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The Immunological System and Neoplasia
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Feline leukemia is a complex disease caused by a horizontally transmitted exogenous retrovirus. One of the common consequences of infection with feline leukemia virus (FeLV) is immunosuppression due mostly to lymphopenia as a result of a reduction in T lymphocytes. The immunosuppression was originally linked to survival of tumor cells rather than to a disease entity in its own right. The discovery of a human immunodeficiency virus (HIV), a retrovirus, as the etiological agent of the acquired immunodeficiency syndrome (AIDS) and the subsequent finding of additional retroviruses linked to immunodeficiencies in other mammalian species including cats stimulated reexamination of retroviral diseases in animals. The isolation of a feline immunodeficiency virus (FTV) was important because it not only provided a model for AIDS research, but because it complicated the clinical picture of the disease syndrome linked to FeLV infection. Furthermore feline leukemia is the first mammalian cancer for which vaccines have been developed and which are marketed by commercial companies in many countries of the world.
HIV and AIDS
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
A virus that attacked the T-lymphocytes of the immune system and was transmitted by body fluids sounded like an HTLV-like retrovirus to Gallo and he immediately began to explore the idea that some version of his newly discovered virus might be the cause of AIDS. At the same time, Max Essex, a Harvard researcher was exploring a potential role for feline leukemia virus, another retrovirus that attacks the immune system of cats. Searching for a retrovirus as the cause of AIDS proved to be a serendipitous first step that arose from conversation between these two scientists.29
Pneumocystis carinii
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Peter D. Walzer, C. Kurtis Kim, Melanie T. Cushion
Cases of naturally acquired P. carinii pneumonia have been reported in animals in whom an immunodeficiency disease was proven (e.g., hairless guinea pig) or strongly suspected (e.g., dogs, goats, swine, horses, primates) (69,274, 278-282). The emergence of AIDS has stimulated interest in retrovirus infection in animals; however, so far, P. carinii has not been the dominant opportunistic infection as in humans. A recent autopsy survey of cats with feline leukemia virus infection failed to reveal P. carinii (283).
A deep dive into future therapies for microcytic anemias and clinical considerations
Published in Expert Review of Hematology, 2023
François Rodrigues, Tereza Coman, Guillemette Fouquet, Francine Côté, Geneviève Courtois, Thiago Trovati Maciel, Olivier Hermine
Dietary iron absorption is usually limited to 1–2 mg per day and mainly serves in adults to compensate for losses, such as bleeding or intestinal cells desquamation [2]. The divalent metal transporter 1 (DMT1) takes up ferrous iron reduced by the duodenal cytochrome B (DCYTB) on the luminal side of enterocyte [15]. As transferrin, DMT1 mRNA possesses an IRE in its 3‘UTR, stabilizing expression during iron deprivation (Galy 2008 Cell Metabolism). DMT1 pathogenic mutations are responsible for a hypochromic microcytic anemia with slowly developing iron overload, suggesting that other absorption mechanisms, such as heme transport by duodenal Feline Leukemia Virus subgroup C Receptor 1 (FLVCR1), can compensate for DMT1 deficiency [16–18]. Indeed, microcytic anemia in this context is not caused by blood iron levels’ depletion but by inefficient iron export from endosomes to the cytosol for heme synthesis after transferrin internalization [5]. Abnormal subcellular iron localization causes ineffective erythropoiesis in this condition. Fascinatingly, erythropoietin (EPO) administration improves hemoglobin levels in patients with DMT1 deficiency [19]. This effect is mediated by inefficient erythropoiesis-linked apoptosis inhibition by EPO.
Clinical and imaging characteristics of posterior column ataxia with retinitis pigmentosa with a specific FLVCR1 mutation
Published in Ophthalmic Genetics, 2018
Jennifer Lee, Hannah L. Scanga, Kunal K. Dansingani, Kenneth J. Taubenslag, Leonid Zlotcavitch, Bharesh K. Chauhan, Christin L. Sylvester, D. Holmes Morton, Ken K. Nischal
Posterior column ataxia with retinitis pigmentosa (PCARP) is an autosomal recessive, slowly progressive, neurodegenerative syndrome due to malfunction of heme-iron transport, that typically presents in early childhood (1). PCARP primarily leads to sensory ataxia due to degeneration of proprioceptive neurons in the posterior column and retinitis pigmentosa (RP), a progressive retinal degenerative disease. This disorder is caused by a known pathogenic mutation in the feline leukemia virus subgroup C cellular receptor 1 (FLVCR1) gene, which encodes for a plasma membrane receptor protein responsible for heme transport. Dysregulation of this pathway results in the accumulation of cytotoxic heme in neurons and consequently, apoptosis (2,3). FLVCR1 genes are abundantly expressed in the retina and the posterior column, accounting for their selective degeneration (4). Patients are usually found to have the following neurologic signs: decreased deep tendon reflexes, loss of deep vibratory and position senses, and ataxic gait (2). Ocular signs in these patients characteristically include irreversible nyctalopia and peripheral vision loss during the first decade of life (5–7).
A splice-site variant in FLVCR1 produces retinitis pigmentosa without posterior column ataxia
Published in Ophthalmic Genetics, 2018
Imran H. Yusuf, Morag E Shanks, Penny Clouston, Robert E. MacLaren
Retinitis pigmentosa (RP) is the most common monogenic cause of blindness. Variants in over 100 genes have been associated with the retinitis pigmentosa phenotype. Homozygous variants in FLVCR1 (feline leukemia virus subgroup c receptor 1), which encodes a transmembrane heme transporter, have been described in association with a clinical syndrome of posterior column ataxia with retinitis pigmentosa (PCARP), (1-4) a syndrome first described in 1997–1998 (5,6). Herein, we describe a patient with a splice-site (intronic) variant in FLVCR1 who exhibited retinitis pigmentosa without posterior column degeneration (therefore, without PCARP). In addition, a novel missense variant was identified in FLVCR1 in the same patient, although with uncertain pathogenicity(7). We suggest a link between intronic splice-site variants in FLVCR1 and the absence of posterior column degeneration and suggest a hypothesis to explain this observation.