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PubMed2006

Hepatitis A virus infection suppresses hepatitis C virus replication and may lead to clearance of HCV.

BACKGROUND/AIMS: The significance of hepatitis A virus (HAV) super-infection in patients with chronic hepatitis C had been a matter of debate. While some studies suggested an incidence of fulminant hepatitis A of up to 35%, this could not be confirmed by others. METHODS: We identified 17 anti-HCV-positive patients with acute hepatitis A from a cohort of 3170 anti-HCV-positive patients recruited at a single center over a period of 12 years. RESULTS: Importantly, none of the anti-HCV-positive patients had a fulminant course of hepatitis A. HCV-RNA was detected by PCR in 84% of the anti-HCV-positive/anti-HAV-IgM-negative patients but only in 65% of anti-HCV-positive patients with acute hepatitis A (p=0.03), indicating suppression of HCV replication during hepatitis A. Previous HAV infection had no effect on HCV replication. After recovery from hepatitis A, an increased HCV replication could be demonstrated for 6 out of 9 patients with serial quantitative HCV-RNA values available while 2 patients remained HCV-RNA negative after clearance of HAV throughout follow-up of at least 2 years. CONCLUSIONS: HAV super-infection is associated with decreased HCV-RNA replication which may lead to recovery from HCV in some individuals. Fulminant hepatitis A is not frequent in patients with chronic hepatitis C recruited at a tertiary referral center.

Acute Disease↗
PubMed2003

Evolution of primate theta-defensins: a serpentine path to a sweet tooth.

Retrocyclins (ancestral human theta-defensins) are cyclic antimicrobial octadecapeptides that interfere with viral uptake and protect human cells from infection by T- and M-tropic strains of HIV-1 in vitro. As are other theta-defensins, retrocyclins are lectins that bind gp120, CD4, and galactosylceramide-all of which are implicated in HIV-1 uptake. Although theta-defensin mRNA transcripts are present in human bone marrow, spleen, thymus, testis, and skeletal muscle, a premature stop codon aborts their translation. We found six theta-defensin (DEFT) genes in the human genome; five on chromosome 8p23 and one on chromosome 1. All six of these pseudogenes, as well as their homologues in chimpanzees and gorillas, contained the same premature stop codon mutation. Whereas we found intact DEFT genes in DNA from several Old World Monkeys, Hylobates syndactylus (a lesser ape) and orangutans, no homologues were present in DNA from six New World Monkeys and five prosimians. We conclude that DEFT genes and theta-defensins arose in Old World Monkeys by mutation of a pre-existing alpha-defensin gene. Although intact DEFT genes survive in some nonhuman primates, our hominid ancestors lost their ability to produce theta-defensins after the orangutan and hominid lineages diverged. It is possible (but may be difficult to prove) that this mutation rendered our species more susceptible to infection by HIV-1.

Amino Acid Sequence↗
PubMed2006

C-E1 fusion protein synthesized by rubella virus DI RNAs maintained during serial passage.

Rubella virus (RUB) replicons are derivatives of the RUB infectious cDNA clone that retain the nonstructural open reading frame (NS-ORF) that encodes the replicase proteins but not the structural protein ORF (SP-ORF) that encodes the virion proteins. RUB defective interfering (DI) RNAs contain deletions within the SP-ORF and thus resemble replicons. DI RNAs often retain the 5' end of the capsid protein (C) gene that has been shown to modulate virus-specific RNA synthesis. However, when replicons either with or without the C gene were passaged serially in the presence of wt RUB as a source of the virion proteins, it was found that neither replicon was maintained and DI RNAs were generated. The majority DI RNA species contained in-frame deletions in the SP-ORF leading to a fusion between the 5' end of the C gene and the 3' end of the E1 glycoprotein gene. DI infectious cDNA clones were constructed and transcripts from these DI infectious cDNA clones were maintained during serial passage with wt RUB. The C-E1 fusion protein encoded by the DI RNAs was synthesized and was required for maintenance of the DI RNA during serial passage. This is the first report of a functional novel gene product resulting from deletion during DI RNA generation. Thus far, the role of the C-E1 fusion protein in maintenance of DI RNAs during serial passage remained elusive as it was found that the fusion protein diminished rather than enhanced DI RNA synthesis and was not incorporated into virus particles.

Animals↗
PubMed2005

Pepper mild mottle virus pathogenicity determinants and cross protection effect of attenuated mutants in pepper.

To determine the pathogenicity domain and to apply cross protection, Pepper mild mottle virus (PMMoV) point-mutations in the replicase (REP) gene between the methyl-transferase and helicase domains, and deletions truncating pseudoknots in the 3' non-coding region (NCR), were constructed. Some mutants substituting a single amino acid in REP residue 348 exhibited mild symptoms in Nicotiana benthamiana or pepper plants. Accumulation of these mutants was higher than that of other REP mutants or wild-type PMMoV. Deletion mutants in the 3' NCR pseudoknot showed the lowest virus replication and accumulation among the mutants tested. Six attenuated mutants, which combined 3' NCR deletions and single or double REP substitution mutations were constructed to investigate cross protection effects on pepper plants. All six of the attenuated mutants showed milder symptom development than wild-type virus. These results suggest that REP and the pseudoknot in the 3' NCR are major pathogenicity determinants of the virus, and engineered PMMoV attenuated mutants can be useful for protection against the virus in pepper plants.

3' Untranslated Regions↗
PubMed1990

Coinhibition of viral interferon induction by benzo[a]pyrene in association with occupation-related particles.

Benzo[a]pyrene (B[a]P) in combination with coal, asbestos, or metal particles was studied for its inhibitory effects on interferon-alpha/beta induction by influenza virus in rhesus monkey kidney (LLC-MK2) cell monolayers. B[a]P per se had no adverse effect on the induction process. However, when cell cultures were pretreated with B[a]P that was bioactivated by rat liver S9 homogenate, from 52 to 65% inhibition of interferon induction occurred. Significantly greater (P less than 0.05) depression (coinhibition) of viral interferon induction (greater than 83%) resulted when bioactivated B[a]P was incorporated with coal particles representative of coal rank (anthracite, bituminous, lignite, peat). Coinhibition affected by bioactivated B[a]P was coal rank-independent but any interferon inhibitory activity affected by coal particles per se was coal rank-dependent. When metals (aluminum, aluminum oxide, ferric oxide, nickel, or chromium) or asbestos fibers (chrysotile, crocidolite, anthophyllite, or amosite) were individually mixed with bioactivated B[a]P, coinhibition of cellular interferon synthesis also resulted which was significantly greater (P less than 0.05) than that manifested by bioactivated B[a]P or particles per se. Coinhibition of interferon induction by silicates (Min-U-Sil, DQ-12, hypersthene, or wollastonite) and the bioactivated hydrocarbon was not in evidence although some silicates alone partially inhibited the induction process. Viral interferon induction was inhibited in a dose-response manner by B[a]P (+/- S9) in combination with selected particles. The adsorption of B[a]P to all types of particles was no more than 5.98 micrograms B[a]P/mg of particles and, moreover, less than 0.5% by weight. These findings provide further evidence that bioactivated B[a]P and occupation-related particles act together to coinhibit a biological defense mechanism, the interferon induction phase of the interferon system.

Animals↗
PubMed1974

Pathogenesis of lipoid nephrosis: a disorder of T-cell function.

Clinical observations suggest that lipoid nephrosis is produced by a systemic abnormality of T-cell function resulting in the secretion of a circulating chemical mediator toxic to an immunologically innocent glomerular basement membrane. The lack of evidence of a humoral antibody response, remission induced by measles which modifies cell-mediated immunity, the therapeutic benefits of steroids and cyclophosphamide which also abate cell-mediated responses, and the occurrence of this syndrome in Hodgkin's disease support this hypothesis. The susceptibility of untreated patients to pneumococcal infections may be of primary or secondary pathogenetic importance. Taken together, the data suggest that this syndrome is a clinical expression of a self-limited primary immune-deficiency disease.

Basement Membrane↗
PubMed1998

Is interferon-alpha a neuromodulator?

Interferons were initially characterized for their ability to 'interfere' with viral replication, slow cell proliferation, and profoundly alter immunity. They are a group of hormone-like molecules synthesized and secreted by macrophages, monocytes, T lymphocytes, glia, and neurons. These cytokines have been shown to have several regulatory roles and diverse biological activities, including control of cellular and humoral immune responses, inflammation, and tumor regression. In addition, there are many reports indicating that interferon-alpha (IFN-alpha) participates in the regulation of various cellular and humoral processes such as the endocrine system modulates behavior, brain activity, temperature, glucose sensitive neurons, feeding pattern and opiate activity. Therefore, IFN-alpha can be considered as a physiological modulator, with only one of its functions being the ability to hinder viral replication intracellularly.

Animals↗
PubMed1998

Transport and mode of action of nucleoside derivatives used in chemical and antiviral therapies.

Nucleoside analogues used in cancer and anti-viral therapies interfere with nucleotide metabolism and DNA replication, thus inducing their pharmacological effects. A long-awaited goal in the understanding of the pharmacological properties of these molecules, that is the molecular characterization of nucleoside plasma-membrane transporters, has been achieved very recently. These carrier proteins are encoded by at least two gene families and new isoforms remain to be identified. Direct demonstration of translocation of these drugs by nucleoside transporters has already been provided and most of them can inhibit natural nucleoside transport, probably in a competitive manner. The expression of these genes is clearly tissue-specific and might depend on the differentiated status of a cell. This is relevant because the sensitivity of a cell to a drug can depend on the type of nucleoside carrier expressed, and the drug itself might modulate nucleoside carrier expression. In this article, Marçal Pastor-Anglada, Antonio Felipe and Javier Casado discuss recent studies on the regulation of nucleoside carrier expression and of the molecular determinants of substrate specificity. Better knowledge of these will contribute to an improved design of therapies based on nucleoside derivatives.

Acquired Immunodeficiency Syndrome↗