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Rozieres, Sohela de; Swan, Christina H.; Sheeter, Dennis A.; Clingerman, Karen J; Lin, Ying‐Chuan; Huitrón‐Reséndiz, Salvador; Henriksen, Steven J.; Torbett, Bruce E.; Elder, John H.

doi:10.1186/1742-4690-1-38

Cited by 17 publications

(6 citation statements)

References 25 publications

(26 reference statements)

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“…FIV-C36 is a highly pathogenic molecular clone of an FIV clade C isolate [23] . Acute FIV-C36 infection is characterized by very high peak viremia and substantial CD4 + T cell loss, leading to early symptoms of immunodeficiency [23] , [36] . Cats received 2×10 5.2 TCID 50 units FIV-C36 on day 0, at the previously determined nadir of CD4 + CD25 hi cell depletion following treatment with anti-CD25 mAb [18] , [22] .…”

Section: Resultsmentioning

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: Resultsmentioning

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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“…Although FIV-C36 infection has been shown to cause acute immunodeficiency without documented neurologic effects, in this study these cats had similar diffusion changes during the inflammatory phase and similar brain histopathology as the FIV-PPR cats, suggesting comparable degree of neurotoxicity effects at those time periods. Therefore, it remains possible that cats with FIV-C36 have lacked clinical neurological problems because they succumb to their disease before neurological signs typically begin, which is at the 14 –15 week time period for FIV-PPR infected cats (de Rozieres et al , 2004a; de Rozieres et al , 2004b; de Rozieres et al , 2008; Hokanson et al , 2000; Phillips et al , 1996). The low level of viral infection detected in brain tissues in this study would also suggest that neuropathogenicity is not directly related to viral load or active viral replication.…”

Section: Discussionmentioning

confidence: 99%

Early detection of neuropathophysiology using diffusion-weighted magnetic resonance imaging in asymptomatic cats with feline immunodeficiency viral infection

et al. 2011

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HIV infection results in a highly prevalent syndrome of cognitive and motor disorders designated as HIV-associated dementia (HAD). Neurologic dysfunction resembling HAD has been documented in cats infected with strain PPR of the feline immunodeficiency virus (FIV), whereas another highly pathogenic strain (C36) has not been known to cause neurologic signs. Animals experimentally infected with equivalent doses of FIV-C36 or FIV-PPR, and uninfected controls were evaluated by magnetic resonance diffusion-weighted imaging (DW-MRI) and spectroscopy (MRS) at 17.5 – 18 weeks post-infection, as part of a study of viral clade pathogenesis in FIV infected cats. Goals of the MR imaging portion of the project were to determine whether this methodology was capable of detecting early neuropathophysiology in the absence of outward manifestation of neurological signs, and to compare MR imaging results for the two viral strains expected to have differing degrees of neurologic effects. We hypothesized that there would be increased diffusion, evidenced by the apparent diffusion coefficient as measured by DW-MRI, and altered metabolite ratios measured by MRS, in the brains of FIV-PPR infected cats relative to C36-infected cats and uninfected controls. Increased apparent diffusion coefficients were seen in the white matter, gray matter, and basal ganglia of both the PPR and C36 infected (asymptomatic) cats. Thalamic MRS metabolite ratios did not differ between groups. The equivalently increased diffusion by DW-MRI suggests similar indirect neurotoxicity mechanisms for the two viral genotypes. DW-MRI is a sensitive tool to detect neuropathophysiological changes in vivo that could be useful during longitudinal studies of FIV.

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“…For example, FIV-CPG derived strains generally result in high initial viral loads and a faster progression to disease, especially in young cats (de Rozieres et al, 2004a; de Rozieres et al, 2004b; de Rozieres et al, 2008). In contrast, cats infected with FIV-A strains often remain asymptomatic for longer periods of time, with lower initial viral loads, though viral growth kinetics are similar in adult cats once the acute stage of infection has passed (de Rozieres et al, 2008; Pedersen et al, 2001; Sparger et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

FIV diversity: FIVPle subtype composition may influence disease outcome in African lions

Troyer

Roelke

Jespersen

et al. 2011

Veterinary Immunology and Immunopathology

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Feline immunodeficiency virus (FIV) infects domestic cats and at least 20 additional species of non-domestic felids throughout the world. Strains specific to domestic cat (FIVFca) produce AIDS-like disease progression, sequelae and pathology providing an informative model for HIV infection in humans. Less is known about the immunological and pathological influence of FIV in other felid species although multiple distinct strains of FIV circulate in natural populations. As in HIV-1 and HIV-2, multiple diverse cross-species infections may have occurred. In the Serengeti National Park, Tanzania, three divergent subtypes of lion FIV (FIVPle) are endemic, whereby 100% of adult lions are infected with one or more of these strains. Herein, the relative distribution of these subtypes in the population are surveyed and, combined with observed differences in lion mortality due to secondary infections based on FIVPle subtypes, the data suggest that FIVPle subtypes may have different patterns of pathogenicity and transmissibility among wild lion populations.

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Cited by 17 publications

References 25 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

Early detection of neuropathophysiology using diffusion-weighted magnetic resonance imaging in asymptomatic cats with feline immunodeficiency viral infection

FIV diversity: FIVPle subtype composition may influence disease outcome in African lions

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