Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human immunodeficiency virus infected persons frequently have manifestations of central nervous system disfunction. These can be primary involvement or secondary processes such as infections or tumors. The present paper presents a short review of radiologic CNS findings in patients with AIDS as seen on CT and or MRI. The radiologic findings of HIV-1 encephalitis, toxoplasmosis, primary CNS lymphoma, PMLE, cryptococcosis, histoplasmosis, CMV encephalitis, HVS and varicella are presented. We expect this will ultimately help in the management of the AIDS patient.
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PMID:CNS involvement in AIDS patients as seen with CT and MR: a review. 181 9

Herpesvirus saimiri strain C488 transforms human CD4+ T-lymphocytes to continuous interleukin-2-dependent growth. Unlike human T-cell lines derived from tumours or those transformed by human T-lymphotropic virus 1, herpesvirus saimiri-immortalized T-cells (HVS T-cells) retain many functions of primary activated T-lymphocytes. We have characterized the course of human immunodeficiency virus types 1 and 2 (HIV-1/-2) infection in three HVS T-cell lines. Our results confirm that HVS T-cells are highly permissive to both HIV-1/-2 prototype viruses and to poorly replicating HIV-2 strains of restricted cell tropism. However, the infection was persistently productive for up to 5 months. The down-regulation of surface CD4 molecules was delayed and virus yields significantly exceeded those obtained in T-cell lines.
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PMID:Herpesvirus saimiri-immortalized human T-cells support long-term, high titred replication of human immunodeficiency virus types 1 and 2. 919 37

In attempts to improve isolation rates and virus yields for human immunodeficiency virus (HIV), the use of herpesvirus saimiri-immortalized T cells (HVS T cells) has been investigated as an alternative to/improvement over peripheral blood mononuclear cells (PBMCs). Here we characterize isolates rescued, in the two cell types, from two asymptomatic, long-term non-progressing HIV-1-infected individuals. All rescued viruses replicated in PBMCs and HVS T cells only, displaying a non-syncytium inducing (NSI) phenotype, and using CCR5 as co-receptor. Furthermore, PBMC/HVS T cell virus pairs displayed similar neutralization profiles. Full-length, expression-competent env genes were rescued from all virus isolates and directly from the patient samples using proviral DNA and viral RNA as templates. Compared with the sequences retrieved directly from the patient samples, both cell types showed similar selection characteristics. Whilst the selections were distinct for individual patient samples, they shared a common characteristic in selecting for viruses with increased negative charge across the V2 domain of the viral glycoproteins. The latter was observed at the env gene sequencing level for three other patients whose HIV strains were isolated in PBMCs only. This further supports a common selection for viral sequences that display a macrophage-tropic/NSI phenotype and shows that HVS T cells are a viable alternative to PBMCs for HIV-1 isolation.
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PMID:Selection following isolation of human immunodeficiency virus type 1 in peripheral blood mononuclear cells and herpesvirus saimiri-transformed T cells is comparable. 1202 49

Apoptosis of uninfected bystander CD4(+) T cells contributes to T-cell depletion during human immunodeficiency virus type 1 (HIV-1) pathogenesis. The viral and host mechanisms that lead to bystander apoptosis are not well understood. To investigate properties of the viral envelope glycoproteins (Env proteins) that influence the ability of HIV-1 to induce bystander apoptosis, we used molecularly cloned viruses that differ only in specific amino acids in Env. The ability of these strains to induce bystander apoptosis was tested in herpesvirus saimiri-immortalized primary CD4(+) T cells (CD4/HVS), which resemble activated primary T cells. Changes in Env that increase affinity for CD4 or CCR5 or increase coreceptor binding site exposure enhanced the capacity of HIV-1 to induce bystander apoptosis following viral infection or exposure to nonreplicating virions. Apoptosis induced by HIV-1 virions was inhibited by CD4, CXCR4, and CCR5 antibodies or by the CXCR4 inhibitor AMD3100, but not the fusion inhibitor T20. HIV-1 virions with mutant Envs that bind CXCR4 but are defective for CD4 binding or membrane fusion induced apoptosis, whereas CXCR4 binding-defective mutants did not. These results demonstrate that HIV-1 virions induce apoptosis through a CXCR4- or CCR5-dependent pathway that does not require Env/CD4 signaling or membrane fusion and suggest that HIV-1 variants with increased envelope/receptor affinity or coreceptor binding site exposure may promote T-cell depletion in vivo by accelerating bystander cell death.
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PMID:Apoptosis of bystander T cells induced by human immunodeficiency virus type 1 with increased envelope/receptor affinity and coreceptor binding site exposure. 1507 35