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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of human epidermoid carcinoma No. 2 cells with herpes simplex virus type 1 (HSV-1) leads to a reorganization of antigens associated with both the small and heterogeneous nuclear ribonucleoprotein complexes (snRNP and hnRNP). The hnRNP core protein antigens remain associated with the host chromatin, which appears to collapse into internal aggregates and along the nuclear envelope. More striking is the formation of prominent clusters of snRNP antigens (both general and U1 snRNP specific), which appear to condense throughout the nucleus then migrate to the periphery. These snRNP clusters have been identified at the fine structure level by immuno-electron microscopy. The HSV-1 presumed transcriptional activator ICP4, DNA-binding protein ICP8, and two capsid proteins ICP5 and p40 are not detectably associated with the snRNP clusters. Similar reorganization of snRNP occurs with HSV-2 and upon infection of African green monkey VERO cells with HSV-1. We speculate that the snRNP clusters arise from an increase in size and density of the interchromatin granule region of the host cell as a result of the partial inactivation of snRNP and host pre-mRNA splicing.
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PMID:Redistribution of nuclear ribonucleoprotein antigens during herpes simplex virus infection. 282 25

The bilayer phase of dioleoylphosphatidylethanolamine (PE) can be stabilized with palmitoyl-IgG monoclonal antibody to the glycoprotein gD of the herpes simplex virus (HSV). Interactions of PE immunoliposomes with the target virions were characterized by analyzing the kinetics of lipid mixing, by liposomal content release, and by ultrastructural studies. As revealed by a resonance energy transfer assay, lipid mixing between PE immunoliposomes and virions was very rapid, with a second-order rate constant (kapp) of 0.173 (min)-1 (microgram/mL virus)-1. In comparison, content release from PE immunoliposomes was much slower and exhibited multiple-phase, mixed-order kinetics, indicating that liposome destabilization involved fusion of liposomes with HSV. The extent and the apparent rate of liposome destabilization were strongly dependent on liposome concentration. This was evident by the fact that only one to two liposomes were destabilized by each virus particle at low liposome concentration (0.1 microM). For higher liposome concentrations (1-10 microM), this value was 35-104. This finding implies that collision among the virus-bound liposomes is essential for the eventual collapse of PE immunoliposomes to form the hexagonal (HII) equilibrium phase which was observed using freeze-fracture electron microscopy. Studies employing soluble gD, immobilized on latex beads, indicated that a multivalent antigen source is essential for PE immunoliposome destabilization. Immediately after liposome-virus binding, fusion of liposome with the viral membrane then follows. Upon growth of the fusion complexes, which increase to 35-104 liposomes for each virus, an eventual collapse of the structure results, driving PE to its equilibrium structure of HII phase.
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PMID:Kinetic and ultrastructural studies of interactions of target-sensitive immunoliposomes with herpes simplex virus. 283 62

Thirty-nine patients with cold urticaria seen over a 12-year-period were re-examined. All but 12 still had positive skin tests for cold and only five of these had shown a spontaneous cure. Fourteen patients were prone to collapse on cold exposure. The incidence of atopy in this group was comparable to that in control groups. Cold urticaria is an extremely chronic disease. The mean disease duration was 9.3 years. Serum antibodies to Epstein-Barr virus, measles virus, cytomegalovirus (CMV), varicella-zoster virus (VZV), herpes simplex virus (HSV), Chlamydia psittaci and Mycoplasma pneumoniae were determined in all 39 patients and compared with control groups. The EBV-antibody patterns (heterophile antibodies and different types of EBV-specific antibodies) showed no evidence of current or of recent primary or secondary infection with EBV. Complement fixing antibody titres to measles virus, CMV, HSV and Mycoplasma pneumoniae were significantly higher in cold urticaria patients than in controls. The existence of a basic immuno-regulatory defect responsible for both the cold urticaria and the elevated antibody levels is proposed.
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PMID:Cold urticaria and virus infections: a clinical and serological study in 39 patients. 395 51

The most well characterized function of pulmonary surfactant is its ability to reduce surface tension at the alveolar air-liquid interface, thereby preventing lung collapse. However, several lines of evidence suggest that surfactant may also have 'non-surfactant' functions: specific components of surfactant (proteins and phospholipids) may interact with different alveolar cells, inhaled particles and micro-organisms modulating pulmonary host defence systems. SP-A, the most abundant surfactant protein, binds to alveolar macrophages via a specific surface receptor with high affinity [128]. Such binding effects the release of reactive oxygen species from resident alveolar macrophages if SP-A is properly presented to the target cell. SP-A also stimulates chemotaxis of alveolar macrophages [142], and serves as an opsonin in the phagocytosis of herpes simplex virus [161] Candida tropicalis [138] and various bacteria [137]. In addition, SP-A enhances the uptake of particles by monocytes and culture-derived macrophages [140] and improves bacterial killing. SP-D, another hydrophobic surfactant-associated protein, might interact with alveolar macrophages as well, stimulating the release of oxygen radicals [148], while for the hydrophilic surfactant proteins SP-B and SP-C no macrophage interactions have been described so far. SP-A and SP-D are members of the so-called 'collectins', pattern recognition molecules involved in first line defence. While some surfactant proteins appear to stimulate certain macrophage defence functions, surfactant phospholipids seem to inhibit those of lymphocytes. Suppressed lymphocyte functions include lymphoproliferation in response to mitogens and alloantigens, B cell immunoglobulin production and natural killer cell cytotoxicity. Concerning surfactant's phospholipid composition phosphatidylglycerol is more suppressive than phosphatidylcholine on a molar basis [38]. Bovine surfactant has an immunosuppressive effect on the development of hypersensitivity pneumonitis in a guinea pig model [150]. Despite these interesting observations, several important questions concerning the interactions of surfactant components with pulmonary host defence systems remain unanswered. Sufficient host defence in the lungs works through various humoral-cellular systems in conjunction with the specific anatomy of the airways and the gas exchange surface--how does the surfactant system fit into this network? Surfactant and alveolar cells are both altered during lung injury--is there a relationship between alveolar cells from RDS patients and the endogenous surfactant isolated from such patients? How does exogenous surfactant as used for substitution therapy modulate the defence system of the host? Some of those artificial surfactants have been shown to inhibit the endotoxin-alveolar macrophages, PMNs and monocytes including IL-1, IL-6 and TNF [139,152].(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Host defence capacities of pulmonary surfactant: evidence for 'non-surfactant' functions of the surfactant system. 782 30

Fulminant hepatic failure as a result of hepatitis A is a rarely diagnosed complication entity in developed countries. With the advent of specific serologic markers for acute hepatitis A virus infection, the incidence and pathology of fulminant hepatitis A can be more clearly defined. We describe four patients (one adult, three children; two males and two females, ages 2 1/2-58 years) referred to our institution for orthotopic liver transplantation subsequent to fulminant hepatic failure following hepatitis A infection. All of these patients had a history of residence in or travel to hepatitis A endemic areas. Hepatitis A infection was documented by the presence of serum IgM against hepatitis A virus prior to transplantation. Infection with hepatitis B virus, cytomegalovirus, Epstein-Barr virus, and herpes simplex virus was excluded by clinical and specific serologic examinations. All patients presented with varying degrees of encephalopathy, progressing to coma. Coagulopathy in the form of prolonged prothrombin time and partial thromboplastin time was present in all patients. Peak liver parenchymal enzymes increased to greater than ten times the upper limit of the normal range. Total and direct bilirubin levels increased to > 20 and 10 mg/dl, respectively. Histologic evaluation of the explanted livers showed a spectrum of changes ranging from periportal hepatocellular necrosis with focal parenchymal collapse and prominent bile duct proliferation to massive necrosis with complete loss of hepatic architecture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fulminant hepatic failure with massive necrosis as a result of hepatitis A infection. 840 20

Somatosensory axon outgrowth is repulsed when soluble semaphorin D (semD) binds to growth cone neuropilin-1 (Npn-1). Here, semD ligand binding studies of Npn-1 mutants demonstrate that the sema domain binds to the amino-terminal quarter, or complement-binding (CUB) domain, of Npn-1. By herpes simplex virus- (HSV-) mediated expression of Npn-1 mutants in chick retinal ganglion cells, we show that semD-induced growth cone collapse requires two segments of the ectodomain of Npn-1, the CUB domain and the juxtamembrane portion, or MAM (meprin, A5, mu) domain. In contrast, the transmembrane segment and cytoplasmic tail of Npn-1 are not required for biologic activity. These data imply that the CUB and MAM ectodomains of Npn-1 interact with another transmembrane growth cone protein that in turn transduces a semD signal into axon repulsion.
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PMID:Neuropilin-1 extracellular domains mediate semaphorin D/III-induced growth cone collapse. 985 46

The herpes simplex virus 1 (HSV-1) tegument protein VP22 has been utilised as a vehicle for trafficking proteins. It has a remarkable property of exiting the cell that is producing it and entering the neighbouring cells, which has been used to deliver therapeutic proteins, p53 and herpes simplex virus thymidine kinase (tk). It has a complex pattern of expression and subcellular localisation. Functions of VP22 include intercellular transport, binding to and bundling of microfilaments, inducing cytoskeleton collapse, nuclear translocation during mitosis, and binding to chromatin and nuclear membrane. The regions of VP22 which contain each of these functions have not been characterised. Finding the region carrying the property of intercellular spread would facilitate enhancement of transport function. By constructing a series of deletion constructs of VP22 tagged by the green fluorescent protein (GFP) we have mapped the functions of VP22 to specific regions in the polypeptide as follows: intercellular transport - aa 81-195; binding and reorganisation of cytoskeleton - aa 159-267; nuclear targeting, inhibition of cytoskeleton collapse - aa 81-121; and nuclear targeting and facilitation of intercellular transport - aa 267-301. Separation of VP22 functions enables focus on the mechanism of VP22-mediated transport and improve the transportation efficiency of VP22.
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PMID:Mapping of herpes simplex virus-1 VP22 functional domains for inter- and subcellular protein targeting. 1152 52

The antisense method is one of the most promising anti-cancer methods, however, the design of antisense oligonucleotides is difficult because many factors affecting their activitiy and stability must be considered. Recently, the oligonucleotide stabilities related to the antisense effects were quantitatively investigated based on nearest-neighbor parameters. We demonstrated that DeltaG(o) (37, hyb), a free energy change for the hybridization of antisense oligodeoxynucleotides (ODNs) with target RNAs is related to the RNase H cleavage of TAg (SV40 large T antigen) mRNA, the expression of a rabbit globin mRNA, and the protein function encoded by hMDR1 (human multidrug resistance-1) mRNA, while DeltaG(o) (37, hp), a free-energy change for hairpin formations of the antisense ODNs significantly affected the arrest efficiency of the DHFR (dihydrofolate reductase) mRNA transcription, the expression of the proalpha1(I) chain of human, and the hybridization extent for HIV-1 alpha-1. For ras RNA (Ha-ras mRNA), DeltaG(o) (37, sc), a free energy change for the conformational change of the mRNA required for antisense ODN binding showed the best correlation with the equilibrium constants for the hybridization with their target RNA. On the other hand, the antisense effects ifor the HSV-1 IE5 (herpes simplex virus type 1 immediate early pre-mRNA5) showed less of a relationship to the hybridization stability of the antisense ODNs with the target pre-mRNA, because the antisense ODNs targeting the pre-mRNA must collapse its secondary structure around the splicing site to cancel out the expected antisense effects. Based on these results, we illustrate a new concept for the design of antisense ODNs based on DeltaG(o) (37, hyb), DeltaG(o) (37, hp), and DeltaG(o) (37, sc).
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PMID:A new concept for the design of antisense oligonucleotides based on nucleic acid thermostability. 1267 72

The inability of herpes simplex virus (HSV) to spread throughout an infected host suggests that the host's immune defense against extracellular HSV is exceptional. Given the basic similarities between HSV and HIV it is reasonable to conclude that the extracellular defense against HIV is similarly potent. HIV hides from this extracellular defense. Because initial hiding place saturation is low, little HIV escapes and it is quickly annihilated. Later, as hiding place saturation increases, the numbers of released HIV increases and the immune system is ultimately overwhelmed. The fact that some perinatally infected infants clear the virus suggests that hiding place saturation is reversible. A critical hiding place re-supplies and increases saturation of other hiding places. The success of bone marrow transplants suggests that bone marrow is a critical hiding place of HIV. The sustained purge of the vulnerable critical hiding place results in a collapse of latency. Steps should be taken to: (1) determine precisely the location of the vulnerable critical hiding place; and (2) determine how to purge this class of cells, as it is purged by infants that clear the virus.
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PMID:A hypothesis on HIV and subsequent implications: effectiveness of 'extracellular defense'; pathogenesis; how the disease might be treated. 1269 28

The repair of double-strand DNA breaks by homologous recombination is essential for the maintenance of genome stability. In herpes simplex virus 1, double-strand DNA breaks may arise as a consequence of replication fork collapse at sites of oxidative damage, which is known to be induced upon viral infection. Double-strand DNA breaks are also generated by cleavage of viral a sequences by endonuclease G during genome isomerization. We have reconstituted a system using purified proteins in which strand invasion is coupled with DNA synthesis. In this system, the viral single-strand DNA-binding protein promotes assimilation of single-stranded DNA into a homologous supercoiled plasmid, resulting in the formation of a displacement loop. The 3' terminus of the invading DNA serves as a primer for long-chain DNA synthesis promoted by the viral DNA replication proteins, including the polymerase and helicase-primase. Efficient extension of the invading primer also requires a DNA-relaxing enzyme (eukaryotic topoisomerase I or DNA gyrase). The viral polymerase by itself is insufficient for DNA synthesis, and a DNA-relaxing enzyme cannot substitute for the viral helicase-primase. The viral single-strand DNA-binding protein, in addition to its role in the invasion process, is also required for long-chain DNA synthesis. Form X, a topologically distinct, positively supercoiled form of displacement-loop, does not serve as a template for DNA synthesis. These observations support a model in which recombination and replication contribute toward maintaining viral genomic stability by repairing double-strand breaks. They also account for the extensive branching observed during viral replication in vivo.
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PMID:Reconstitution of recombination-dependent DNA synthesis in herpes simplex virus 1. 1292 2


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