Downmodulation of CD3ε expression in CD8α + β − T cells of feline immunodeficiency virus-infected cats

Nishimura, Yorihiro; Shimojima, Masayuki; Sato, Eiji; Izumiya, Yoshihiro; Tohya, Yukinobu; Mikami, Takeshi; Miyazawa, Takayuki

doi:10.1099/vir.0.80102-0

Cited by 21 publications

(19 citation statements)

References 39 publications

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“…Antibodies against feline CD3 (NZM1) [27], CD4 (30A) [28], CD8α (3.357) [28], and IFN-γ (E6D4A5) [29] were purified from hybridoma supernatants in our lab. Anti-CD80 (B7.1.66) was generously provided by Dr. Mary Tompkins of North Carolina State University [30].…”

Section: Methodsmentioning

confidence: 99%

Partial Regulatory T Cell Depletion Prior to Acute Feline Immunodeficiency Virus Infection Does Not Alter Disease Pathogenesis

et al. 2011

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Feline immunodeficiency virus (FIV) infection in cats follows a disease course similar to HIV-1, including a short acute phase characterized by high viremia, and a prolonged asymptomatic phase characterized by low viremia and generalized immune dysfunction. CD4+CD25hiFoxP3+ immunosuppressive regulatory T (Treg) cells have been implicated as a possible cause of immune dysfunction during FIV and HIV-1 infection, as they are capable of modulating virus-specific and inflammatory immune responses. Additionally, the immunosuppressive capacity of feline Treg cells has been shown to be increased during FIV infection. We have previously shown that transient in vivo Treg cell depletion during asymptomatic FIV infection reveals FIV-specific immune responses suppressed by Treg cells. In this study, we sought to determine the immunological influence of Treg cells during acute FIV infection. We asked whether Treg cell depletion prior to infection with the highly pathogenic molecular clone FIV-C36 in cats could alter FIV pathogenesis. We report here that partial Treg cell depletion prior to FIV infection does not significantly change provirus, viremia, or CD4+ T cell levels in blood and lymphoid tissues during the acute phase of disease. The effects of anti-CD25 mAb treatment are truncated in cats acutely infected with FIV-C36 as compared to chronically infected cats or FIV-naïve cats, as Treg cell levels were heightened in all treatment groups included in the study within two weeks post-FIV infection. Our findings suggest that the influence of Treg cell suppression during FIV pathogenesis is most prominent after Treg cells are activated in the environment of established FIV infection.

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Section: Methodsmentioning

confidence: 99%

Partial Regulatory T Cell Depletion Prior to Acute Feline Immunodeficiency Virus Infection Does Not Alter Disease Pathogenesis

et al. 2011

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“…Lymphocytes may lose the ability to proliferate in response to stimulation with mitogens or antigens, and priming of lymphocytes by immunogens may be impaired [105,133,134,135,136,137,138,139]. Lymphocyte function may be reduced by altered expression of cell surface molecules, such as CD4, major histocompatibility complex II antigens, or cytokines and cytokine receptors [140,141,142,143,144], or through over-expression of abnormal molecules, such as receptors [145], leading to disrupted production of cytokines or receptor function. Impaired neutrophil adhesion and emigration in response to bacterial products have been described in FIV-infected cats [146,147,148].…”

Section: Clinical Signsmentioning

confidence: 99%

Clinical Aspects of Feline Retroviruses: A Review

Hartmann¹

2012

Viruses

274

301

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Feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) are retroviruses with global impact on the health of domestic cats. The two viruses differ in their potential to cause disease. FeLV is more pathogenic, and was long considered to be responsible for more clinical syndromes than any other agent in cats. FeLV can cause tumors (mainly lymphoma), bone marrow suppression syndromes (mainly anemia), and lead to secondary infectious diseases caused by suppressive effects of the virus on bone marrow and the immune system. Today, FeLV is less commonly diagnosed than in the previous 20 years; prevalence has been decreasing in most countries. However, FeLV importance may be underestimated as it has been shown that regressively infected cats (that are negative in routinely used FeLV tests) also can develop clinical signs. FIV can cause an acquired immunodeficiency syndrome that increases the risk of opportunistic infections, neurological diseases, and tumors. In most naturally infected cats, however, FIV itself does not cause severe clinical signs, and FIV-infected cats may live many years without any health problems. This article provides a review of clinical syndromes in progressively and regressively FeLV-infected cats as well as in FIV-infected cats.

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“…Moreover, HIV-1 specific CD8+ T cells have been detected prior to the detection of a humoral response [34]–[37]. The acute phase of FIV infection is accompanied by the rapid expansion of a CD8+ lymphocyte population that is thought to represent an activated T cell population responding to virus replication [31], [38], [39]. Both Group 1 and Group 2 cats displayed such an expanded population (Fig.…”

Section: Resultsmentioning

confidence: 99%

Selective Expansion of Viral Variants following Experimental Transmission of a Reconstituted Feline Immunodeficiency Virus Quasispecies

et al. 2013

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Following long-term infection with virus derived from the pathogenic GL8 molecular clone of feline immunodeficiency virus (FIV), a range of viral variants emerged with distinct modes of interaction with the viral receptors CD134 and CXCR4, and sensitivities to neutralizing antibodies. In order to assess whether this viral diversity would be maintained following subsequent transmission, a synthetic quasispecies was reconstituted comprising molecular clones bearing envs from six viral variants and its replicative capacity compared in vivo with a clonal preparation of the parent virus. Infection with either clonal (Group 1) or diverse (Group 2) challenge viruses, resulted in a reduction in CD4+ lymphocytes and an increase in CD8+ lymphocytes. Proviral loads were similar in both study groups, peaking by 10 weeks post-infection, a higher plateau (set-point) being achieved and maintained in study Group 1. Marked differences in the ability of individual viral variants to replicate were noted in Group 2; those most similar to GL8 achieved higher viral loads while variants such as the chimaeras bearing the B14 and B28 Envs grew less well. The defective replication of these variants was not due to suppression by the humoral immune response as virus neutralising antibodies were not elicited within the study period. Similarly, although potent cellular immune responses were detected against determinants in Env, no qualitative differences were revealed between animals infected with either the clonal or the diverse inocula. However, in vitro studies indicated that the reduced replicative capacity of variants B14 and B28 in vivo was associated with altered interactions between the viruses and the viral receptor and co-receptor. The data suggest that viral variants with GL8-like characteristics have an early, replicative advantage and should provide the focus for future vaccine development.

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Downmodulation of CD3ε expression in CD8α + β − T cells of feline immunodeficiency virus-infected cats

Abstract: Feline immunodeficiency virus (FIV) infection in cats is

Cited by 21 publications

References 39 publications

Partial Regulatory T Cell Depletion Prior to Acute Feline Immunodeficiency Virus Infection Does Not Alter Disease Pathogenesis

Partial Regulatory T Cell Depletion Prior to Acute Feline Immunodeficiency Virus Infection Does Not Alter Disease Pathogenesis

Clinical Aspects of Feline Retroviruses: A Review

Selective Expansion of Viral Variants following Experimental Transmission of a Reconstituted Feline Immunodeficiency Virus Quasispecies

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