Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchiolitis obliterans organizing pneumonia (BOOP) is increasingly recognized as an important cause of diffuse infiltrative lung disease. It is a diagnostic consideration in patients with a febrile flu-like illness of a few weeks' duration and a roentgenogram showing bilateral patchy infiltrates that are not responsive to a typical course of antibiotics. It is defined as granulated tissue plugs within lumens of small airways that extend into alveolar ducts and alveoli. Clinically, a flu-like illness, cough, and crackles are common. Pulmonary function studies of patients show a decreased vital capacity, normal flow rates (except in smokers), and a decreased diffusing capacity. It is generally idiopathic, but it may occur during the resolution of a viral or mycoplasma pneumonia. It is also associated with a variety of systemic illnesses and clinical settings. These include the connective tissue disorders, antineoplastic and other drugs, and immunological disorders, as well as bone marrow and lung transplantation. There are numerous related disorders, including human immunodeficiency virus infection, radiation therapy, thyroiditis, and alcoholic cirrhosis. In idiopathic BOOP, complete resolution occurs in 65% to 85% of patients treated with corticosteroid therapy. This type of therapy is often effective in patients with associated systemic disorders or in other clinical settings, but there may be limited or no response in patients with dermatomyositis, immunosuppression, or interstitial opacities at the lung bases. Respiratory failure leading to death may occur in 5% of patients. It is important to add BOOP to the differential diagnosis of febrile, noninfectious illnesses that are mimics of pneumonia.
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PMID:Bronchiolitis obliterans organizing pneumonia. 756 1

A series of polyanionic compounds was synthesized and evaluated for their activity against human immunodeficiency virus (HIV-1, HIV-2) and various other RNA and DNA viruses. Several compounds, i.e., 2p, 3p, 8p, 13p, 14p, 15p, 17p, 18p, and 19p, proved active against HIV-1 within the concentration range of 0.1-3 micrograms/mL while not being toxic to the host cells (CEM, MT-4) at concentrations up to 100 micrograms/mL or higher. As a rule, these polyanionic compounds proved also active, albeit at somewhat higher concentrations than those required for HIV-1 inhibition, against a number of other enveloped viruses, including HIV-2, human cytomegalovirus, influenza A virus, respiratory syncytial virus, and arenaviruses (Junin and Tacaribe). Among the most potent HIV-1 inhibitors ranked compounds 18p and 19p, the sodium salts of N-methylamides obtained by polymerization of monomers prepared starting from 10-undecenoyl chloride and omega-aminoalkanoic acids.
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PMID:Polyanion inhibitors of human immunodeficiency virus and other viruses. 1. Polymerized anionic surfactants. 760 8

The steam distillate prepared from fresh plants of Houttuynia cordata Thunb. (Saururaceae) was found to have direct inhibitory activity against herpes simplex virus type 1 (HSV-1), influenza virus, and human immunodeficiency virus type 1 (HIV-1) without showing cytotoxicity, but not against poliovirus and coxsackie-virus. The loss of viral infectivity was related to the duration of drug treatment. Three major components of the distillate, methyl n-nonyl ketone, lauryl aldehyde, and capryl aldehyde, also inactivated HSV-1, influenza virus, and HIV-1. These in vitro findings demonstrate that the essential oils provide virucidal activity against enveloped viruses by interfering with the function of virus envelope.
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PMID:Virucidal effects of the steam distillate from Houttuynia cordata and its components on HSV-1, influenza virus, and HIV. 761 66

Despite considerable evidence that cell activation enhances human immunodeficiency virus-type 1 (HIV-1) replication in vitro, there is very little data on the role of immune activation on in vivo HIV-1 replication. In this study, we examined the effect of influenza vaccination on HIV-1 replication in the peripheral blood of 20 study subjects, and in 14 control subjects who did not receive influenza vaccination. Blood was obtained from each subject on three occasions during the month before vaccination and again on three occasions during the following month. Over the study period, there was little change in levels of proviral DNA in peripheral blood mononuclear cells (PBMCs). However, peak PBMC viral RNA levels after influenza vaccination were significantly increased over the mean of prevaccination values. This change was not observed to the same extent in unvaccinated controls. Therefore, this is the first report showing that HIV-1 replication can increase in temporal association with influenza vaccination. Our results suggest that continued immunologic (antigenic) stimulation may result in increased virus load in vivo. To address the appropriateness of influenza vaccination in HIV-infected patients, expanded studies will be required to examine specific and generalized immune responses to vaccination, and differences in patient response based on disease stage.
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PMID:Human immunodeficiency virus-type 1 replication can be increased in peripheral blood of seropositive patients after influenza vaccination. 762 Jan 62

Liposomes have been proposed as vehicles for vaccines against parasitic and viral illnesses. Experimental vaccines against malaria, HIV, hepatitis A, and influenza virus have been shown to be safe and highly immunogenic in several human trials. Analysis of the intracellular trafficking patterns of liposomal antigen reveals that after being phagocytosed by macrophages, liposomal antigen readily escapes from endosomes into the cytoplasm of the macrophages. It is proposed that liposomal peptide antigen can enter either the Golgi apparatus or the endoplasmic reticulum and thereby interact with MHC class II or class I molecules. The intracellular cytoplasmic trafficking patterns of liposomal antigens raise the possibility that liposomes may have utility in human vaccines for induction of either humoral immunity or cytotoxic T lymphocytes.
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PMID:Liposomal vaccines: clinical status and immunological presentation for humoral and cellular immunity. 762 48

Viral variation has been proposed to play a role in the pathogenesis of human immunodeficiency virus type-1 (HIV-1) infection, and is an important consideration in vaccine design. During the course of an infection, isolates with sequence changes in CD8 T-cell and B-cell epitopes arise. To determine whether sequence variation within the V3 loop of HIV-1 gp120 affects HLA-DR beta 1*0101-restricted CD4 T-cell recognition, we have generated CD4 T-cell clones (TLC) specific to gp120 V3 loop peptides. Four HLA-DR beta 1*0101-restricted groups of TLC were defined by distinct patterns of responses to a panel of peptides, consistent with a highly diverse T-cell repertoire recognizing the 30 amino acid stretch (296-326) of the gp120 V3 loop. Nevertheless, a single residue change at position 311 was found to abolish the recognition of two of the four groups of TLC. This was not due to an effect of the residue at 311 on binding to major histocompatibility complex (MHC), because: (1) irrespective of the residue at 311, peptides competed well with the influenza haemagglutinin peptide 307-319 for binding to cell-bound DR1; and (2) R311-specific TLC were also HLA DR beta 1*0101 restricted. Instead, the substitution of arginine for serine at position 311 blocked the interaction of the peptide with the T-cell receptor. Thus, despite the diversity of the T-cell response to the V3 loop of HIV-1, a single amino acid change can have a considerable influence on the responding T-cell population. As residue 311 is one of the most variable of the V3 loop residues, these results suggest that CD4 recognition can also exert pressure on viral variation consistent with a role for these cells in antiviral immunity.
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PMID:The effect of a single amino acid substitution within the V3 loop of HIV-1 gp120 on HLA-DR1-restricted CD4 T-cell recognition. 764 8

Much is known about the mechanism by which mRNAs cross the nuclear envelope (the translocation stage of nucleocytoplasmic transport), but far less is known about the preceding (intranuclear migration/release) and succeeding (cytoplasmic binding) stages. Therefore, existing information suffices for articulating detailed kinetic models of translocation, but not models for the overall mRNA transport process. In this paper, we show that simple kinetic models of translocation can (i) accommodate data about nucleocytoplasmic distributions of endogenous transcripts; (ii) predict the overall effects on these distributions of effectors such as insulin and epidermal growth factor; (iii) throw some light on the mechanism(s) of action of the HIV-1 protein Rev and produce experimentally testable predictions about this mechanism; and (iv) account for the action of influenza virus NS1 protein. However, the simplest forms of translocation models apparently fail to account for some properties of viral regulators such as HIV Rev and adenovirus E1B-E4 complex. To elucidate these topics, less narrowly focused models of mRNA transport are required, describing intranuclear binding/release as well as translocation. On the basis of our examination of translocation models, we suggest some criteria that the requisite broadly based models must satisfy.
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PMID:Kinetic models for nucleocytoplasmic transport of messenger RNA. 764 11

A virus may express multiple simple mutations producing a set of viral subspecies called quasispecies: the quasispecies are considered the same species as the original virus. We are interested in reducing the point mutation space to enumerate that sequence space. We form a point mutation by applying a single bit mutation to a strand of viral DNA. How many differing viruses are possible if we allow any of the base pairs to change along the strand? For a strand of arbitrary length n we see that there is a possible sequence space of 4n-1.4 = 4n combinations. We can further remove identical sequences due to redundant amino acid codon encoding. This requires the use of a computer, but this time the complexity is a product: the number of possible amino acids times the number of codons. This substantial reduction from an exponential complexity O(4n) to a product O(n.amino-acid-number) gives us the complete list of mutant viral entities which are one mutation away from the original. Further reduction is possible, but requires biological insight regarding the viability of the mutation. By recognizing the possible sequence space, prediction can be made toward identifying future viral strains of HIV and influenza (to name two important viral particles), and perhaps develop a predictive intervention.
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PMID:Use of computer algorithms to reduce viral quasispecies sequence space. 765 89

Genetic immunization is a new vaccine technology, where antigen encoding DNA plasmids are directly injected into muscle or skin with the purpose of eliciting an immune response to the gene product. The gene products are correctly glycosylated, folded and expressed by the host cell. This is an advantage when the antigens are difficult to obtain in the desired purity, amount or correctly glycosylated form or when only the genetic sequences are known e.g. HCV. The DNA plasmids are injected into muscles or delivered coated onto gold microparticles into the skin by a particle bombardment device, a "gene gun". Genetic immunization has demonstrated induction of both a specific humoral but also a more broadly reacting cellular immune response in animal models of cancer, mycoplasma, TB, malaria, and many virus infections including influenza and HIV. Thus, the DNA vaccine mimics a live vaccine without the biohazard. Many animal species have responded to genetic immunization and gene vaccine has also been used to induce a desired immuneresponse in patients with cancer and HIV. The technique was first described in 1992 but is developing fast. This review describes the history and principle of the technology, its advantages, problems and possible applications.
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PMID:[Genetic immunization--"the biological equivalent of cold fusion"?]. 767 26

The ability of minigene-encoded viral peptide epitopes to be presented by class I molecules in the absence of MHC-encoded transporters has been evaluated in mutant T2 cells. These cells have a large deletion in the class II MHC region that includes the known transporter protein for antigenic peptides and proteasome genes and they are defective in presenting viral epitopes to CTL. T2 cells that express minigenes encoding the influenza virus matrix peptide 58-66 (GILGFVFTL) and two HTLV 1 Tax peptides 11-19 (LLFGYPVYV) and 12-19 were lysed by HLA-A2-restricted peptide-specific CTL. Minigene expression of a HLA-A2-restricted HIV reverse transcriptase peptide 476-484 (ILKEPVHGV) with three charged residues sensitized T2 cells poorly for lysis by HIV-specific CTL unless the peptide was preceded by an endoplasmic reticulum translocation signal sequence. Expression of an influenza virus nucleoprotein peptide 383-391 (SRYWAIRTR) with three charged arginine residues did sensitize HLA-B27+ T2 cells for lysis by peptide-specific CTL. These and other results with endogenously expressed peptide analogs in which hydrophobic and charged amino acids were interchanged demonstrate that antigenic peptides can be translocated from the cytoplasm into the class I Ag presentation pathway independent of MHC-encoded transporters; and that peptide hydrophobicity appears not to be a major determinant in selecting peptides for this alternate pathway.
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PMID:Presentation of endogenous peptides to MHC class I-restricted cytotoxic T lymphocytes in transport deletion mutant T2 cells. 767 94


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