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At least 1,099 records · Page 61Linked to original sources
PubMed2002

Antigenic drift, antigenic shift and interferon antagonists: how bunyaviruses counteract the immune system.

Members of the Bunyaviridae family are amongst the most widespread viruses in the world. They can be found on every inhabited continent at virtually every latitude, and are able to infect a wide range of arthropods, plants and mammals including humans. More than 300 named viruses are contained within the family Bunyaviridae (Virus Taxonomy: Seventh Report of the International Committee on Taxonomy of Viruses (2000) 599), and several members cause significant disease in humans or domestic animals. Despite being recognised as an emerging threat, relatively little is known about their virulence mechanisms. Here, we try to summarise the current state of knowledge about how the viruses of the Bunyaviridae succeed in establishing infection in the face of a powerful immune system.

Animals↗
PubMed1996

The entry of reovirus into L cells is dependent on vacuolar proton-ATPase activity.

Inhibitors of vacuolar proton-ATPase activity (5 microM bafilomycin A1 or 50 nM concanamycin A) prevented infection by reovirus particles but not by infectious subviral particles (ISVPs). Neither compound affected virus attachment or internalization. However, both compounds potently blocked cleavage of the viral protein mu 1C. Finally, both reovirus particles and ISVPs efficiently translocated the toxin alpha-sarcin to the cytosol during virus entry. Bafilomycin A1 blocked translocation of alpha-sarcin by reovirus particles but not by ISVPs.

Animals↗
PubMed2004

A cellular RNA-binding protein enhances internal ribosomal entry site-dependent translation through an interaction downstream of the hepatitis C virus polyprotein initiation codon.

Translational initiation of hepatitis C virus (HCV) mRNA occurs by internal entry of ribosomes into an internal ribosomal entry site (IRES) at the 5' nontranslated region. A region encoding the N-terminal part of the HCV polyprotein has been shown to augment the translation of HCV mRNA. Here we show that a cellular protein, NS1-associated protein 1 (NSAP1), augments HCV mRNA translation through a specific interaction with an adenosine-rich protein-coding region within the HCV mRNA. The overexpression of NSAP1 specifically enhanced HCV IRES-dependent translation, and knockdown of NSAP1 by use of a small interfering RNA specifically inhibited the translation of HCV mRNA. An HCV replicon RNA capable of mimicking the HCV proliferation process in host cells was further used to confirm that NSAP1 enhances the translation of HCV mRNA. These results suggest the existence of a novel mechanism of translational enhancement that acts through the interaction of an RNA-binding protein with a protein coding sequence.

Amino Acid Sequence↗
PubMed1967

Soluble antigens of vaccinia-infected mammalian cells. II. Time course of synthesis of soluble antigens and virus structural proteins.

Virus-induced soluble antigens produced in mammalian cells after infection with vaccinia virus can be divided into two classes on the basis of molecular weight. Synthesis of the low molecular weight antigens begins early in the course of infection (1 to 2 hr), and is switched-off rather abruptly 4 to 5 hr after infection in a manner similar to that reported for the early enzymes characteristic of this same system. It was demonstrated, however, that these antigens do not include virus-induced thymidine kinase, a major virus-induced enzyme, nor is it likely that the low molecular weight antigens described here share identity with any of the virus-induced enzymes. A portion of the low molecular weight antigens appear to be incorporated into the structure of newly synthesized virus, probably as internal proteins. In contrast, synthesis of the high molecular weight antigen class is initiated later in the course of infection (4 to 5 hr), just prior to the appearance of newly synthesized virus. Antiserum directed specifically against virus structural proteins forms precipitin bands with all of the high molecular weight antigens recognizable by immunoelectrophoresis. This evidence, coupled with the observation that the high molecular weight antigen fraction elicits production of specific virus-neutralizing antibody, strongly suggests that this antigen class represents virus structural subunits produced in excess.

Antigens↗
PubMed2005

A mutant fusion (F) protein of simian virus 5 induces hemagglutinin-neuraminidase-independent syncytium formation despite the internalization of the F protein.

The fusion (F) protein of simian virus 5 strain W3A induces syncytium formation independently of coexpression of the hemagglutinin-neuraminidase protein. This property can be transferred to the F protein of strain WR by replacing the leucine at position 22 with the W3A F counterpart, proline. The resulting mutant L22P has a conformation that is distinct from that of the WR F protein. Se-L22P is a cleavage site mutant of L22P that is cleavable only by addition of exogenous trypsin. We showed here that the cell surface-localized L22P was internalized with a t1/2 of 25 min and degraded in the cell, while the WR F protein was not. The cell surface-localized Se-L22P underwent a significant conformational change upon cleavage. Intriguingly, it disappeared from the cell surface due to its internalization, while inducing extensive syncytium formation. These results indicate that L22P may display an internalization signal during the course of fusion induction.

Amino Acid Substitution↗
PubMed2026

Nipah virus in the era of global connectivity: molecular evolution, transmission risk, and preparedness strategies.

Nipah virus (NiV) is a highly pathogenic zoonotic RNA virus belonging to the genus Henipavirus within the family Paramyxoviridae, representing a continuing global health concern due to its high case fatality rate and potential for epidemic expansion in the era of increasing international connectivity. The virus demonstrates strong evolutionary adaptability driven by the absence of proofreading mechanisms during RNA replication, enabling genetic diversification that may influence host range, virulence, and transmission dynamics. Molecular pathogenesis of NiV is primarily mediated through interaction of viral glycoproteins with ephrin-B2 and ephrin-B3 receptors, facilitating host cell entry, endothelial damage, and neuroinvasion. Immune evasion facilitated by the action of accessory proteins encoded by the P gene (P, V, W, and C) acts to suppress innate antiviral immunity through the inhibition of interferon induction and JAK/STAT signaling. Human-to-human transmission of Nipah virus remains limited, with epidemiological evidence indicating basic reproduction numbers generally below unity; however, respiratory involvement and healthcare-associated exposure may enhance cluster outbreaks. Global travel, ecological disruption, and fragmented surveillance systems contribute to spillover risk, particularly in South and Southeast Asia where fruit bats of the genus Pteropus serve as natural reservoirs. Despite advances in vaccine technology, including subunit, viral vector, mRNA-based platforms, and monoclonal antibody therapies, no licensed prophylactic or therapeutic agent is currently available for human use. Global preparedness remains challenged by the scarcity of high-containment biosafety facilities, limited research funding, and absence of integrated One Health surveillance networks. Ethical considerations surrounding wildlife population control further complicate disease mitigation strategies. Emerging genomic surveillance, artificial intelligence-assisted predictive modeling, and regional data-sharing frameworks are essential for early detection and response. Strengthening molecular research on viral-host interactions and transmission determinants will be critical for preventing future Nipah virus outbreaks in an increasingly interconnected world.

Genomic surveillance↗
PubMed1992

Internal ribosome entry site within hepatitis C virus RNA.

The mechanism of initiation of translation on hepatitis C virus (HCV) RNA was investigated in vitro. HCV RNA was transcribed from the cDNA that corresponded to nucleotide positions 9 to 1772 of the genome by using phage T7 RNA polymerase. Both capped and uncapped RNAs thus transcribed were active as mRNAs in a cell-free protein synthesis system with lysates prepared from HeLa S3 cells or rabbit reticulocytes, and the translation products were detected by anti-gp35 antibodies. The data indicate that protein synthesis starts at the fourth AUG, which was the initiator AUG at position 333 of the HCV RNA used in this study. Efficiency of translation of the capped methylated RNA appeared to be similar to that of the capped unmethylated RNA. However, a capped methylated RNA showed a much higher activity as mRNA than did the capped unmethylated RNA in rabbit reticulocyte lysates when the RNA lacked a nucleotide sequence upstream of position 267. The results strongly suggest that HCV RNA carries an internal ribosome entry site (IRES). Artificial mono- and dicistronic mRNAs were prepared and used to identify the region that carried the IRES. The results indicate that the sequence between nucleotide positions 101 and 332 in the 5' untranslated region of HCV RNA plays an important role in efficient translation. Our data suggest that the IRES resides in this region of the RNA. Furthermore, an IRES in the group II HCV RNA was found to be more efficient than that in the group I HCV RNA.

Base Sequence↗
PubMed2005

The antiviral activity of sulfated polysaccharides against dengue virus is dependent on virus serotype and host cell.

Two homogeneous sulfated polysaccharides obtained from the red seaweeds Gymnogongrus griffithsiae and Cryptonemia crenulata, the kappa/iota/nu carrageenan G3d and the dl-galactan hybrid C2S-3, were assayed for their antiviral properties against the four serotypes of dengue virus (DENV) in different host cell types. Both seaweed derivatives were selective inhibitors of DENV-2 multiplication in Vero cells with inhibitory concentration 50% (IC50) values around 1 microg/ml and selectivity indices > 1000. The compounds had a lower antiviral effect against DENV-3 (IC50 values in the range 13.9-14.2 microg/ml), an even lower effect against DENV-4 (IC50 values in the range 29.3 to > 50 microg/ml) and were totally inactive against DENV-1. With respect to the host cell, the polysulfates were inhibitors of DENV-2 and DENV-3 in the human hepatoma HepG2 and foreskin PH cells, with similar antiviral effectiveness as in Vero cells, but were totally inactive in mosquito C6/36 HT cells. Mechanistic studies demonstrated that G3d and C2S-3 were active DENV-2 inhibitors only when added together with the virus or early after infection, and both initial processes of virus adsorption and internalization are the main targets of these compounds. Therefore, the variations in antiviral activity of the polysaccharides depending on the viral serotype and the host cell may be ascribed to differences in the virus-cell interaction leading to virus entry.

Animals↗
PubMed2003

Differences in virus-induced cell morphology and in virus maturation between MVA and other strains (WR, Ankara, and NYCBH) of vaccinia virus in infected human cells.

Live recombinants based on attenuated modified vaccinia virus Ankara (MVA) are potential vaccine candidates against a broad spectrum of diseases and tumors. To better understand the efficacy of MVA as a human vaccine, we analyzed by confocal and electron microscopy approaches MVA-induced morphological changes and morphogenetic stages during infection of human HeLa cells in comparison to other strains of vaccinia virus (VV): the wild-type Western Reserve (WR), Ankara, and the New York City Board of Health (NYCBH) strains. Confocal microscopy studies revealed that MVA infection alters the cytoskeleton producing elongated cells (bipolar), which do not form the characteristic actin tails. Few virions are detected in the projections connecting neighboring cells. In contrast, cells infected with the WR, Ankara, and NYCBH strains exhibit a stellated (multipolar) or rounded morphology with actin tails. A detailed transmission electron microscopy analysis of HeLa cells infected with MVA showed important differences in fine ultrastructure and amounts of the viral intermediates compared to cells infected with the other VV strains. In HeLa cells infected with MVA, the most abundant viral forms are intracellular immature virus, with few intermediates reaching the intracellular mature virus (IMV) form, at various stages of maturation, which exhibit a more rounded shape than IMVs from cells infected with the other VV strains. The "IMVs" from MVA-infected cells have an abnormal internal structure ("atypical" viruses) with potential alterations in the core-envelope interactions and are unable to significantly acquire the additional double envelope to render intracellular envelope virus. The presence of potential cell-associated envelope virus is very scarce. Our findings revealed that MVA in human cells promotes characteristic morphological changes to the cells and is able to reach the IMV stage, but these virions were not structurally normal and the subsequent steps in the morphogenetic pathway are blocked.

Animals↗
PubMed2003

Global distribution of rubella virus genotypes.

Phylogenetic analysis of a collection of 103 E1 gene sequences from rubella viruses isolated from 17 countries from 1961 to 2000 confirmed the existence of at least two genotypes. Rubella genotype I (RGI) isolates, predominant in Europe, Japan, and the Western Hemisphere, segregated into discrete subgenotypes; international subgenotypes present in the 1960s and 1970s were replaced by geographically restricted subgenotypes after approximately 1980. Recently, active subgenotypes include one in the United States and Latin America, one in China, and a third that apparently originated in Asia and spread to Europe and North America, starting in 1997, indicating the recent emergence of an international subgenotype. A virus that potentially arose as a recombinant between two RGI subgenotypes was discovered. Rubella genotype II (RGII) showed greater genetic diversity than did RGI and may actually consist of multiple genotypes. RGII viruses were limited to Asia and Europe; RGI viruses were also present in most of the countries where RGII viruses were isolated.

Base Sequence↗
PubMed1986

Chemical crosslinking of lipids and proteins within Mason-Pfizer monkey and squirrel monkey type D retroviruses.

Nearest neighborhoods between lipids and proteins were investigated in Mason-Pfizer monkey virus (MPMV) and squirrel monkey retrovirus (SMRV) using the chemical crosslinking reagent dimethyl suberimidate (DMS). Analysis of DMS-induced lipid-protein complexes by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that in both viruses the major internal structural protein, p27 (MPMV) and p35 (SMRV), is linked to the lipid bilayer. Additionally, in SMRV a second protein (p20) was found to have a vicinal relationship to the lipid bilayer of the virus. Electron microscopic investigations of MPMV and SMRV particles indicated that, in accord with the crosslinking data, the core shell of these type D retroviruses is in close proximity to the viral membrane.

Animals↗
PubMed1995

Human immunodeficiency virus nucleocapsid protein stimulates strand transfer from internal regions of heteropolymeric RNA templates.

We have examined the influence of HIV nucleocapsid protein (NCp) on strand transfer from internal regions of a heteropolymeric RNA template. The system consisted of a DNA-primed 225 nucleotide RNA donor template, on which reverse transcriptase initiated primer extension, and a 189 nucleotide RNA acceptor template, to which extended primers could transfer. The last 133 nucleotides on the 3' end of the acceptor were homologous to an internal region on the donor, limiting homologous strand transfer to this region. Primers extended to the end of the donor were 212 nucleotides while those transferred to, and extended on the acceptor were 259 nucleotides in length. The rate of strand transfer and the level of transfer products increased several-fold when nucleocapsid was included in the reactions. The increase was due, at least in part, to the transfer to, and extension on the acceptor, of incompletely elongated primer-extension products that were "chased" into transfer products in the presence of nucleocapsid. Nucleocapsid did not directly influence reverse transcriptase elongation as the enzyme processivity (number of nucleotides incorporated before the enzyme dissociates from the primer-template) was approximately the same in the presence and absence of nucleocapsid.

Capsid↗
PubMed2005

Survival of severe acute respiratory syndrome coronavirus.

BACKGROUND: The primary modes of transmission of severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) appear to be direct mucus membrane contact with infectious droplets and through exposure to formites. Knowledge of the survival characteristics of the virus is essential for formulating appropriate infection-control measures. METHODS: Survival of SARS-CoV strain GVU6109 was studied in stool and respiratory specimens. Survival of the virus on different environmental surfaces, including a laboratory request form, an impervious disposable gown, and a cotton nondisposable gown, was investigated. The virucidal effects of sodium hypochlorite, house detergent, and a peroxygen compound (Virkon S; Antec International) on the virus were also studied. RESULTS: SARS-CoV GVU6109 can survive for 4 days in diarrheal stool samples with an alkaline pH, and it can remain infectious in respiratory specimens for >7 days at room temperature. Even at a relatively high concentration (10(4) tissue culture infective doses/mL), the virus could not be recovered after drying of a paper request form, and its infectivity was shown to last longer on the disposable gown than on the cotton gown. All disinfectants tested were shown to be able to reduce the virus load by >3 log within 5 min. CONCLUSIONS: Fecal and respiratory samples can remain infectious for a long period of time at room temperature. The risk of infection via contact with droplet-contaminated paper is small. Absorbent material, such as cotton, is preferred to nonabsorptive material for personal protective clothing for routine patient care where risk of large spillage is unlikely. The virus is easily inactivated by commonly used disinfectants.

Animals↗
PubMed1995

Quantitation of human immunodeficiency virus type 1 DNA and RNA by a novel internally controlled PCR assay.

A novel internally controlled PCR (ICPCR) assay was developed to accurately quantitate human immunodeficiency virus type 1 (HIV-1) DNA and RNA in peripheral blood mononuclear cells and plasma. The ICPCR assay was sensitive and reproducible within a linear range of amplification of 10(0) to 10(3) copies for HIV-1 DNA and 10(1) to 10(4) copies for HIV-1 RNA. The assay detected HIV-1 RNA in plasma and peripheral blood mononuclear cells from all HIV-1 subjects regardless of disease stage. ICPCR was compared with a branched-DNA signal amplification assay for subjects beginning antiretroviral therapy. The reductions in plasma HIV-1 RNA in response to therapy were comparable with the two assays. The ICPCR assay should be useful in monitoring HIV-1 RNA levels both in natural history studies and in clinical trials of antiretroviral agents.

DNA, Viral↗
PubMed2005

Mumps virus-specific antibody titers from pre-vaccine era sera: comparison of the plaque reduction neutralization assay and enzyme immunoassays.

Mumps virus-neutralizing antibodies are believed to be the most predictable surrogate marker of protective immunity. However, assays used to detect neutralizing antibodies, such as the plaque reduction neutralization (PRN) assay, are labor- and time-intensive and consequently are often supplanted by the more rapid and inexpensive enzyme immunoassay (EIA) technique. For virus infections for which international antibody standards exist and are bridged to clinical studies of protection (e.g., measles and rubella), the EIA has been successfully used to determine immune surrogate endpoints, yet no such international reference exists for mumps serology. Since both virus-neutralizing and nonneutralizing antibodies are measured in the EIA, in the absence of a mumps serological standard, the EIA may be prone to yielding false-positive results when utilized for assessing surrogate markers of protective immunity. Moreover, since mumps virus-specific antibody titers are generally low in comparison to antibody levels induced by other viruses and EIA procedures often employ relatively high serum dilution factors, the EIA may be prone to yielding false-negative results. To examine these issues, a PRN assay and two commercially available EIA kits were used to evaluate wild-type mumps virus serological responses in human serum samples from the pre-mumps vaccine era. Our results indicate that the PRN assay is a more sensitive and specific method of measuring serological responses to wild-type mumps virus.

Adolescent↗
PubMed1992

Neutralization of influenza virus by low concentrations of hemagglutinin-specific polymeric immunoglobulin A inhibits viral fusion activity, but activation of the ribonucleoprotein is also inhibited.

High concentrations of hemagglutinin-specific neutralizing polymeric monoclonal immunoglobulin A (IgA) inhibit attachment of the majority of type A influenza virus virions to cell monolayers and tracheal epithelium (H. P. Taylor and N. J. Dimmock, J. Exp. Med. 161:198-209, 1985; M. C. Outlaw and N. J. Dimmock, J. Gen. Virol. 71:69-76, 1990). A minority of virions attaches but is not infectious. Here, we report that a different mechanism operates when influenza virus A/Puerto Rico/8/34 (H1N1) is neutralized by low concentrations of monoclonal polymeric IgA or when A/fowl plague virus/Rostock/34 (H7N1) is neutralized by low concentrations of polyclonal rat secretory IgA. Under these conditions, neutralized virus attaches to cells and is taken up by them. However, upon entering the cell, the nucleoprotein (NP) of neutralized virus is found in the perinuclear cytoplasm, whereas NP from nonneutralized virus is concentrated in the nucleus itself. Further data show that the low-pH-mediated cell fusion activity of virions is inhibited by IgA in proportion to loss of infectivity. The possibilities that neutralization by low amounts of polymeric IgA is caused by inhibition of the virion fusion activity and that the aberrant distribution of NP from neutralized virus results from its failure to escape from the endosomal system were investigated by using A/PR/8/34 and the fusogenic agent polyethylene glycol (PEG) at pH 5.4. A/PR/8/34 attached to cells at 4 degrees C, with minimal internalization of the virus; treatment with PEG at pH 5.4 and 4 degrees C for 1 min led to infectious fusion of nonneutralized virus with the plasma membrane and, under these conditions, was more efficient than PEG at pH 7 or medium at pH 5.4. Neutralized virus which was attached to cells and treated with acidified PEG appeared to undergo primary and secondary uncoating, with its NP protein becoming concentrated in the nucleus and M1 becoming concentrated in the perinuclear cytoplasm. Although the distribution of NP and M1 was indistinguishable from infectious virus, infectivity was not restored. Thus, even when IgA-induced inhibition of fusion is reversed, virus is still neutralized. We suggest that infectious influenza virus undergoes an activation stage which may be the relaxation of the ribonucleoprotein structure needed to permit transcription or may be the removal of M1 bound to the ribonucleoprotein.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1981

Reactivity of antisera to antigens of C-type viruses with leucocytes from patients with acute leukaemia.

A number of previous studies have suggested that certain C-type viruses from non-human primates are associated with acute leukaemia in humans. The present study sought to examine this association further by detection of antigens related to these viruses on the surface of acute leukaemia cells. Antisera against the whole viruses or the major internal protein of simian sarcoma, endogenous baboon and Rauscher viruses were tested against mononuclear cells from patients with acute leukaemia at various stages of their disease in 51Cr release leucocyte dependent cytotoxic assays. A high proportion of the patients had antigens related to these viruses detectable on their blood leucocytes at some stage in their disease whereas with one exception blood leucocytes from non-leukaemic subjects did not. The expression of these antigens did not show a close relation to the number of blast cells in blood detected on morphological grounds. Antigens related to the non-human primate viruses were detected on mononuclear cells from bone marrow samples of several non-leukaemic patients which indicated they were not specifically associated with leukaemia. Antigens related to the Rauscher virus were detected on cells of practically all bone marrow samples tested. These results suggest that assays to detect these antigens would be of limited usefulness to monitor disease activity in patients with acute leukaemia. Their expression on blood leucocytes however appeared strongly associated with acute leukaemia and further studies to assess the prognostic and epidemiological significance of detection of these antigens appears warranted.

Animals↗