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At least 937 records · Page 52Linked to original sources
PubMed1991

Persistent infection with lymphocytic choriomeningitis virus enhances expression of MHC class I glycoprotein on cultured mouse brain endothelial cells.

Brain endothelial cells (EC) represent a major component of the blood/brain barrier, which activated CTL cross to enter the central nervous system. Several viruses also penetrate the central nervous system through the blood stream via the brain EC. The studies reported here focus on understanding the principles and consequences of interactions among viruses, lymphocytes, and EC in the brain. As shown persistent but not acute infection by lymphocytic choriomeningitis virus enhances the expression of MHC class I glycoproteins on the brain EC of mice. This increase in MHC expression during viral infection does not seem to result from the release of cytokines. However, replicative virus is required, because UV inactivated virus fails to enhance MHC expression. Viral determinants appear on EC surfaces after infection and serve as targets for CTL directed lysis. In contrast, neurons (OBL 21 neuronal cell line), which express negligible amounts of MHC class I glycoproteins, show no gain in MHC markers during persistent viral infection and are not targets for virus-specific CTL killing.

Animals↗
PubMed2002

Bone marrow chimeras reveal non-H-2 hematopoietic control of susceptibility to Theiler's virus persistent infection.

The DA strain of Theiler's murine encephalomyelitis virus persists in the white matter of the spinal cords of susceptible mice. Previous results showed that the difference in susceptibility to viral persistence between the susceptible SJL/J strain and the resistant B10.S strain was due to multiple non-H-2 loci. The respective roles of hematopoietic and nonhematopoietic cells in this difference have been evaluated with bone marrow chimeras. The results show that non-H-2 loci with a major effect on susceptibility are expressed in hematopoietic cells. However, the study of the SJL.B10-D10Mit180-D10Mit74 congenic line suggests that other loci expressed in nonhematopoietic cells also play a role.

Animals↗
PubMed1995

Mice as carriers of Salmonella enteritidis on persistently infected poultry units.

Evidence of the possible role of wild mice in the epidemiology of Salmonella enteritidis infection on broiler breeder and layer breeder units was obtained by a bacteriological examination of local mice. Persistent S enteritidis infection in birds on these units had been a problem and a high proportion of the mice were found to carry salmonella. S enteritidis was isolated from the liver and the intestine of most of the mice, indicating a systemic infection. Three-week-old chicks were infected by contact with droppings from mice which had been infected experimentally with S enteritidis two and five months previously. Wild mice infected artificially or naturally excreted S enteritidis intermittently, with up to 10(4) organisms in some individual droppings. A naturally infected mouse which died after intermittently excreting small numbers of S enteritidis in its droppings for 19 weeks had 10(4) organisms/g of liver and 10(3)/g of macerated intestine and contents. S enteritidis was also found in fetal tissue in a naturally infected mouse suggesting the possibility that the organism might be transmitted vertically.

Animal Husbandry↗
PubMed1994

[Evolution of hepatitis C virus (HCV) viremia and adaptation of HCV in persistent infection in patients with acute hepatitis].

HCV viremia had ceased in majority of patients with acute resolving hepatitis C, and it continued for at least 1 year in all patients with chronicity. The HCV RNA titer in serum decreased markedly after the onset of acute hepatitis and then re-elevated in patients with chronicity. During this period, amino acid substitution rate in the E2/NS1 region (especially in HVR) was significantly higher in patients with acute hepatitis than in patients with chronic hepatitis. When patients with acute hepatitis C became persistent HCV carriers, the substitution rate decreased to the level seen in patients with chronic hepatitis. These observations suggest that rapid substitution of the amino acid sequence in the HVR of the E2/NS1 region may be one of the mechanisms of persistent HCV infection.

Acute Disease↗
PubMed1995

Association of hepatitis C virus particles with immunoglobulin: a mechanism for persistent infection.

The physical properties of hepatitis C virus (HCV) particles were determined by ultracentrifugation on 20-60% isopycnic sucrose density gradients. We report that (i) two populations of HCV particles were found in the sera of patients with chronic HCV infection [at high density (1.186-1.213 g/ml) and at low density (1.099-1.127 g/ml)], (ii) virus particles with high density values were associated with immunoglobulin, and (iii) virus particles with low density values accumulated base changes within a hypervariable region (HVR) of the E2 envelope domain of the RNA genome. The results indicate that base changes within the HVR of E2 lead to the accumulation of immunoglobulin-free virus particles. Therefore, these findings imply that persistent HCV infection is established as a consequence of sequence variation in the E2 envelope domain.

Amino Acid Sequence↗
PubMed1992

Absence of persistent infection with enteroviruses in muscles of patients with inflammatory myopathies.

We searched for enteroviral nucleic acid sequences using the polymerase chain reaction and slot-blot hybridization in coded muscle biopsy specimens from 39 patients with active inflammatory myopathies (polymyositis, dermatomyositis, and inclusion-body myositis) and from 16 patients with other neuromuscular diseases, including patients with postpolio syndrome. For primers, we used sequences of the noncoding region at the 5' end of the viral RNA. We failed to detect specific enteroviral nucleic acid sequences in the muscle biopsy specimens. Because this sensitive technique can amplify even low copy numbers of the viral genome, it appears unlikely that a persistent enteroviral infection is the cause of inflammatory myopathies.

Base Sequence↗
PubMed2004

Hyperthermic pre-conditioning promotes measles virus clearance from brain in a mouse model of persistent infection.

Nervous tissue subjected to hyperthermic pre-conditioning is resistance to numerous insults although in vitro, the same treatment can increase gene expression and cytopathic effect of neurotropic paramyxoviruses, including measles virus (MV). The present work determined whether the in vivo relationship between hyperthermic pre-conditioning and MV infection would be to increase neuropathogenicity or, conversely, to promote clearance. Balb/c mice 36 h of age were exposed to a 41 degrees C hyperthermic treatment for 30 min. Intracranial inoculation of mice with Edmonston MV was performed at 6 h following the heat treatment, a time point exhibiting elevated levels of the major inducible 70-kDa heat shock protein in brain, a hallmark of pre-conditioning. Forty-seven percent of the non-heated animals supported a persistent cytopathic infection at 21-day post infection (PI) based upon the quantitative detection of viral RNA in brain using real time RT-PCR. Cytopathic effect in the infected brains was proportionate to viral RNA burden. In contrast, infected stress conditioned mice lacked significant cytopathic effect and clearance was demonstrated in 95% of the animals. Analysis of shorter post-infection intervals showed that levels of viral RNA in brain were equivalent between stress conditioned and non-conditioned mice at 2 and 7 days PI, with clearance being first evident in both groups at 14 days. The temporal onset and progression of clearance was correlated to splenocyte blastogenic responsiveness to purified MV antigen but not the production of MV-specific antibody. Collectively, these results support the hypothesis that stress conditioning enhances the efficacy of cell-mediated immune responses known to mediate viral clearance from brain.

Animals↗
PubMedDate not supplied

Mathematical modelling of American cutaneous leishmaniasis: incidental hosts and threshold conditions for infection persistence.

We present a model for the dynamics of transmission of American Cutaneous Leishmaniasis (ACL) that includes a population of incidental hosts for parasites (that is, they act only as sinks of infection), along with species that are reservoir hosts (that is, both source and sink of infection). Although, there is evidence that suggests the existence of incidental hosts for Leishmania parasites, there are no mathematical models developed to account for this. Based on this model we obtained expressions that allow computing the threshold conditions for the persistence of the infection using three different approaches. The three expressions agree in the parameters involved in the computation of the threshold, and also in the parameters that are excluded from it, which are those related to the transmission in incidental hosts. We also suggest alternatives for future development in the modelling of the dynamics of transmission of ACL, according to the needs of a more realistic, precise, or general character of the model.

Animals↗
PubMed1971

Lytic and turbid plaque-type mutants of lymphocytic choriomeningitis virus as a cause of neurological disease or persistent infection.

Mouse-passaged lymphocytic choriomeningitis (LCM) virus was found to contain a mixture of two different plaque-type mutants when plated on BHK-21/13S cells in agarose suspension. One mutant gave rise to clear plaques, with death of the cells, whereas the other produced turbid plaques which were sometimes very difficult to see. The clear-plaque variant caused a pronounced cytopathic effect on BHK-21 cells, but the turbid variant caused none; it also interfered with the cytopathic effect due to the clear variant. Brain-passed LCM virus was found to consist mainly of the clear-plaque-type, whereas liver-passed virus was mainly turbid-plaque-type. The clear type induced convulsions and early death after intracerebral inoculation of adult mice; the turbid variant caused no convulsions and late deaths. In newborn mice, the clear-plaque-type was uniformly fatal, whereas the turbid variant caused no deaths but instead induced persistent tolerant infection.

Animals↗
PubMed1985

Transfusion-associated acquired immunodeficiency syndrome. Evidence for persistent infection in blood donors.

To investigate whether infection with human T-cell lymphotropic virus/lymphadenopathy-associated virus (HTLV-III/LAV) may be persistent in asymptomatic persons and to correlate infection with seropositivity, we performed virologic and serologic studies in 25 of 30 persons who were identified as being at high risk for the acquired immunodeficiency syndrome (AIDS) and who had donated blood to patients who later contracted transfusion-associated AIDS. High-risk donors were those who belonged to a high-risk population, had AIDS or a closely related condition, or had a low ratio of helper to suppressor T lymphocytes. We performed similar studies in 6 of the 24 patients with AIDS who had received donations from this group. HTLV-III/LAV was isolated from 22 of the 25 donors, between 12 and 52 months (mean, 28) after they had donated blood, and from all 6 recipients, between 14 and 37 months (mean, 26) after they had received blood. Of the 22 virus-positive donors, 2 have contracted AIDS, 5 have generalized lymphadenopathy, and 15 (68 per cent) remain asymptomatic. Antibodies to HTLV-III/LAV were detectable by the enzyme-linked immunosorbent assay in serum samples obtained from each person at the time the virus was isolated. We conclude that infection with HTLV-III/LAV may be persistent and asymptomatic for years. This demonstration that viremic patients may be asymptomatic supports the use of serologic screening of donated blood to supplement current procedures for the prevention of transfusion-associated AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Expression of members of the 28-kilodalton major outer membrane protein family of Ehrlichia chaffeensis during persistent infection.

The 28-kDa immunodominant outer membrane proteins (P28 OMPs) of Ehrlichia chaffeensis are encoded by a multigene family. As an indirect measure of the in vivo expression of the members of the p28 multigene family of E. chaffeensis, sera from two beagle dogs experimentally infected with E. chaffeensis were evaluated for the presence of specific antibodies to P28 OMPs by enzyme-linked immunosorbent assay. Antigenic peptides unique to each of the P28s were identified within the first hypervariable region of each P28 OMP. Serological responses to peptides derived from all P28 OMPs were detected from day 30 postinoculation to day 468 and from day 46 until day 159 in the two beagles. Although antibody titers to the peptides fluctuated, the peak response to all of the peptides appeared simultaneously in each dog. The antibody responses to another outer membrane protein of E. chaffeensis (GP120) showed similar temporal and quantitative changes. These data suggest that the P28 OMPs are expressed concurrently during persistent Ehrlichia infection.

Amino Acid Sequence↗
PubMed1992

Cytomegalovirus infection persists in the liver graft in the vanishing bile duct syndrome.

Cytomegalovirus infection is one factor implicated in the cause of the vanishing bile duct syndrome complicating liver transplantation. To further investigate the role of cytomegalovirus in this syndrome, we studied serial liver biopsy material by in situ hybridization for cytomegalovirus DNA using a highly sensitive technique that allows the localization of viral replication. Cytomegalovirus DNA was identified in hepatocytes in 10 of 12 patients with the vanishing bile duct syndrome, 1 of whom had no serological evidence of cytomegalovirus infection. It was also present in all 18 patients with uncomplicated cytomegalovirus infection but was not identified in any of 10 subjects with transplants who had neither complication. Nine of the patients in this series underwent a diagnostic liver biopsy at 1 wk and subsequently had cytomegalovirus infection develop; cytomegalovirus DNA was identified in liver tissue of all nine patients, indicating that cytomegalovirus replication commences at an early stage. In those with uncomplicated cytomegalovirus, infection occurred earlier (p less than 0.05) but was eliminated more quickly (p less than 0.0005), and the number of infected hepatocytes was greater (p less than 0.05) when compared with those with the vanishing bile duct syndrome; in these, cytomegalovirus DNA was detectable until death or retransplantation. Cytomegalovirus DNA was never identified in either biliary or endothelial tissue. These data indicate that the vanishing bile duct syndrome is associated with persistent cytomegalovirus replication within hepatocytes.

Cholestasis↗
PubMed1996

Frequent detection of reviraemia in ducks persistently infected with avian leukosis retroviruses.

Ducks intraembryonally infected with avian leukosis viruses of subgroup C (ALV-C) were followed for a long period (up to 6.8 years), and the viraemia and production of virus-neutralizing antibodies were measured. In three independent experiments comprising ducks inoculated with uncloned and/or molecularly cloned ALV-C, we found that after the elimination of primary post-hatching viraemia, reviraemia could be detected in 60-70% of infected animals. Based on the course of viraemia, the individual ducks were assigned to four different groups: Group I (no reviraemia), Group II (one transient reviraemic period), Group III (one persistent reviraemic period), Group IV (fluctuating reviraemia). In comparison to sera from ducks included in Group I and/or II, a significant decrease in neutralizing activity of sera from animals comprised in Group III and/or IV was observed. Two out of four reviraemic viruses were not neutralized by antiserum against ALV-C, instead their infectivity was enhanced. Long-term follow-up of the cell-associated virus revealed that its rescuability by cocultivation with chicken embryo fibroblasts fluctuated in about 50% of animals. In the reviraemic phase of infection, integrated proviruses could be detected by Southern blotting in a majority of tissues examined. Our data document that many features recognized in lentiviruses are valid also for oncoviruses transmitted to heterologous hosts and substantiate further the suitability of ALV-C-infected ducks as a model for studying persistent retroviral infection.

Animals↗
PubMed1997

AIDS pathogenesis: the role of accessory gene mutations, leading to formation of long-lived persistently infected cells and/or apoptosis-inducing HIV-1 particles.

Human immunodeficiency virus type 1 (HIV-1) infection indirectly induces activation-dependent apoptosis in bystander immune CD4+ T-cells, a hallmark of AIDS pathogenesis. It is well known that this pathogenetic event is significantly correlated with a high virus load. Active viral replication occurs in HIV-1 asymptomatic carriers throughout all stages of clinical disease. Most of the HIV-1 in plasma is derived from short-lived infected cells with a half life of a few days; however, a minor population of virus is derived from long-lived persistently and latently infected cells. Recently, the importance of such latent reservoirs for HIV-1 has come to the forefront because of studies with potent antiretroviral inhibitors that block only new rounds of infection. An initial large drop in viral load occurs within two weeks as noted by a decrease in plasma viremia. This is then followed by a slower second-phase decay, since only a small fraction of latently infected resting CD4+ T-cells carry replication-competent, integrated provirus. This review highlights the mechanisms of apoptosis induction in bystander immune cells by both protease-defective, gp120-containing HIV-1 particles, as well as by wild-type virus that appears to be derived predominantly from long-lived infected cells. A model involving the NH2-terminal Nef domain (p7) in this 'bystander apoptosis' event is also presented.

Acquired Immunodeficiency Syndrome↗
PubMed1990

The budding of defective human immunodeficiency virus type 1 (HIV-1) particles from cell clones persistently infected with HIV-1.

Three cell clones producing large numbers of infectious or noninfectious particles of human immunodeficiency virus type 1 (HIV-1), designated M 10/LAV-2, M 16/LAV-3, and MT/LAV-17, were isolated from persistently HIV-1-infected MT-4 cells. In M 10/LAV-2, the HIV-1 proteins were defective in the cleavage of gag precursor protein, and the particles were doughnut-shaped with a double-ring structure. These particles were produced by budding at the cell surface from crescentic structures followed by the formation of double-ring structures. The viral proteins in M 16/LAV-3 were defective in the cleavage of env precursor protein. The morphology of the virus particles was intact, and an electron dense bar-shaped core was seen inside a single-ring enveloped structure. The intact particles were released from the cell surface by a budding process in which crescent shape structures first appeared at the cell membrane, then subsequently just before release matured to a complete structure with an electron dense core. In MT/LAV-17, the synthesis of HIV-1 proteins was normal, and the particles were teardrop-shaped with an intact core structure. These particles were produced by budding with an electron dense core at the cell surface. Thus, it was suggested that the morphological maturation of HIV-1 particles was completed just before release from the cell surface in several cell clones producing HIV-1 particles of different morphology.

Antibodies, Monoclonal↗
PubMed1987

Demonstration of bovine viral diarrhoea virus in peripheral blood mononuclear cells of persistently infected, clinically normal cattle.

Peripheral blood mononuclear cells (PBL) from cattle known to be persistently viraemic with bovine viral diarrhoea virus (BVDV) following a foetal infection, were examined for the presence of viral antigens and cell-associated infectious virus. Using immunocytochemical techniques, physical separations of PBL subsets and virus isolation techniques (directly and by cocultivation) it was found that infection occurred in B and T lymphocytes, monocytes, and a group of cells designated null cells for lack of more specific classification. The latter three groups also supported viral replication, as infectious virus could be isolated from enriched cell populations. BVDV-like particles in cytoplasmic vesicles of PBL subsets were detected by electron microscopy.

Animals↗
PubMed1989

Viral antigen distribution in the central nervous system of cattle persistently infected with bovine viral diarrhea virus.

Distribution of viral antigens in the central nervous system of 25 cattle with a persistent bovine viral diarrhea virus (BVDV) infection was studied. Using a polyclonal antiserum produced in pigs and the direct immunofluorescence and immunoperoxidase technique, BVDV antigen was located exclusively in neurons. Predilection sites for viral persistence were cerebral cortex and hippocampus; in other areas of brain and spinal cord, viral antigens were in single neurons or small groups of neurons. There was no morphological evidence of cellular alteration due to viral persistence. Perivascular lymphocytic infiltrations were in affected nervous tissue. It is concluded that the central nervous system is an important location for persistence of BVDV.

Animals↗
PubMed1999

Persistent infection of a lymphoma cell line by herpes simplex virus.

The peripheral blood cells from a patient with a B-cell lymphoma were established in long-term tissue culture. Two years after establishment of the cells in culture they were infected with herpes simplex virus type 2 and the productivity and duration of viral persistence investigated. One week after infection the lymphoblastoid cells were productively infected and have remained so for a period of over 3 years. Expression of a viral glycoprotein antigen was evaluated by using a fluorescein-labeled monoclonal anti-herpes simplex virus type 2 antibody and revealed a spectrum of staining reactions grading from a lightly stippled to very intense pattern. Polymerase chain reaction analysis of the infected cells revealed the presence of the herpes simplex virus type 2 DNA polymerase gene in the infected cells that was absent from the uninfected lymphoblastoid cells. These results taken together with the long-term growth characteristics of both the infected and uninfected lymphoblastoid cells suggest that this cell line may be a good model system for studying viral infection, viral replication, viral latency, and clinical application for the isolation of human herpes virus.

Adult↗