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At least 271 records · Page 15Linked to original sources
PubMed1984

Virus replication and induction of interferon in human epidermal keratinocytes following infection with herpes simplex virus.

Keratinocyte cultures derived from surgical skin specimens of healthy newborns and adults were infected with herpes simplex virus (HSV) type 1 or 2. Typical HSV cytopathic effects involved all cell layers in stratified colonies, and paralleled the production of infectious virus. Virus growth curves and production of virus were comparable in newborn and adult keratinocytes. Interferon (IF) production by keratinocytes paralleled the yield of virus over at least 72 h, and was greater in cultures of adult cells than cultures from newborns. UV irradiation of HSV resulted in progressive virus inactivation and a parallel reduction in induced IF. This suggests that IF production was related to virus replication, and that irradiated (noninfectious) HSV DNA did not contribute significantly to the generation of IF in this system. These results establish that human epidermal keratinocytes can serve as a model system for quantitative assessment of herpes simplex virus infection.

Adult↗
PubMed2006

Negative regulation of hepatitis B virus replication by cellular Hsp40/DnaJ proteins through destabilization of viral core and X proteins.

The hepatitis B virus core protein consists of an amino-terminal capsid-assembly domain and a carboxyl-terminal RNA-binding domain. By using the yeast two-hybrid system, two Hsp40/DnaJ chaperone-family proteins, Hdj1 and hTid1, that interact with the carboxyl-terminal region (aa 94-185) of the core protein were identified. Hdj1 is the prototype member of the family and hTid1 is the human homologue of the Drosophila tumour-suppressor protein Tid56. Binding of the viral core protein with the Hsp40 proteins was confirmed by affinity chromatography and immunoprecipitation of transiently expressed proteins. Moreover, in a sucrose gradient, the precursor form of hTid1 co-sedimented with capsid-like particles composed of the full-length core protein. Unlike the general perception of the role of the cellular chaperone proteins in assisting viral protein folding and thus enhancing virus replication, ectopic expression of Hdj1 and hTid1 suppressed replication of HBV in transfected human hepatoma cells. Conversely, RNA interference-mediated knock-down of hTid1 resulted in increased HBV replication. It was found that both Hsp40 proteins specifically accelerated degradation of the viral core and HBx proteins. Our results suggest that the cellular chaperones, through destabilization of viral proteins, exert inhibitory functions on virus replication and hence may play suppressive roles in hepatocellular carcinoma.

Animals↗
PubMed1994

Newcastle disease virus vaccines: differences between Line C and Line 15I chickens with respect to virus replication and IgA responses in the gut and Harderian gland.

The Ulster 2C and Hitchner B1 strains of Newcastle disease virus were inoculated into inbred White Leghorn birds of the Reaseheath-C and 15I lines by the oculonasal route. Both viruses replicated in the Harderian gland (HG) and induced virus-specific IgA in the tears and bile. Ulster 2C but not Hitchner B1 replicated in the small intestine and induced virus-specific antibody forming cells (AFC) in the small intestine. Line 15I birds produced 120-fold more virus and 13-fold more IgA-AFC in the small intestine than Line C birds. Line C birds produced 20-fold more virus in the HG and at least three-fold higher titres of lacrimal IgA than Line 15I birds. The level of local virus replication in the HG or small intestine, which varied according to the line of bird, positively predicted the local antibody response in the same organ. When low doses of Ulster 2C were inoculated into Line C birds virus replication was low and irregular in birds older than 18 days whereas low doses of Hitchner B1 replicated in all ages of bird.

Aging↗
PubMed1998

Clinical significance of serum HBeAg and HBV-DNA-specific values of virus replication in chronic hepatitis-B virus infection.

The prevalence of serum HBV-DNA and that of HBeAg was evaluated in 44 subjects (27 males and 17 females) aged between 3 and 59 years. They were divided in two groups: (A) chronic asymptomatic HBsAg carriers; and (B) chronic HBsAg carriers with a history of HBV infection. The patients had been chronic HBV carriers between 8 months and 15 years. All underwent clinical and biochemical evaluation. The serological markers of HBV infection were tested using ABBOTT assay kits. The serum HBV-DNA was quantified using a hemiluminiscence molecular hybridization assay (Digene-Murex). HBV-DNA+ were 13 patients (29.55 +/- 6.88%). The highest level of viral replication (up to 50%) was measured in the patients aged from 3 to 29 years while in the others a 3 to 4-fold decrease of the viral replication was detected. HBV-DNA+ were 8 (23.53 +/- 6.39%) of the chronic asymptomatic hepatitis B carriers and 5 (50.00 +/- 7.5%) of the chronic HBV carriers with former acute hepatitis B infection. Similar results were obtained for the other index of viral replication--HBeAg/anti-HBe. Eight (23.53 +/- 6.39%) patients from group I and 4 (40.00 +/- 7.38%) patients from group II were HBeAg+ while anti-HBe+ were 26 (76.47 +/- 6.39%) and 6 (60.00 +/- 7.38%) patients from group I and II, respectively, i.e., about a quarter of the chronic asymptomatic HBsAg carriers and half of the chronic HBV carriers that had had an acute hepatitis B virus infection had HBV replication in their bodies. HBeAg+ patients had high levels of serum HBV-DNA (625.70-3328.00 pg/ml) which indicated extremely intensive viral replication. The presence of HBeAg and especially of HBV-DNA as markers of viral replication in chronic asymptomatic HBsAg carriers and chronic HBsAg carriers with a prior acute hepatitis B virus infection provide important information for the clinical decisions.

Adolescent↗
PubMed2003

Disulfide-linked integrase oligomers involving C280 residues are formed in vitro and in vivo but are not essential for human immunodeficiency virus replication.

The human immunodeficiency virus type 1 integrase (IN) forms an oligomer that integrates both ends of the viral DNA. The nature of the active oligomer is unclear. Recombinant IN obtained under reducing conditions is always in the form of noncovalent oligomers. However, disulfide-linked oligomers of IN were recently observed within viral particles. We show that IN produced from a baculovirus expression system can form disulfide-linked oligomers. We investigated which residues are responsible for the disulfide bridges and the relationship between the ability to form covalent dimers and IN activity. Only the mutation of residue C280 was sufficient to prevent the formation of intermolecular disulfide bridges in oligomers of recombinant IN. IN activity was studied under and versus nonreducing conditions: the formation of disulfide bridges was not required for the in vitro activities of the enzyme. Moreover, the covalent dimer does not dissociate into individual protomers on disulfide bridge reduction. Instead, IN undergoes a spontaneous multimerization process that yields a homogenous noncovalent tetramer. The C280S mutation also completely abolished the formation of disulfide bonds in the context of the viral particle. Finally, the replication of the mutant virus was investigated in replicating and arrested cells. The infectivity of the virus was not affected by the C280S IN mutation in either dividing or nondividing cells. The disulfide-linked form of the IN oligomers observed in the viral particles is thus not required for viral replication.

Cysteine↗
PubMed1991

Reactivation of hepatitis B virus replication in patients receiving cytotoxic therapy. Report of a prospective study.

One hundred Chinese patients who received induction cytotoxic therapy for malignant lymphoma were prospectively studied to determine the incidence, morbidity, mortality, and predisposing factors for reactivation of hepatitis B virus replication during cytotoxic therapy. In 18 (67%) hepatitis B surface antigen-positive and 10 (14%) hepatitis B surface antigen-negative patients, hepatitis developed during cytotoxic therapy (P less than 0.0001). Hepatitis could be attributed to exacerbation or reactivation of chronic hepatitis B in 13 (72%) hepatitis B surface antigen-positive patients but in only 2 (20%) hepatitis B surface antigen-negative patients (P less than 0.0001). Sudden increase or reactivation of hepatitis B virus replication gave rise to icteric hepatitis, nonfatal hepatic failure, and death in 22.3%, 3.7%, and 3.7% of patients who were positive for hepatitis B surface antigen; in 2%, 2%, and 0% of those positive for hepatitis B antibodies; and in none of those who were seronegative. Among the hepatitis B surface antigen-positive patients, male sex was the only factor that was associated with an increased risk of reactivation of hepatitis B virus replication. We recommend that hepatitis B surface antigen-positive patients with malignancies receiving cytotoxic therapy be closely monitored.

Adolescent↗
PubMed1983

Persistent infection of cultivated cells with lymphocytic choriomeningitis virus: regulation of virus replication. Brief report.

L cells were infected with lymphocytic choriomeningitis virus (LCM virus). They were subcultivated and infectious virus and interfering virus were quantified at intervals. Both entities fluctuated in perfect parallelism. Superinfection with LCM virus revealed a pattern of interference that bore no simple relationship with the quantity of interfering virus present. We explain the oscillating pattern of virus replication, which characterizes this type of LCM virus carrier cultures, as being due to spontaneous shutdown of virus synthesis in conjunction with the action of a resistance factor produced by cells coinfected with infectious virus and interfering virus.

Animals↗
PubMed1993

Anti-glycoprotein B monoclonal antibody protects T cell-depleted mice against herpes simplex virus infection by inhibition of virus replication at the inoculated mucous membranes.

A monoclonal antibody (MAb 2c) specific for glycoprotein B of herpes simplex virus (HSV) mediated clearance of the virus from the infected mucous membranes. Young adult C57BL/6J mice were inoculated intravaginally with HSV type 1 and injected intraperitoneally either 24 and 72 h or 65 and 265 h post-inoculation with a polyclonal immune serum or the MAb 2c, both adjusted to the same neutralizing capacity. Immunization with the polyclonal immune serum did not alter the duration of virus shedding from the genital mucous membranes although a lethal outcome of infection was clearly prevented. Immunization with the MAb, however, resulted in a rapid clearance of the virus from the genital tract thus completely inhibiting genital inflammation and lethality. The same effects were achieved in mice depleted in vivo of CD4+ T cells although peripheral virus replication continued longer in these mice. In mice depleted of both CD4+ and CD8+ T cells the polyclonal immune serum was no longer able to protect against lethality, and virus replication in the mucous membranes persisted until the mice died. In contrast, after treatment with the MAb peripheral infection was quickly eliminated and all mice survived. These findings indicate that clearance of the virus from the primary site of replication can be mediated by humoral immunity. The relevance of this observation for vaccination against HSV is discussed.

Animals↗
PubMed2007

Bleomycin treatment causes enhancement of virus replication in the lungs of SHIV-infected macaques.

Pneumonia is a major complication of human immunodeficiency virus (HIV) pathogenesis but it develops only after prolonged infection. We used the macaque model to explore a hypothesis that the disease is a two-stage process, the first stage being establishment of the viral infection in the lung and the second being amplification of virus replication by host factors induced by chemical agents or opportunistic pathogens in the lung. Bleomycin, a chemical known to induce diffuse alveolar damage and pulmonary fibrosis with accumulation of macrophages and a rich T helper type 2 (Th2) cytokine environment, was inoculated intratracheally into five of eight SHIV 89.6P-infected macaques and into one uninfected macaque. Three additional simian HIV (SHIV)-infected macaques without bleomycin treatment served as untreated virus controls. Although none of the animals became clinically ill, bleomycin induced classical host responses in the lungs of all the treated, virus-infected macaques. There was enhanced production of the chemokine, monocyte chemotactic protein-1 (MCP-1), that had previously been shown to cause enhanced replication of the virus. Four of the five treated animals developed more productive SHIV infection in the lungs compared with the infected untreated animals. Enhanced virus replication was found primarily in infiltrating macrophages. Enhanced replication of the virus in the lungs was associated with host factors induced by the drug and supported the hypothesis for a two-stage process of pulmonary pathogenesis.

Animals↗
PubMed1984

Suppression of influenza virus replication in infected mice by protease inhibitors.

Administration of the protease inhibitors, epsilon-aminocaproic acid or aprotinins, to mice infected with mouse-adapted influenza virus strain A/PR/8/34 (HON1) and A/Aichi/2/68 (H3N2) reduced virus replication in the lungs. Up to 100-fold reduction of virus titre and virus-induced neuraminidase activity were revealed in mouse lungs under protease inhibitor treatment. As a result, drug-treated mice rapidly cleared the virus from their lungs. The predominant synthesis was of non-infectious virions with uncleaved haemagglutinin in the lungs of drug-treated mice, in contrast to the production of highly infectious virions with proteolytically cleaved haemagglutinin in untreated mice. These observations suggest that protease inhibitors suppress influenza virus replication in mouse lungs due to prevention of haemagglutinin cleavage and virus proteolytic activation.

Aminocaproic Acid↗
PubMed1976

Interactions of murine leukemia virus (MuLV) with isolated lymphocytes. I. Virus replication in lymphocytes infected with Friend virus and cultures in diffusion chambers in vivo.

A new technique for infection of mature lymphocytes with murine leukemia virus (Friend) MuLV-F) is described. Spleen cells for normal, non-infected donors were placed into diffusion chambers (constructed with 0.22 mum por size Millipore filters) which were then implanted into the peritoneal cavities of normal syngeneic recipient mice. The cells were infected with an injection of MuLV-F into the peritoneal cavity and, in some instances, also by placing virus into the chambers. Cells were recovered by treating the chamber content with elastase and collagenase. The infection was determined in two ways: (1) cells with replicating MuLV were enumerated as infection centers (IC) on S+L- indicator cells; and (2) virus-related cell membrane antigen (MA) was detected by immunofluorescence. Cells recovered from chambers after 2-3 weeks of culture represented about 10% of the original inoculum; viability was approximately 90%. The number of IC in MuLV-F-infected chambers was about 10 times higher than obtained by infection and cultivation of spleen cells in vitro. The kinetics of IC and MA in chamber-cultured. MuLV-F-infected spleen cells was similar to that in the spleen of infected mice during the first 10 days after infection. Later on, the process of infection within the chambers slowed down, reaching about 50% MA-positive and about 10% IC-positive cells, whereas the number of both IC- and MA-positive cells in the spleen reached 80% or more. The infection of splenic lymphocytes in diffusion chambers occurred equally well when chambers were implanted into: (1) syngeneic, virus susceptible hosts; (2) syngeneic, lethally irradiated hosts; and (3) allogeneic, virus-resistant hosts, suggesting that the process within the chamber is independent of MuLV replication in the tissues of the chamber-bearing mouse. The diffusion chamber technique seems to provide an environment in which various types of isolated lymphocytes of different mouse strains can interact with MuLV almost as efficiently as in vivo.

Animals↗
PubMed1990

Influence of hepatitis delta virus replication in the presence of hepatitis B virus DNA in peripheral blood mononuclear cells.

The presence of hepatitis B virus DNA was studied in peripheral blood mononuclear cell samples from 259 HBsAg carriers (229 anti-hepatitis delta negative, 30 anti-hepatitis delta positive), 16 anti-HBc-positive HBsAg-negative patients and 30 patients without hepatitis B virus markers. Hepatitis B virus DNA sequences were detected in peripheral blood mononuclear cell from 115 (44.4%) of the chronic HBsAg carriers and from two (12%) of the anti-HBc-positive, HBsAg-negative patients. In anti-hepatitis delta-negative patients, viral DNA was positive in peripheral blood mononuclear cell from 74 (46%) and from 24 (35.5%) with and without serum HBV-DNA, respectively. With respect to anti-hepatitis delta-positive patients, viral DNA was found in peripheral blood mononuclear cell in 8 of 13 (61.5%) of the patients with circulating hepatitis delta virus RNA and in 9 of 17 (53%) of the hepatitis delta virus RNA-negative subjects. Regarding hepatitis B virus DNA in serum and peripheral blood mononuclear cell, 71% (5 of 7) of the patients with serum hepatitis B virus DNA had this marker in peripheral blood mononuclear cell, whereas 52% (12 of 23) of the patients without serum hepatitis B virus DNA had hepatitis B virus DNA in peripheral blood mononuclear cell. A Southern blot analysis was also carried out on peripheral blood mononuclear cell samples from 30 patients. Hepatitis B virus DNA was detected in 16 patients as free forms, in 12 patients as dimers and free forms and as free circular together with free linear forms in the remaining two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Effect of novobiocin and other DNA gyrase inhibitors on virus replication and DNA synthesis in herpes simplex virus type 1-infected BHK cells.

The four known inhibitors of the bacterial DNA gyrase (nalidixic acid, oxolinic acid, novobiocin and coumermycin A) were investigated with respect to their effect on the growth of uninfected BHK cells and the yield of virus from herpes simplex virus type 1 (HSV-1)-infected BHK cells. High concentrations of nalidixic acid and oxolinic acid (about 10 mM) were needed for 50% inhibition of cellular and viral multiplication with less than fourfold preferential inhibition of virus over cell growth. Novobiocin and coumermycin were effective at lower molar concentrations and the amount needed for 50% inhibition was 10-fold higher for cell growth than for virus yield. At 5 x 10(-4) M, novobiocin inhibited DNA synthesis in uninfected cells to approx. 20% of non-treated controls, while virus DNA in infected cells was almost completely inhibited (approx. 1% of controls). Residual cellular DNA synthesis in infected cells was rather insensitive (approx. 90% of controls) to this concentration of novobiocin.

Aminocoumarins↗
PubMed1996

A double blind, placebo-controlled study to assess the effect of famciclovir on virus replication in patients with chronic hepatitis B virus infection.

This is the first double-blind controlled study of famciclovir, an oral antiviral agent, as potential therapy for chronic hepatitis B virus (HBV) carries. A fall of more than 90% in HBV DNA levels was noted in six of 11 evaluable patients treated with a 10 day course of oral famciclovir. Further studies with more prolonged therapy are ongoing.

2-Aminopurine↗
PubMed1986

Biochemical and genetic evidence for the hepatitis B virus replication strategy.

Hepatitis B viruses synthesize their open circular DNA genomes by reverse transcription of an RNA intermediate. The details of this process have been examined with the use of mammalian hepatitis B viruses to map the sites for initiation and termination of DNA synthesis and to explore the consequences of mutations introduced at short, separated direct repeats (DR1 and DR2) implicated in the mechanisms of initiation. The first DNA strand to be synthesized is initiated within DR1, apparently by a protein primer, and the completed strand has a short terminal redundancy. In contrast, the second DNA strand begins with the sequence adjacent to DR2, but its 5' end is joined to an oligoribonucleotide that contains DR1; thus the putative RNA primer has been transposed to the position of DR2. It is now possible to propose a detailed strategy for reverse transcription by hepatitis B viruses that can be instructively compared with that used by retroviruses.

Animals↗
PubMed1996

Conditional human immunodeficiency virus type 1 protease mutants show no role for the viral protease early in virus replication.

The human immunodeficiency virus type 1 protease plays a critical role in the proteolytic processing of precursor polyproteins during virion maturation. Contradictory evidence has been obtained for a possible role for the protease early after infection, i.e., during DNA synthesis and/or integration. We have reexamined this question by using conditional mutants of the protease. In one set of experiments, protease mutants that confer a temperature-sensitive phenotype for processing were used to assess the need for protease activity early after infection. No significant difference from results with wild-type virus was seen when infections were carried out at either 35 or 40 degrees C. In a separate set of experiments, infections were carried out in the presence of a protease inhibitor. In this case, both wild-type virus and a drug-resistant variant were used, the latter as a control to ensure a specific effect of the inhibitor. Infection with either virus was not inhibited at drug concentrations that were up to 10-fold higher than those needed to inhibit intracellular processing by the viral protease. The results obtained by both of these experimental protocols provide evidence that the human immunodeficiency virus type 1 protease does not play a role early after infection.

Cell Line↗