Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0349506 (photosensitivity)
 4,145 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The feline homologue of CD134 (fCD134) is the primary binding receptor for feline immunodeficiency virus (FIV), targeting the virus preferentially to activated CD4+ helper T cells. However, with disease progression, the cell tropism of FIV broadens such that B cells and monocytes/macrophages become significant reservoirs of proviral DNA, suggesting that receptor utilization may alter with disease progression. We examined the receptor utilization of diverse strains of FIV and found that all strains tested utilized CD134 as the primary receptor. Using chimeric feline x human CD134 receptors, the primary determinant of receptor function was mapped to the first cysteine-rich domain (CRD1) of fCD134. For the PPR and B2542 strains, the replacement of CDR1 of fCD134 (amino acids 1 to 64) with human CD134 (hCD134) alone was sufficient to confer nearly optimal receptor function. However, evidence of differential utilization of CD134 was revealed, since strains GL8, CPGammer (CPG41), TM2, 0827, and NCSU1 required determinants in the region spanning amino acids 65 to 85, indicating that these strains may require a more stringent interaction for infection to proceed.
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PMID:Differential utilization of CD134 as a functional receptor by diverse strains of feline immunodeficiency virus. 1653 6

The feline homologue of CD134 is the primary binding receptor for feline immunodeficiency virus (FIV), targeting the virus preferentially to activated CD4+ helper T cells. However, strains of FIV differ in utilization of CD134; the prototypic strain PPR requires a minimal determinant in the first cysteine-rich domain (CRD1) of feline CD134 to confer near-optimal receptor function, while strains such as GL8 require additional determinants in the CD134 CRD2. We map this determinant to a loop in CRD2 governing the interaction between the receptor and its ligand; the amino acid substitutions S78N-S79Y-K80E restored full viral receptor activity to the CDR2 of human CD134 in the context of feline CD134, with tyrosine-79 appearing to be the critical residue for restoration of receptor function.
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PMID:Mapping the domains of CD134 as a functional receptor for feline immunodeficiency virus. 1684 Mar 53

A feline immunodeficiency virus (FIV) provirus with a vif gene deletion (FIVDelta vifATGgamma) that coexpresses feline gamma interferon (IFN-gamma) was tested as a proviral DNA vaccine to extend previous studies showing efficacy with an FIV-pPPRDelta vif DNA vaccine. Cats were vaccinated with either FIVDelta vifATGgamma or FIV-pPPRDelta vif proviral plasmid DNA or with both FIV-pPPRDelta vif DNA and a feline IFN-gamma expression plasmid (pCDNA-IFNgamma). A higher frequency of FIV-specific T-cell proliferation responses was observed in cats immunized with either FIVDelta vifATGgamma or FIV-pPPRDelta vif plus pCDNA-IFNgamma, while virus-specific cytotoxic-T-lymphocyte responses were comparable between vaccine groups. Antiviral antibodies were not observed postvaccination. Virus-specific cellular and humoral responses were similar between vaccine groups after challenge with a biological FIV isolate (FIV-PPR) at 13 weeks postimmunization. All vaccinated and unvaccinated cats were infected after FIV-PPR challenge and exhibited similar plasma virus loads. Accordingly, inclusion of plasmids containing IFN-gamma did not enhance the efficacy of FIV-pPPRDelta vif DNA immunization. Interestingly, the lack of protection associated with FIV-pPPRDelta vif DNA immunization contrasted with findings from a previous study and suggested that multiple factors, including timing of FIV-pPPRDelta vif inoculations and challenge, as well as route of challenge virus delivery, may significantly impact vaccine efficacy.
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PMID:Vaccination of cats with attenuated feline immunodeficiency virus proviral DNA vaccine expressing gamma interferon. 1707 9

The feline immunodeficiency virus (FIV) targets activated CD4-positive helper T cells preferentially, inducing an AIDS-like immunodeficiency in its natural host species, the domestic cat. The primary receptor for FIV is CD134, a member of the tumor necrosis factor receptor superfamily, and all primary viral strains tested to date use CD134 for infection. We examined the expression of CD134 in the cat using a novel anti-feline CD134 monoclonal antibody (MAb), 7D6, and showed that as in rats and humans, CD134 expression is restricted tightly to CD4+, and not CD8+, T cells, consistent with the selective targeting of these cells by FIV. However, FIV is also macrophage tropic, and in chronic infection the viral tropism broadens to include B cells and CD8+ T cells. Using 7D6, we revealed CD134 expression on a B220-positive (B-cell) population and on cultured macrophages but not peripheral blood monocytes. Moreover, macrophage CD134 expression and FIV infection were enhanced by activation in response to bacterial lipopolysaccharide. Consistent with CD134 expression on human and murine T cells, feline CD134 was abundant on mitogen-stimulated CD4+ T cells, with weaker expression on CD8+ T cells, concordant with the expansion of FIV into CD8+ T cells with progression of the infection. The interaction between FIV and CD134 was probed using MAb 7D6 and soluble CD134 ligand (CD134L), revealing strain-specific differences in sensitivity to both 7D6 and CD134L. Infection with isolates such as PPR and B2542 was inhibited well by both 7D6 and CD134L, suggesting a lower affinity of interaction. In contrast, GL8, CPG, and NCSU were relatively refractory to inhibition by both 7D6 and CD134L and, accordingly, may have a higher-affinity interaction with CD134, permitting infection of cells where CD134 levels are limiting.
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PMID:Probing the interaction between feline immunodeficiency virus and CD134 by using the novel monoclonal antibody 7D6 and the CD134 (Ox40) ligand. 1760 74

Bloom syndrome is an autosomal recessive disorder characterized by proportionate short stature, photosensitivity, immunodeficiency, hypogonadism and a tendency to develop various malignancies. The greatly increased frequency of sister chromatid exchanges (reciprocal exchange of homologous segments between the two sister chromatids of a chromosome) is regarded as pathognomonic for BS. We describe an 18-year old girl who presented with short stature. She was diagnosed with BS based on an extremely increased frequency of sister chromatid exchanges. Ophthalmological examination revealed mild lens opacities bilaterally, which, to our knowledge, has not been previously reported to be associated with BS.
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PMID:Lens opacities in Bloom syndrome: case report and review of the literature. 1789 17

A 45-year-old previously healthy man presented with minimally itchy spiny papular lesions of 3 years' duration and discharging nodular cystic lesions for the past 2 years. Initially, lesions appeared on his ears, followed by the gradual appearance of similar lesions over his face, back, and extremities. The lesions were not associated with photosensitivity. Over the years, the patient continued to have similar lesions without any significant response to various topical medications and oral antibiotics. There was no history of fever or any other systemic complaints and the patient denied any other significant medical problems in the past. Cutaneous examination revealed multiple, grouped, spiny papular lesions coalescing to form plaques at places over the ears, extremities, and trunk (Figure 1). Elongated, horny, follicular spires were noted on the top of the papular lesions. Multiple discharging nodular lesions with crusting were seen predominantly over the chest, abdomen, and back (Figure 2), and closed comedonal lesions were noted on the face and trunk. Multiple orange-brown scaly plaques were seen over the extensor aspect of the patient's thighs (Figure 1, inset). A few nails showed wedge-shaped thickening without subungual hyperkeratosis or other nail changes. Palms, soles, and oral mucosa were normal. Considering the atypical cutaneous findings, the clinical possibility of pityriasis rubra pilaris (human immunodeficiency virus [HIV]-associated type 6 PRP) was considered. Hematoxylin and eosin stain of skin biopsy specimens taken from the spiny papular and plaque lesions revealed marked hyperkeratosis with alternating orthokeratosis and parakeratosis with follicular keratotic plugging (Figure 3; Figure 3, inset). Irregular broad acanthosis was also detected in the epidermis. Dermis showed moderate perivascular lymphomononuclear inflammatory infiltrate. Thus, the skin biopsy was consistent with PRP. HIV serology by enzyme-linked immunosorbent assay (ELISA) with 3 different kits was found to be positive for HIV-1. The patient denied any risk factors associated with acquiring HIV infection, and laboratory values for complete blood cell count, routine serum biochemical profile, and lipid profile were normal. The patient was prescribed oral isotretinoin and asked to come for follow-up for CD4 T-cell count, but did not return.
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PMID:Pityriasis rubra pilaris in a HIV-positive patient (Type 6 PRP). 1817 6

Feline immunodeficiency virus (FIV) causes progressive immunodeficiency in domestic cats, with clinical course dependent on virus strain. For example, clade A FIV-PPR is predominantly neurotropic and causes a mild disease in the periphery, whereas clade C FIV-C36 causes fulminant disease with CD4(+) T-cell depletion and neutropenia but no significant pathology in the central nervous system. In order to map pathogenic determinants, chimeric viruses were prepared between FIV-C36 and FIV-PPR, with reciprocal exchanges involving (i) the 3' halves of the viruses, including the Vif, OrfA, and Env genes; (ii) the 5' end extending from the 5' long terminal repeat (LTR) to the beginning of the capsid (CA)-coding region; and (iii) the 3' LTR and Rev2-coding regions. Ex vivo replication rates and in vivo replication and pathologies were then assessed and compared to those of the parental viruses. The results show that FIV-C36 replicates ex vivo and in vivo to levels approximately 20-fold greater than those of FIV-PPR. None of the chimeric FIVs recapitulated the replication rate of FIV-C36, although most replicated to levels similar to those of FIV-PPR. The rates of chloramphenicol acetyltransferase gene transcription driven by the FIV-C36 and FIV-PPR LTRs were identical. Furthermore, the ratios of surface glycoprotein (SU) to capsid protein (CA) in the released particles were essentially the same in the wild-type and chimeric FIVs. Tests were performed in vivo on the wild-type FIVs and chimeras carrying the 3' half of FIV-C36 or the 3' LTR and Rev2 regions of FIV-C36 on the PPR background. Both chimeras were infectious in vivo, although replication levels were lower than for the parental viruses. The chimera carrying the 3' half of FIV-C36 demonstrated an intermediate disease course with a delayed peak viral load but ultimately resulted in significant reductions in neutrophil and CD4(+) T cells, suggesting potential adaptation in vivo. Taken together, the findings suggest that the rapid-growth phenotype and pathogenicity of FIV-C36 are the result of evolutionary fine tuning throughout the viral genome, rather than being properties of any one constituent.
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PMID:Replication properties of clade A/C chimeric feline immunodeficiency viruses and evaluation of infection kinetics in the domestic cat. 1855 Jun 65

Infection by multiple lentiviral strains is recognized as a major driving force in the human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) epidemic, but the neuropathogenic consequences of multivirus infections remain uncertain. Herein, we investigated the neurovirulence and underlying mechanisms of dual lentivirus infections with distinct viral strains. Experimental feline immunodeficiency virus (FIV) infections were performed using cultured cells and an in vivo model of AIDS neuropathogenesis. Dual infections were comprised of two FIV strains (FIV-Ch and FIV-PPR) as copassaged or superinfected viruses, with subsequent outcome analyses of host immune responses, viral load, neuropathological features, and neurobehavioral performance. Dual infections of feline macrophages resulted in greater IL-1beta (interleukin-1beta), TNF-alpha (tumor necrosis factor alpha), and IDO (indoleamine 2,3-dioxygenase) expression and associated neurotoxic properties. FIV coinfection and sequential superinfection in vivo also induced greater IL-1beta, TNF-alpha, and IDO expression in the basal ganglia (BG) and cortex (CTX), compared to the monovirus- and mock-infected groups, although viral loads were similar in single virus- and dual virus-infected animals. Immunoblot analyses disclosed lower synaptophysin immunoreactivity in the CTX resulting from FIV super- and coinfections. Cholinergic and GABAergic neuronal injury was evident in the CTX of animals with dual FIV infections. With increased glial activation and neuronal loss in dual FIV-infected brains, immunohistochemical analysis also revealed elevated detection of cleaved caspase-3 in dysmorphic neurons, which was associated with worsened neurobehavioral abnormalities among animals infected with the copassaged viruses. Dual lentivirus infections caused an escalation in neuroinflammation and ensuing neurodegeneration, underscoring the contribution of infection by multiple viruses to neuropathogenesis.
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PMID:Dual lentivirus infection potentiates neuroinflammation and neurodegeneration: viral copassage enhances neurovirulence. 1911 33

Feline immunodeficiency virus (FIV) DNA vaccine approaches that included a vif-deleted FIV provirus (FIV-pPPRDeltavif) and feline cytokine expression plasmids were tested for immunogenicity and efficacy by immunization of specific pathogen free cats. Vaccine protocols included FIV-pPPRDeltavif plasmid alone; a combination of FIV-pPPRDeltavif DNA and feline granulocyte macrophage-colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)-alpha expression plasmids; or a combination of FIV-pPPRDeltavif and feline interleukin (IL)-15 plasmids. Cats immunized with FIV-pPPRDeltavif, GM-CSF and TNF-alpha plasmids demonstrated an increased frequency of FIV-specific T cell proliferation responses compared to other vaccine groups. Immunization with FIV-pPPRDeltavif and IL-15 plasmids was distinguished from other vaccine protocols by the induction of antiviral antibodies. Suppression of virus loads was not observed for any of the FIV-pPPRDeltavif DNA vaccine protocols after challenge with the FIV-PPR isolate. However, prior immunization with FIV-pPPRDeltavif, GM-CSF, and TNF-alpha plasmids resulted in preservation of CD4 T cell functions, including mitogen-induced cytokine expression and antigen-specific proliferation upon infection with FIV. These findings justify further examination of cytokine combinations as adjuvants for lentiviral DNA vaccines.
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PMID:Vaccination with vif-deleted feline immunodeficiency virus provirus, GM-CSF, and TNF-alpha plasmids preserves global CD4 T lymphocyte function after challenge with FIV. 1946 59

Bloom syndrome (congenital telangiectatic erythema) is a rare autosomal recessive disorder characterized by telangiectasias and photosensitivity, growth deficiency of prenatal onset, variable degrees of immunodeficiency, and increased susceptibility to neoplasms of many sites and types. We are reporting Bloom syndrome in two brothers from Kashmir (India), 8 and 6 years of age, who presented with erythematous rashes on the face, photosensitivity, and growth retardation.
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PMID:Bloom syndrome in two siblings. 2053 70


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