Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Virus Replication”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed2005

Cinanserin is an inhibitor of the 3C-like proteinase of severe acute respiratory syndrome coronavirus and strongly reduces virus replication in vitro.

The 3C-like proteinase (3CLpro) of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is one of the most promising targets for anti-SARS-CoV drugs due to its crucial role in the viral life cycle. In this study, a database containing structural information of more than 8,000 existing drugs was virtually screened by a docking approach to identify potential binding molecules of SARS-CoV 3CLpro. As a target for screening, both a homology model and the crystallographic structure of the binding pocket of the enzyme were used. Cinanserin (SQ 10,643), a well-characterized serotonin antagonist that has undergone preliminary clinical testing in humans in the 1960s, showed a high score in the screening and was chosen for further experimental evaluation. Binding of both cinanserin and its hydrochloride to bacterially expressed 3CLpro of SARS-CoV and the related human coronavirus 229E (HCoV-229E) was demonstrated by surface plasmon resonance technology. The catalytic activity of both enzymes was inhibited with 50% inhibitory concentration (IC50) values of 5 microM, as tested with a fluorogenic substrate. The antiviral activity of cinanserin was further evaluated in tissue culture assays, namely, a replicon system based on HCoV-229E and quantitative test assays with infectious SARS-CoV and HCoV-229E. All assays revealed a strong inhibition of coronavirus replication at nontoxic drug concentrations. The level of virus RNA and infectious particles was reduced by up to 4 log units, with IC50 values ranging from 19 to 34 microM. These findings demonstrate that the old drug cinanserin is an inhibitor of SARS-CoV replication, acting most likely via inhibition of the 3CL proteinase.

Animals↗
PubMed2002

TT virus replicates in stimulated but not in nonstimulated peripheral blood mononuclear cells.

TT virus (TTV) is an unenveloped, single-stranded, circular-DNA virus which resembles members of the Circoviridae, that is commonly found in humans and which lacks pathological consequences for the infected host. TTV replication has been demonstrated in bone marrow cells but not in peripheral blood mononuclear cells (PBMC), suggesting that hematopoietic cells must be activated to support TTV replication. To test this hypothesis, PBMC from two naturally TTV-infected individuals and from two healthy TTV-DNA negative donors infected in vitro with a TTV-DNA-positive serum were cultured in the presence (stimulated) or absence (unstimulated) of phytohemagglutinin, lipopolysaccharide, and interleukin-2. TTV-DNA was detected in both stimulated and unstimulated PBMC. However, TTV-DNA replicative intermediates and mRNA were detected only in stimulated PBMC. Furthermore, TTV-DNA and mRNA were detected in PBMC from two TTV negative donors reinfected with supernatants from TTV-infected stimulated cells but not when using culture supernatants from unstimulated cells. These results demonstrate that TTV replicates in PBMC only when stimulated.

Cells, Cultured↗
PubMed1985

In vitro effect of haemagglutination inhibition antibodies on measles virus replication.

Children between the ages of 6 and 15 years were studied for the presence of serum levels of measles haemagglutination inhibition antibodies in relation to the continual measles epidemics in Nigeria. The neutralization of Edmonston B strain of live measles virus by such antibodies was also studied in Vero cells. The results indicate that in Vero cells, replication of the virus could be inhibited for up to 3 days by haemagglutination inhibition antibody at a concentration of 1:16.

Adolescent↗
PubMedDate not supplied

Hepatitis B virus replication in dark reddish patchy markings appearing on the hepatic surface.

We investigated the localization of hepatitis B virus (HBV) antigens and HBV DNA in dark reddish patchy markings (DRPM) on the hepatic surface in three patients with chronic active hepatitis B. The number of hepatitis B core antigen-positive hepatocytes in areas of DRPM was less than that in areas not appearing as DRPM. The grain concentration indicating HBV DNA on autoradiography in hepatocytes in areas of DRPM was less than that in areas not appearing as DRPM. These findings suggest that replication of the hepatitis B virus is reduced in pre-nodular lesions which are appearing as DRPM in chronic active hepatitis.

Adult↗
PubMed1997

The kappaB sites in the human immunodeficiency virus type 1 long terminal repeat enhance virus replication yet are not absolutely required for viral growth.

The dependence of human immunodeficiency virus type 1 (HIV-1) on its NF-kappaB binding sites (kappaB sites) for replication in transformed and primary T-cell targets was examined by infecting cells with HIV-1 reporter viruses containing kappaB site enhancer mutations. Viral transcription was measured either with luciferase-expressing HIV-1 that infects for a single round or by flow cytometric analyses with HIV-1 expressing placental alkaline phosphatase (PLAP) or green-fluorescent protein (GFP). Both PLAP- and GFP-expressing viruses spread from cell to cell and allowed analysis of viral gene expression patterns in single cells. Infection of a panel of T-cell lines with different basal levels of NF-kappaB demonstrated a direct correlation between the amount of constitutive nuclear NF-kappaB and the degree to which a wild-type virus outperformed kappaB site mutants. One T-cell line with a constitutively high level of nuclear NF-kappaB, PM1, showed a 20-fold decrease in transcription when its kappaB sites were mutated. In contrast, in a T-cell line with a low basal level of NF-kappaB, SupT1, mutation of the kappaB site in the enhancer had no effect on viral transcription or growth rate. Phytohemagglutinin-activated peripheral blood mononuclear cells showed a large dependence on the kappaB sites for optimal virus growth. Viruses without marker genes corroborated the finding that mutations to the kappaB sites impair virus production in cells with a high basal level of NF-kappaB. These data show that in T cells, HIV-1 can use NF-kappaB to enhance its growth but the virus is clearly able to grow in its absence.

Base Sequence↗
PubMed2002

Molecular evidence that the hepatitis C virus replicates in the oral mucosa.

BACKGROUND/AIMS: Patients infected with the hepatitis C virus (HCV) often have extrahepatic manifestations, which significantly contribute to HCV-related morbidity, but whose pathogenesis is largely unknown. Our aim was to evaluate the HCV replication in oral mucosa of chronic hepatitis C patients. METHODS: We collected oral mucosa specimens from 17 anti-HCV-positive and four anti-HCV-negative patients. Fifteen had oral lichen (12 anti-HCV-positive). Total mucosa RNA was extracted and analyzed for presence and titer of genomic and negative-strand HCV RNA. Findings were compared with clinical and pathological features. RESULTS: Genomic and negative-strand HCV RNA were detected, respectively, in 12 of 17 (70.6%) and four of 17 (23.5%) specimens from the chronic hepatitis C patients. No negative-strand HCV RNA was detected in five anti-HCV-positive patients without lichen (including three with normal mucosa). Presence and titer of the negative-strand HCV RNA were independent of HCV genotype, serum viral load, and histological diagnosis of liver lesions. The phylogenetic analysis of the envelope 2 region cloned from a normal mucosa and the corresponding serum further suggested that only lichen tissues appear to harbor replicating HCV. CONCLUSIONS: HCV may occasionally replicate in oral lichen tissue, possibly contributing to the pathogenesis of mucosa damage.

Adult↗
PubMed1989

Effect of dexamethasone on herpes simplex virus replication in mouse neuroblastoma cells (NB41A3): receptor characteristics.

Monolayers of NB41A3 (MNB) cells were exposed to pharmacologic doses of dexamethasone (DXM). After 24-h, the cells were infected with herpes simplex virus type 1 (HSV-1) at a multiplicity of infection (m.o.i.) = 0.1. After every 24-h period, extracellular and intracellular virus aliquots were collected and frozen. The aliquots were titered in a standard plaque-forming assay. It was shown that the hormone led to a statistically significant increase of extra- and intracellular virus titers above the titers exhibited by these cells without added hormone. The same experiment was repeated in Vero cells, but the hormone did not elevate the resultant HSV-1 titers. A binding assay was performed on these two cell lines by use of 3H-DXM to determine if a DXM receptor was present. Specific binding was seen, but only in the MNB cell line. The Bmax of this receptor was 480 fmol/mg protein and it had a Kd of 2.3 nM. The S value of the receptor ligand complex equalled 8.0. These results indicate that cells possessing hormone receptors allow for a more efficient replication of the virus and suggest that these hormones may play an important role in the exacerbation of herpes simplex virus infection in vivo.

Animals↗
PubMed2000

Selection of functional tRNA primers and primer binding site sequences from a retroviral combinatorial library: identification of new functional tRNA primers in murine leukemia virus replication.

Retroviral reverse transcription is initiated from a cellular tRNA molecule and all known exogenous isolates of murine leukemia virus utilise a tRNA(Pro)molecule. While several studies suggest flexibility in murine leukemia virus primer utilisation, studies on human immunodeficiency virus and avian retro-viruses have revealed evidence of molecular adapt-ation towards the specific tRNA isoacceptor used as replication primer. In this study, murine leukemia virus tRNA utilisation is investigated by in vivo screening of a retroviral vector combinatorial library with randomised primer binding sites. While most of the selected primer binding sites are complementary to the 3'-end of tRNA((Pro)), we also retrieved PBS sequences matching four other tRNA molecules and demonstrate that Akv murine leukemia virus vectors may efficiently replicate using tRNA(Arg(CCU)), tRNA(Phe(GAA))and a hitherto unknown human tRNA(Ser(CGA)).

3T3 Cells↗