRRSV in infected tissues. PRRSV-specific T cells, enumerated by gamma interferon enzyme-linked immunospot assay, did not appear until 2 weeks after PRRSV inoculation, and their abundance exhibited substantial variation over time and among animals. In all cases the T-cell response was transient. High levels of viral RNA were present in lymphoid tissues of all animals in the acute phase of infection. Viral loads were decreased 1,000-fold or more in persistent infections, with the primary sites of persistence being tonsil, sternal lymph node, and inguinal lymph node. The abundance of virus-specific T cells in either acutely or persistently infected animals was highly variable and showed no correlation to the level of virus in lymphoid tissues. No significant difference in antigen-specific T-cell abundance was observed in secondary lymphoid tissues in either acute or persistent infection except for tonsil, in which the number of responding cells was extremely low. CD4؉ -and CD8 ؉ -T-cell frequencies did not change after PRRSV infection, though a decrease in ␥␦ T cells was observed. Macrophages, the permissive cell type for PRRSV, were present in various levels in all tissue preparations and were not in proportion to local virus load. These findings indicate that a weak CMI response contributes to prolonged PRRSV infection and suggests that PRRSV suppresses T-cell recognition of infected macrophages. Thus, the slow but eventual resolution of PRRSV infection may be dependent on limiting permissive macrophages and on innate immune factors.

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Anti-Feline Immunodeficiency Virus (FIV) Soluble Factor(s) Produced from Antigen-Stimulated Feline CD8⁺T Lymphocytes Suppresses FIV Replication

Cited by 30 publications

References 47 publications

Characterization of a Highly Pathogenic Molecular Clone of Feline Immunodeficiency Virus Clade C

Characterization of a Highly Pathogenic Molecular Clone of Feline Immunodeficiency Virus Clade C

Involvement of cytolytic and non-cytolytic T cells in the control of feline immunodeficiency virus infection

The Level of Virus-Specific T-Cell and Macrophage Recruitment in Porcine Reproductive and Respiratory Syndrome Virus Infection in Pigs Is Independent of Virus Load

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Anti-Feline Immunodeficiency Virus (FIV) Soluble Factor(s) Produced from Antigen-Stimulated Feline CD8+T Lymphocytes Suppresses FIV Replication

Cited by 30 publications

References 47 publications

Characterization of a Highly Pathogenic Molecular Clone of Feline Immunodeficiency Virus Clade C

Characterization of a Highly Pathogenic Molecular Clone of Feline Immunodeficiency Virus Clade C

Involvement of cytolytic and non-cytolytic T cells in the control of feline immunodeficiency virus infection

The Level of Virus-Specific T-Cell and Macrophage Recruitment in Porcine Reproductive and Respiratory Syndrome Virus Infection in Pigs Is Independent of Virus Load

Contact Info

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Anti-Feline Immunodeficiency Virus (FIV) Soluble Factor(s) Produced from Antigen-Stimulated Feline CD8⁺T Lymphocytes Suppresses FIV Replication