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

Transmission of human T cell leukemia virus type I (HTLV-I) to a T cell line (MOLT-4#8) was studied using cell-free virus infection or cocultivation with an HTLV-I-transformed T cell line (MT-2). Immunofluorescence and FACS analyses showed that HTLV-I was efficiently adsorbed onto MOLT-4#8 cells. However, after adsorption, no extrachromosomal viral DNA in the cells was detected by the Southern blot method. In contrast, when MT-2 cells were cocultured with MOLT-4#8 cells, generation of extrachromosomal DNA was clearly observed. These data suggest that the cell-free HTLV-I may have difficulties in penetration, uncoating or reverse transcription. After cocultivation, MOLT-4#8 cells chronically infected with HTLV-I were cloned and analyzed. Only four provirus-positive cell lines were obtained. The transmission rate of the virus by cocultivation seemed to be low in our experimental system, although marked cell fusion was observed. Moreover, none of the cloned cell lines which harbored HTLV-I provirus expressed any viral protein. Inefficient integration and expression of the provirus might be hypothesized as compared with human immunodeficiency virus type 1 transmission.
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PMID:Inefficient transmission of HTLV-I to MOLT-4 cells by cell-free virus and cocultivation. 130 3

A total of 40 multiple sclerosis (MS) patients from Denmark and 10 from the Faroes were examined for antibodies with affinity to human T cell leukemia/lymphoma virus type 1 (HTLV-I) and human immunodeficiency virus type 1 and 2 (HIV-1 and HIV-2). Using ELISA, MS patients and a group of healthy controls did not differ significantly in their reactivities to HTLV-I. However, elevated reactivities were recorded with 5 MS sera, whereas only 2 of the sera from the controls produced highly values. Ten patients with other neurological diseases all seemed to exhibit low reactivity in HTLV-I ELISA. The reactivities of 2 MS sera decreased considerably by absorption with an HTLV-I lysate. In immunofluorescence assay, two other MS sera reacted with HTLV-I transformed cell lines as well as with non-infected cells. Examined by Western blotting (WB), a single MS serum produced a distinct HTLV-I p19 band. With ELISA for detection of HIV-1 and HIV-2 antibodies, 2 MS sera exhibited borderline reactions. Further examination of these two sera by WB revealed weak reactivities against p24 and p53 of HIV-1. One the whole, the present observations do not suggest that a putative MS retrovirus would be closely related with HTLV-I, HIV-1 or HIV-2.
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PMID:Seroreactivity to human T cell leukemia/lymphoma virus type 1 and related retroviruses in multiple sclerosis patients from Denmark and the Faroes. 132 31

The majority of lymphomas in the setting of acquired, iatrogenic, or congenital immunodeficiencies are B-cell lymphoproliferations. We describe a rare T-cell lymphoma in a fulminantly ill patient infected with human immunodeficiency virus type 1 (HIV-1). The T-cell nature of the process was defined genotypically (monoclonal T-cell receptor beta-chain [CT beta] rearrangement) and phenotypically (CD45RO+, CD4+, CD5+, CD25+, CD8-, CD3- and negative for a variety of B-cell and monocyte markers). The CD4+, CD25+ (interleukin-2 receptor [IL-2R]) phenotype with production of IL-2 and IL-2R RNA is analogous to human T-lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATLL); however, no HTLV-1 could be detected. Southern blot analysis did demonstrate monoclonally integrated HIV-1 within the tumor genome. Furthermore, the tumor cells were producing HIV p24 antigen as shown by immunohistochemistry. This is the first case of acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's lymphoma in which HIV-1 infection may have played a central role in the lymphocyte transformation process.
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PMID:Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1-associated T-cell transformation. 137 87

Transcription from the human immunodeficiency virus type 1 (HIV-1) provirus is activated by a cellular factor, NF kappa B, recognizing the tandemly repeated 10-base-pair sequences, termed the kappa B sequence, present in the enhancer region within the viral long terminal repeat (LTR). Using electrophoretic mobility shift assay (EMSA), which demonstrates specific DNA-protein interaction in vitro, we could demonstrate that reducto-oxidative modulation of NF kappa B dramatically changes its DNA binding activity and that a cellular physiological reducing catalyst, thioredoxin (TRX) also known as adult T cell leukemia derived factor (ADF), fully restored the DNA-binding activity of the oxidized NF kappa B. We also observed that purified TRX/ADF protein could augment gene expression from HIV LTR as demonstrated by transient chloramphenicol acetyltransferase (CAT) assay. These observations confirmed the previous notion that ADF might be an inducing factor of cellular interleukin-2 receptor alpha subunit (IL-2R alpha) through the kappa B sequence that is a common central cis-regulatory element in both IL-2R alpha and HIV gene expression. These observations indicate that reducto-oxidative regulation (or redox regulation) of a cysteine residue(s) on the NF kappa B molecule might play an important role in its specific DNA interaction and that it might provide a clue to the understanding of a pathway of cellular signal transduction to NF kappa B that is independent from the known pathways involving protein phosphorylation.
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PMID:Human thioredoxin/adult T cell leukemia-derived factor activates the enhancer binding protein of human immunodeficiency virus type 1 by thiol redox control mechanism. 149 89

A wide range of enveloped viruses, including human herpes simplex virus type 1, human cytomegalovirus, human T cell leukemia/lymphoma virus type I, human immunodeficiency virus type 1, Sindbis virus, and Friend erythroleukemia virus, are highly susceptible to merocyanine 540 (MC 540)-sensitized photoinactivation. By contrast, human pluripotent hematopoietic stem cells, red cells, factor VIII, and von Willebrand factor are much less sensitive. This suggests that MC 540 may be useful for the inactivation of enveloped viruses in blood and blood products. The dye has a low acute systemic toxicity, is rapidly eliminated from the blood stream, and has little or no mutagenic potential. The currently available data support the view that MC 540-sensitized photo-inactivation interferes with early events in the infectious process, notably the ability of the virus to adhere to and penetrate its host cell. The viral envelope is a major target of photodynamic damages which appear to be mediated at least in part by singlet molecular oxygen.
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PMID:Merocyanine-sensitized photoinactivation of enveloped viruses. 161 87

Adult T-cell leukemia (ATL), a disease entity first described by Takatsuki et al., is endemic in southwestern Japan, the Caribbean Islands, and in some parts of Africa. ATL patients are classified into four subtypes according to the clinical picture: acute, chronic, smoldering, and lymphoma type. The diagnosis of ATL is made from the characteristic clinical findings, the detection of serum antibodies to HTLV-I, and when necessary, the confirmation of monoclonal integration of HTLV-I proviral DNA in cellular DNA of ATL cells. Recently, diagnostic criteria for clinical subtypes of ATL were proposed by the Lymphoma Study Group in Japan: 1) smoldering type, normal lymphocyte level, no hypercalcemia, lactate dehydrogenase (LDH) value 1.5 times the upper limit of normal or lower, no lymphadenopathy, no involvement of liver, spleen, central nervous system (CNS), bone or gastrointestinal tract, and no ascites or pleural effusion: 2) chronic type, absolute lymphocytosis with T-lymphocytosis of greater than 3 x 10(9)/1, LDH value twice the upper limit of normal or lower, no hypercalcemia, no involvement of CNS, bone, or gastrointestinal tract, and no ascites or pleural effusion: 3) lymphoma type, no lymphocytosis, 1% or less abnormal lymphocytes, and histologically-proven lymphadenopathy: 4) acute type, remaining ATL patients who are not classified as any of the above types. Infection with HTLV-I is a direct cause of ATL. Furthermore, infection with this virus can indirectly cause many other diseases via the induction of immunodeficiency, such as chronic lung diseases, opportunistic lung infections, cancer of other organs, monoclonal gammopathy, chronic renal failure, strongyloidiasis, non-specific dermatomycosis, non-specific lymph node swelling, HTLV-I associated myelopathy (HAM/TSP), and HTLV-I uveitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Natural history of HTLV-I infection]. 163 39

Although the human immunodeficiency virus type 1 (HIV-1) is frequently isolated from the cerebrospinal fluid of infected patients, only a small percentage of patients are found to have clinical dementia or neuropathies (or both). The reasons for this remain unclear. In our study, serum neutralizing antibody titers against the human T cell leukemia virus-IIIB isolate of HIV-1 were tested in 10 patients with acquired immunodeficiency syndrome (AIDS) with neurologic complications and 20 patients with HIV infection without neurologic complications. Titers were significantly lower in the neuro-AIDS group, suggesting that impaired neutralizing antibody responses in this subpopulation of patients may be involved in the immunopathogenesis of AIDS encephalopathy.
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PMID:Neutralizing antibody responses in patients with AIDS with neurologic complications. 174 7

Human T-cell lymphotrophic virus I (HTLV-I) and human T-cell lymphotrophic virus II (HTLV-II) are closely related retroviruses that are highly prevalent in injection drug users (IDUs). The bulk of infection in this group probably occurs with HTLV-II, with a lower prevalence of HTLV-I. HTLV-I is known to cause adult T-cell leukemia/lymphoma and tropical spastic paraparesis. HTLV-II has not been proven to cause any human pathology, but may be immunosuppressive and is almost indistinguishable serologically from HTLV-I. As with human immunodeficiency virus (HIV), infection with these viruses is likely to be lifelong and the disease may have a latent period of many years. Unlike HIV, HTLV-I and/or HTLV-II are not likely to be transmitted from mother to child prenatally, and usually require breast-feeding for vertical transmission. It is likely that HTLV-I and/or HTLV-II has been prevalent in IDUs for far longer than the HIV epidemic. HTLV-I and/or HTLV-II are relevant to the AIDS epidemic in that they may function as biologic markers of behavioral risk status for HIV infection in IDUs or their sexual partners, and they may accelerate the course of HIV infection in persons coinfected with HTLV-I and/or HTLV-II and HIV. Coinfection will be more likely as the HIV epidemic progresses. Pregnant addicts entering outpatient methadone maintenance treatment in San Francisco County or Contra Costa County during 1990 were found to have an HTLV-II prevalence of 21% (n = 24). Important issues in counseling infected methadone patients are described.
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PMID:Human T-cell lymphotrophic virus in California's injection drug users. 176 94

Immunohistological and electron microscopy studies of lymph nodes from patients infected with the human immunodeficiency virus 1 (HIV-1) demonstrated that follicular dendritic cells (FDC), the antigen-presenting cells of the B cell system, contain and may produce the virus. To elucidate the mode of infection of FDC with HIV-1 in vitro we developed an improved method for the preparation of single-cell suspensions of viable FDC with high purity (greater than 90% FDC). These isolated FDC were subjected to human T cell leukemia virus IIIB infection, which was monitored after 4 days in culture using the polymerase chain reaction. We were able to demonstrate that normal human FDC are highly susceptible to infection by HIV-1. Inhibition experiments with the monoclonal antibody OKT4a demonstrate that this infection is independent of the CD4 molecule.
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PMID:Isolation of normal human follicular dendritic cells and CD4-independent in vitro infection by human immunodeficiency virus (HIV-1). 186 73

A nucleolar localizing rev gene mutant M10 of human immunodeficiency virus type 1 (HIV-1) lost a Rev function completely, instead, gained a Rex activity of human T cell leukemia virus type 1 (HTLV-1). The obtained compatibility between Rev M10 and Rex with their own nucleolar targeting signal (NOS) suggests a common molecular mechanism of their post-transcriptional regulation, despite no sequence similarities of both proteins and their responsive RNA elements, respectively.
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PMID:Functional conversion from HIV-1 Rev to HTLV-1 Rex by mutation. 187 42


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