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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus type 1 (Z321 designate, HIV-1Z321), the oldest known HIV, was isolated from a serum sample collected in Zaire in 1976 and was molecularly cloned. Restriction enzyme analysis of unintegrated viral DNA revealed the presence of conserved restriction enzyme cleavage sites in the long terminal repeat sequences. Nucleotide sequence analysis of the 3' end of the viral DNA revealed a pattern similar to other HIV-1 isolates described. However, some of the common restriction sites present in other isolates were absent in HIV-1Z321. The extent of differences between HIV-1Z321 and recent isolates from North America and Zaire was 17.86-18.36% on the nucleotide sequence level and 26.5-33.2% difference in the predicted amino acid sequence in the envelope gene. Differences were also noted in 3'-orf (nef: according to HIV gene nomenclature; see Ref. 42) gene and U3 region of the long terminal repeat sequences of HIV-1Z321 and other isolates. Nucleotide sequence of a HIV-1 isolate, 12 years apart from the present isolates, will provide an important time calibration point for the evolutionary divergence of HIV isolates. Hybrid HIV was also generated by transfecting HIV-1Z321 and HIV-1HTLV-III viral DNAs into cells.
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PMID:Molecular characterization of HIV-1 isolated from a serum collected in 1976: nucleotide sequence comparison to recent isolates and generation of hybrid HIV. 271 63

Human immunodeficiency virus type 1 (HIV-1) core antigen was assayed in the plasma of children at risk for infection with HIV to determine its usefulness in the diagnosis of infection and to correlate it with the clinical stage of disease. Antigen was detected in the plasma of all children less than 15 months of age with acquired immunodeficiency syndrome (AIDS). Two thirds of children with AIDS-related illnesses and half of children with asymptomatic infection had antigen. Although 53% of plasma specimens originating from HIV-infected children younger than 6 months of age contained antigen, only 25% of plasma specimens from children younger than 6 months who had no symptoms and none of the 10 specimens from HIV-infected newborn infants contained antigen. Half of the specimens containing core antigen also contained anticore antibody. Quantitative mean antigen levels were more likely to be elevated in children with AIDS (516 pg/ml) than in children with AIDS-related illnesses (295 pg/ml) or in those who had no symptoms (70 pg/ml). Antigen levels tended to increase over time in children with advancing clinical illness, but they tended to decrease over time after a diagnosis of AIDS was made. Antigen was detected in the plasma of 4 of 14 children without symptoms who subsequently reverted to an HIV seronegative state. We conclude that the detection of core antigen occurs with high frequency in children, even young infants, with symptomatic HIV infection. Plasma core antigen was less frequent in children without symptoms and was not detected in 10 infected children when they were tested at birth.
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PMID:Human immunodeficiency virus type 1 antigenemia in children. 272 8

Human immunodeficiency virus type 1 (HIV-1) encodes a nuclear trans-activator, termed Rev, that is required for the expression of the viral structural proteins and, hence, for viral replication. The Rev protein acts posttranscriptionally to induce the sequence-specific nuclear export of unspliced HIV-1 mRNA species that are otherwise excluded from the cell cytoplasm. We have used site-directed mutagenesis to identify two distinct regions of the HIV-1 Rev protein that are required for in vivo biological activity. The larger and more N-terminal of these two regions includes, but extends beyond, an arginine-rich sequence element required for nuclear localization. Mutation of a second, more C-terminal Rev protein sequence element was found to yield defective Rev proteins that act as trans-dominant inhibitors of Rev function. These Rev mutants are shown to inhibit HIV-1 replication when expressed in transfected cells and may have potential application in the treatment of HIV-1 related disease.
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PMID:Functional dissection of the HIV-1 Rev trans-activator--derivation of a trans-dominant repressor of Rev function. 275 19

Human immunodeficiency virus type 1 (HIV-1) replication requires the expression of two classes of viral mRNA. The early class of HIV-1 transcripts is fully spliced and encodes viral regulatory gene products. The functional expression of one of these nuclear regulatory proteins, termed Rev (formerly Art or Trs), induces the cytoplasmic expression of the incompletely spliced, late class of HIV-1 mRNAs that encode the viral structural proteins, including Gag and Env. Here, we provide evidence that this induction reflects the export from the cell nucleus to the cytoplasm of a pool of unspliced viral RNA constitutively expressed in the nucleus. The hypothesis that Rev acts on RNA transport, rather than splicing, is further supported by the observation that the cytoplasmic expression of a non-spliceable HIV-1 env gene sequence is also subject to Rev regulation. Here we show that this Rev response requires a specific target sequence which coincides with a complex RNA secondary structure present in the env gene. The response to Rev is fully maintained when this sequence is relocated to other exonic or intronic locations within env but is ablated by inversion. These results indicate that the HIV-1 rev gene product induces HIV-1 structural gene expression by activating the sequence-specific nuclear export of incompletely spliced HIV-1 RNA species.
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PMID:The HIV-1 rev trans-activator acts through a structured target sequence to activate nuclear export of unspliced viral mRNA. 278 94

Human immunodeficiency virus type 1 (HIV-1) isolates from various patients were divided into two major groups, rapid/high and slow/low, according to their replication properties in vitro. Rapid/high isolates grow well in cell lines and induce the formation of syncytia in peripheral blood mononuclear cells. In contrast, slow/low isolates do not replicate in cell lines and rarely induce syncytia in peripheral blood mononuclear cells. To understand the differences in replicative capacity of these isolates, a panel of indicator cell lines was used. These cell lines were generated for sensitive detection of HIV-1 isolates and show characteristics of T-lymphoid or monocytoid cells. As a result of infection, chloramphenicol acetyltransferase expression is activated. Rapid/high viruses activate chloramphenicol acetyltransferase expression in T-cell and monocytoid indicator cell lines, whereas slow/low isolates activate chloramphenicol acetyltransferase expression only in monocytoid cell lines. The block in infection of T-lymphoid cells by the slow/low isolates appears to occur early in the infection cycle, prior to the production of the virally encoded tat protein. HIV-1 isolates can thus be distinguished according to target-cell tropism. Monocyte-derived cells seem to be a more general target for the various HIV-1 isolates.
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PMID:Rapidly and slowly replicating human immunodeficiency virus type 1 isolates can be distinguished according to target-cell tropism in T-cell and monocyte cell lines. 278 83

Human immunodeficiency virus type 1 (HIV-1) is the aetiologic agent of AIDS (acquired immune deficiency syndrome) in most countries and probably originated in Central Africa like the AIDS epidemic itself. Evidence for a second major group of human immunodeficiency-associated retroviruses came from a report that West African human populations like wild-caught African green monkeys had serum antibodies that reacted more strongly with a simian immunodeficiency virus (STLV-3Mac) (ref.6) than with HIV-1. Novel T-lymphotropic retroviruses were reported to have been isolated from healthy Senegalese West Africans (HTLV-4) (ref. 4) and from African green monkeys (STLV-3AGM) (ref. 7), and a different retrovirus (HIV-2) was identified in other West African AIDS patients. Genomic analysis of HIV-2 clearly distinguished it from STLV-3 (ref. 9), but restriction enzyme site-mapping of three different HTLV-4 isolates and six different STLV-3AGM isolates showed them to be essentially indistinguishable. In this report we clone, restriction map, and partially sequence three isolates of HTLV-4 (PK82, PK289, PK190) (ref. 4). We find that these viruses differ in nucleotide sequence from each other and from three isolates of STLV-3AGM (K78, K6W, K1) (ref. 7) by 1% or less. We also report the isolation of a T-lymphotropic retrovirus from the peripheral blood of a healthy Senegalese woman which hybridizes preferentially to HIV-2 specific DNA probes. We conclude that HTLV-4 (ref. 4) and STLV-3AGM (ref. 7) are not independent virus isolates and that HIV-2 is present in Senegal as it is in other West African countries.
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PMID:Relation of HTLV-4 to simian and human immunodeficiency-associated viruses. 282 48

Human immunodeficiency virus type 1 (HIV-1) can infect CD4+ lymphocytes, monocytes-macrophages, and various other cell lines, including B-cell lines. To study the parameters of B-cell infections, we examined the susceptibility of 24 B-lymphoid cell lines to both HIV-1 and HIV-2 infections. These cell lines included a series of Epstein-Barr virus (EBV) genome-negative Burkitt's lymphoma cell lines and their EBV-converted counterparts. To infect these cells we used two HIV-1 isolates and one HIV-2 isolate. Infections were monitored with a cytoplasmic RNA dot-blot and a syncytium assay. HIV infection was also studied by a novel method based on electrophoresis of DNA liberated from cells that were lysed in situ in the well of an agarose gel. All human B-cell lines could be infected with HIV-1, regardless of the presence of EBV genomes; thus, EBV infection had no major effect on HIV susceptibility of B-cell lines. Integrated proviral HIV genomes could be detected by Southern blot analysis of DNA extracted from long-term, non-HIV-producing B-cell lines. This study suggests that B-lymphoid cells may serve as reservoirs for latent or persistent HIV infections in vivo, even in the absence of EBV infection.
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PMID:Epstein-Barr virus-positive and -negative B-cell lines can be infected with human immunodeficiency virus types 1 and 2. 284 99

Human immunodeficiency virus type-1 (HIV-1) antigen was assayed in paired serum/cerebrospinal fluid (CSF) specimen from 85 adults and 58 children with acquired immunodeficiency syndrome and was compared with clinical neurological status. A quantitative comparison of HIV-1 antigen levels in matched serum and CSF specimens indicated that HIV-1 antigen expression in these compartments is independent and is correlated with acquired immunodeficiency syndrome dementia complex in adults and progressive encephalopathy in children. In a longitudinal study (n = 47), 16 patients tested positive for HIV-1 antigen in the CSF before (n = 2) or coincident (n = 14) with neurological deterioration. Six patients who tested positive for HIV-1 antigen in the CSF remained neurologically normal for a median duration of follow-up of 11 months. Six of 25 patients who tested negative for HIV-1 antigen in the CSF, subsequently showed neurological deterioration. These data indicate that HIV-1 antigen expression in the CSF is not useful in predicting neurological deterioration.
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PMID:Human immunodeficiency virus type 1 antigen in cerebrospinal fluid. Correlation with clinical neurologic status. 291 78

Human immunodeficiency virus type 1 (HIV-1), in contrast with most other retroviruses, encodes trans-regulatory proteins for virus gene expression. It is shown in this study, by means of an in vitro splicing system, that nuclear extracts obtained from cells infected with HIV-1 contain a factor (or factors) that specifically inhibits splicing of a synthetic SP6/HIV pre-messenger RNA (pre-mRNA)-containing donor and acceptor splice sites in the coding region for the envelope protein. It is also shown that the SP6/HIV pre-mRNA is not capable of assembly in a ribonucleoprotein complex, spliceosome, in extracts from infected cells. These findings raise the possibility that specific inhibition of pre-mRNA splicing in the envelope protein coding region by HIV-1 trans-regulatory factors might be one control mechanism for efficient production of structural viral proteins and virion assembly.
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PMID:Virus-specific splicing inhibitor in extracts from cells infected with HIV-1. 264 56

Human immunodeficiency virus type I (HIV-1) is associated with a spectrum of neurological disorders. At the time of primary HIV-1 infection, an acute aseptic meningitis or encephalitis indicates central nervous system invasion. Evidence of HIV-1 infection is found in the CSF of most asymptomatic seropositive individuals, suggesting viral persistence in the nervous system. After a long incubation period, viral activation is signaled by expression of HIV-1 antigen in the CSF, which correlates with a profound dementia in adults or with an analogous progressive encephalopathy in children. The neuropathological substrate of this dementing process consists of multinucleated giant cells and diffuse white matter pallor. Immunocytochemical and in situ hybridization studies demonstrate that antigen presenting cells, including blood derived macrophages and resident brain microglia, are directly infected by HIV-1, and participate in the formation of the syncytial giant cells. Astrocytes and endothelial cells may also be infected, but evidence for infection of oligodendroglia and neurons is lacking. Studies of lentiviral encephalitides in ungulates and non-human primates emphasize the importance of specific viral antigenic stimulation and the role of inflammatory cells as direct or indirect mediators of tissue damage. The disorders of the peripheral nervous system described in patients with HIV-1 infection have not been convincingly linked to direct viral infection. At least two of the neuromuscular complications, the inflammatory motor neuropathy and polymyositis are likely to have an autoimmune pathogenesis.
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PMID:Human immunodeficiency virus type 1 (HIV-1) infection of the nervous system: a review. 307 11


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