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At least 901 records · Page 50Linked to original sources
PubMed2000

Enhanced susceptibility to subcutaneous abscess formation and persistent infection around catheters is associated with sustained interleukin-1beta levels.

A persistent Staphylococcus epidermidis infection in mice around a subcutaneous polyvinylpyrrolidone-grafted silicon elastomer catheter (SEpvp) but not around a conventional silicon elastomer catheter was observed. With SEpvp pericatheter tissue, protracted and exaggerated interleukin-1beta (IL-1beta) production was found. Apparently, sustained levels of IL-1beta are associated with enhanced susceptibility to biomaterial-associated S. epidermidis infection.

Abscess↗
PubMed2006

Repeated intravaginal inoculation with cell-associated simian immunodeficiency virus results in persistent infection of nonhuman primates.

The goal of the present study was to develop a nonhuman primate model of intravaginal human immunodeficiency virus (HIV) transmission with cell-associated virus. Reproductively mature, cycling cynomolgus macaques with or without chemically induced, transient ulcers of the lower female reproductive tract repeatedly received challenge with a variable amount of in vitro simian immunodeficiency virus mac239-infected peripheral blood mononuclear cells. Persistent viremia was established with surprisingly few infectious lymphocytes containing physiologically relevant quantities of cell-associated virus. This model will be indispensable for the testing of vaccines and topical agents that are aimed toward the prevention of heterosexual transmission of HIV.

Administration, Intravaginal↗
PubMed2005

Persistent diarrhea in the returning traveler: think beyond persistent infection.

The report describes a young female United Nations worker, stationed in East Timor for an extended duration, who presented with persistent travelers' diarrhea and who was convinced that she was harboring a persistent infestation. In fact, careful history, laboratory evaluation and endoscopy with duodenal biopsies found all the classical hallmarks of unmasked celiac sprue. The patient then had a dramatic response to a gluten-free diet, with complete resolution of symptoms. Persistent travelers' diarrhea is an entity which carries an interesting and extensive differential diagnosis beyond persistent enteric infections or infestations. Rather, many sufferers have long been cleared of the initial offending pathogen and are left with either a post-infectious disorder of absorption, digestion, motility or visceral sensation or carry a chronic gastrointestinal disorder which has been unmasked by an enteric infection, such as idiopathic inflammatory bowel disease, gastrointestinal malignancy or celiac sprue. Other key issues raised by the case include the vanishing incidence of tropical sprue, an entity to which most clinicians would have mistakenly attributed this malabsorptive syndrome arising in a traveler, and the under-recognition of the protean manifestations of celiac sprue, to which we would add persistent travelers' diarrhea.

Adult↗
PubMed2001

Tissue distribution of bovine viral diarrhea virus antigens in persistently infected cattle.

The tissue distribution and cellular localization of viral antigens in three cattle with persistent bovine viral diarrhea virus (BVDV) infection was studied. In three cases, necropsy findings of oral ulcers, abmasal ulcers and necrosis of Peyer's patches were suspected have been caused by BVDV infection. Non-cytopathic BVDV was isolated from a tissue pool of liver, kidneys and spleen. Immunohistochemical detection of BVDV showed that BVDV antigens were detected in both epithelial and nonepithelial cells in all examined organs, including the gastrointestinal tract, liver, pancreas, lung, lymphatic organs (spleen, lymph nodes), adrenal gland, ovary, uterus, and the mammary gland. These findings support the hypothesis that animals with persistent BVDV infection spread BVDV through all routes, and that infertility in BVDV infection is associated with the infection of BVDV in the ovaries and uteri.

Adrenal Glands↗
PubMed1998

Oral administration of human T-cell leukemia virus type 1 induces immune unresponsiveness with persistent infection in adult rats.

The major route of human T-cell leukemia virus type 1 (HTLV-1) infection is mother-to-child transmission caused by breast-feeding. We investigated the host immune responses to orally established persistent HTLV-1 infection in adult rats. HTLV-1-producing MT-2 cells were inoculated into immunocompetent adult rats either orally, intravenously, or intraperitoneally. HTLV-1 proviruses were detected in the peripheral blood and several organs for at least 12 weeks. Transmission of HTLV-1 to these animals was confirmed by analysis of HTLV-1 flanking regions. Despite persistent HTLV-1 presence, none of the orally inoculated rats produced detectable levels of anti-HTLV-1 antibodies, whereas all intravenously or intraperitoneally inoculated rats showed significant anti-HTLV-1 antibody responses. T-cell proliferative responses against HTLV-1 were also absent in orally inoculated rats. Our findings suggest that gastrointestinal exposure of adult rats to HTLV-1-infected cells induces persistent HTLV-1 infection in the absence of both humoral and cellular immune responses against HTLV-1. This immune unresponsiveness at primary infection may subsequently affect the host defense ability against HTLV-1.

Administration, Oral↗
PubMed1990

In vivo selection of lymphocyte-tropic and macrophage-tropic variants of lymphocytic choriomeningitis virus during persistent infection.

This study demonstrates cell-specific selection of viral variants during persistent lymphocytic choriomeningitis virus infection in its natural host. We have analyzed viral isolates obtained from CD4+ T cells and macrophages of congenitally infected carrier mice and found that three types of variants are present in individual carrier mice: (i) macrophage-tropic, (ii) lymphotropic, and (iii) amphotropic. The majority of the isolates were amphotropic and exhibited enhanced growth in both lymphocytes and macrophages. However, some of the lymphocyte-derived isolates grew well in lymphocytes but poorly in macrophages, and a macrophage-derived isolate replicated well in macrophages but not in lymphocytes. In striking contrast, the original wild-type (wt) Armstrong strain of lymphocytic choriomeningitis virus that was used to initiate the chronic infection and from which the variants are derived grew poorly in both lymphocytes and macrophages. These three types of variants also differed from the parental virus in their ability to establish a chronic infection in immunocompetent hosts. Adult mice infected with the wt Armstrong strain cleared the infection within 2 weeks, whereas adult mice infected with the variants harbored virus for several months. These results suggest that the ability of the variants to persist in adult mice is due to enhanced replication in macrophages and/or lymphocytes. This conclusion is further strengthened by the finding that the variants and the parental wt virus grew equally well in mouse fibroblasts and that the observed growth differences were specific for cells of the immune system.

Animals↗
PubMed2004

Persistent infection and suppression of host response by alphaviruses.

Alphaviruses cause chronic noncytopathic infection in mosquito cells and develop a highly cytopathic infection in a wide variety of cells of vertebrate origin. Upon infection, alphaviruses modify cellular processes to meet the virus needs for propagation. Downregulation of translation and transcription caused by viral infection appears to reduce interferon (IFN) and cytokine gene expression and allows more efficient dissemination of infection. Alphaviruses with mutations in nonstructural protein nsP2 can become less cytopathic and capable of persisting in some vertebrate cell lines for a number of passages. nsP2 likely functions as an important regulator of virus-host cell interactions and plays a significant role in suppressing the antiviral response. Mammalian cells having no defects in type I IFN system react to replication of the nsP2 viral mutants by more efficient activation of IFN and IFN-dependent genes and are capable of eliminating established alphavirus infection. Blocking of IFN-alpha/beta signaling makes mouse fibroblasts unable to stop replication of Sindbis virus (SINV) with mutated nsP2 and leads to persistent infection. Downregulation of transcription and translation during alphavirus infection are quite independent events, and both probably are involved in inhibition of the antiviral response.

Alphavirus↗
PubMed1980

Further studies on subacute encephalitis and hydrocephalus in hamsters caused by measles virus from persistently infected cell cultures.

Newborn hamsters were inoculated intracerebrally (IC) with disrupted measles carrier Lu 106 cells. No acute neurological disease developed, but limited, persistent neural infection was identified by immune fluorescence and by virus isolation. By ten days after inoculation, virus could be recovered only by cocultivation of explant cultures of central nervous system (CNS) tissue and Vero cells. Virus was still demonstrable in CNS by both techniques 50 days after inoculation, the latest sample collected. Animals inoculated as newborns developed a poor hemagglutination-inhibiting (HI) antibody response. In three-week-old hamsters inoculated IC no detectable replication of carrier virus occurred. The serum HI antibody response was more than 20 times higher than that in animals inoculated as newborns. Hydrocephalus developed in a fraction of animals inoculated at birth or at the age of three weeks. Both infectious and heat-inactivated disrupted virus carrier material, but not control material of Lu 106 cells, gave hydrocephalus. The precise mechanism leading to hydrocephalus is unclear. Carrier virus material may produce a meningeal irritation causing disturbances of the extraventricular flow or resorption of cerebrospinal fluid, leading to communicating hydrocephalus. Infectious carrier virus may replicate in and destroy ependymal cells, further contributing to hydrocephalus.

Age Factors↗
PubMed1986

Biology of cloned cytotoxic T lymphocytes specific for lymphocytic choriomeningitis virus. VI. Migration and activity in vivo in acute and persistent infection.

Cloned cytotoxic T lymphocytes (CTL) specific for lymphocytic choriomeningitis virus (LCMV) were adoptively transferred to syngeneic mice acutely or persistently (carrier mice) infected with LCMV. Although infectious virus was cleared from the spleens during acute LCMV infection begun 24 hr earlier and the spleens remained clear of virus for the 4 days of testing, there was no concomitant reduction of viral titers in lymph nodes. In contrast, adoptive transfer of cloned CTL into animals with persistent rather than acute LCMV infection resulted in deaths of syngeneic but not allogeneic recipients. LCMV-immune spleen cells taken 30 to 50 days after a primary immunization and activated by in vitro stimulation before transfer also caused death of syngeneic carrier mice. However, LCMV-immune spleen cell per se provoked no clinical manifestations when transferred but cleared infectious virus and viral nucleic acid sequences from syngeneic carrier mice. The migration of 51Cr-labeled, LCMV-specific, H-2-restricted cloned CTL was assessed in vivo. The circulation of these CTL clearly differed from that of spleen cells freshly isolated from uninfected mice and from non-LCMV-specific CTL clone. Further, the circulatory pattern of LCMV-specific, H-2-restricted, cloned CTL in carrier mice was markedly different than in uninfected animals; only 7% of the injected cells remained in the lungs of uninfected mice 8 hr after injection, whereas 30% had accumulated in the liver. However, 55% of the cells injected into carrier mice still remained in their lungs 8 to 16 hr later. Hence, LCMV-specific, H-2-restricted, cloned CTL have unique trafficking patterns in the presence of LCMV antigens and immune activities in vivo.

Acute Disease↗
PubMed1991

Human immunodeficiency virus type 1 vif, vpr, and vpu mutants can produce persistently infected cells.

A series of human immunodeficiency virus type 1 (HIV-1) mutants in vif, vpr, vpu, and nef were constructed from an infectious plasmid (pNL 432) containing the full-length HIV-1 DNA by frameshift mutations. The capacities for replication and cell killing of these mutant viruses were examined in a clonal cell line (M 10) isolated from HTLV-I-transformed MT-4 cells. In all cases, the mutant viruses replicated, expressed HIV-1 antigens, and induced drastic cytopathic effects. However, some M 10 cells survived infection with vif, vpr, and vpu mutant viruses and became persistently HIV-1-infected, whereas no cells survived infection with the nef mutant as well as the wild-type virus. The HIV-1 particles produced from the surviving cells after infection with the vif, vpr, or vpu mutant viruses were fully replicative in M 10 cells without apparent cytopathic effects.

Cell Death↗
PubMed1986

Regulation of expression of the wound tumor virus genome in persistently infected vector cells is related to change in translational activity of viral transcripts.

The interaction between a plant virus and its insect vector was studied at the molecular level by examining wound tumor virus (WTV) gene expression in cultured cells derived from its leafhopper vector. Infection of vector cells by WTV is noncytopathic and results in an acute phase (through day 5), followed by persistence beginning with the first cell passage. Viral-specific polypeptide synthesis and viral genome RNA accumulation increased to a maximum level during the first 5 days following inoculation and then decreased as infected cells were passaged (to 5 to 20% of the level observed during the acute phase by passages 10 to 15). In contrast, viral-specific mRNAs were present at approximately the same level in the acute phase and in the early stage (passage 10) of the persistent phase of infection. Although viral transcripts isolated at different times after inoculation exhibited identical electrophoretic migration patterns, they had different functional activities in cell-free translation systems. Transcripts isolated from persistently infected cells were inefficiently translated in vitro, reflecting the situation in infected cells. These results indicate that the decline in the level of viral polypeptide synthesis associated with the persistent phase of WTV infection is related to a change in the translational activity of viral transcripts.

Cells, Cultured↗
PubMed2005

The role of genome diversity and immune evasion in persistent infection with Helicobacter pylori.

Helicobacter pylori is an important human pathogen that chronically colonizes the stomach of half the world's population. Infection typically occurs in childhood and persists for decades, if not for the lifetime of the host. How is bacterial persistence possible despite a vigorous innate and adaptive immune response? Here we describe the complex role of bacterial diversity and specific mechanisms to avoid or subvert host immunity in bacterial persistence. We suggest that H. pylori finely modulates the extent to which it interacts with the host in order to promote chronic infection, and that it uses diverse mechanisms to do so.

Antibodies, Bacterial↗
PubMed1998

The efficacy of nucleoside analogs against JC virus multiplication in a persistently infected human fetal brain cell line.

The effectiveness of nucleoside analogs in blocking viral multiplication was evaluated using an immortalized human neuroglial cell line capable of sustaining a persistent JCV infection, SVG-JC. Results from in situ DNA hybridization and hemagglutination assays performed on drug treated cultures were used as a measure of viral DNA replication and multiplication, respectively. Of the three drugs tested, Ara-C (cytosine arabinoside), AZT (3'-azido-3'-deoxythymidine), and cidofovir (S)-1-[3-hydroxy-2-(phosphonylmethoxypropyl] cytosine), only Ara-C showed a significant effect in decreasing active JCV replication and multiplication. In vitro data, using different cell types and virus strains have shown that specific drugs can indeed modulate viral infection. However, such modulation has not previously been demonstrated in those cells of the CNS which are specifically targeted by JCV. The SVG-JC cells represent a unique system with which further studies can be conducted on the effects of drugs on brain derived cells that are susceptible to viral infection.

Anti-HIV Agents↗
PubMed2002

Persistent infection of human thymic epithelial cells by coxsackievirus B4.

Persistent replication of coxsackievirus B4 (CVB4) E2 (diabetogenic) and CVB4 JBV (nondiabetogenic) strains in thymic epithelial cell (TEC)-enriched cultures (>or=95%) was proved by detection of positive- and negative-strand viral RNA by reverse transcription-PCR in extracted RNA from cell cultures, VP1 capsid protein detection by immunofluorescence (IF) staining, and release of infectious particles up to 30 days after infection without obvious cytolysis. By double-IF staining, cytokeratin-containing cells were shown to be susceptible to CVB4. The persistence of CVB4 was associated with a significantly increased rate of TEC proliferation (up to 70%) after 20 days of culture and a significantly increased chronic production of immunoreactive interleukin-6 (IL-6), leukemia inhibitory factor, and granulocyte-macrophage colony-stimulating factor in supernatant after 3 days of culture. The CVB4 replication and the release of cytokines were not restricted to the CVB4 E2 diabetogenic strain and did not depend on the genetic background of the host; however, TEC were more responsive to CVB4 E2 than CVB4 JBV as far as the production of cytokines.

Cell Division↗
PubMed1996

Latent and persistent infections of monocytes and macrophages.

Human cytomegalovirus (HCMV), like all herpesviruses, persists in the host after primary infection, with reactivation often occurring as a result of immunosuppression. The lack of a model system has made analysis of HCMV latency and reactivation difficult. However, the ability to analyse which specific cell types in vivo carry the virus and the relative levels of permissiveness of these cell types for viral gene expression and productive infection is beginning to help us understand these complex molecular events.

Animals↗
PubMed2000

Detection of granulocytic Ehrlichia species DNA by PCR in persistently infected dogs.

Three female beagle dogs inoculated with granulocytic Ehrlichia species were monitored for four to six months to determine whether there was evidence that the organisms persisted. The dogs were inoculated intravenously with blood containing an Ehrlichia species closely related to Ehrlichia equi and Ehrlichia phagocytophila, and identical to the human granulocytic ehrlichiosis agent with respect to its 16S rRNA gene sequence. The clinical signs were evaluated, and blood samples were collected for haematology, serum biochemistry and serology. Ehrlichial inclusions in the blood were monitored by microscopy, and ehrlichial DNA was detected by the polymerase chain reaction (PCR). Two of the dogs were injected with prednisolone on days 54 to 56 and days 152 to 154 after infection, and the other was injected with prednisolone on days 95 to 97 after infection. The dogs were euthanased and examined postmortem. Ehrlichial inclusions were demonstrated in the neutrophils and seroconversion occurred shortly after inoculation. Two of the dogs developed acute disease with rectal temperatures above 39.0 degrees C, after which no further clinical signs were observed. The administration of corticosteroids seemed to facilitate the detection of ehrlichial inclusions. Ehrlichial DNA was detected intermittently by PCR in blood samples from two of the dogs throughout the study. Persistent infection was demonstrated up to five-and-a-half months after inoculation.

Acute Disease↗
PubMed2006

Attacking HIV provirus: therapeutic strategies to disrupt persistent infection.

The therapeutic armamentarium for human immunodeficiency virus type 1 (HIV-1) infection continues to expand. New targets such as entry and integration have recently been successfully exploited. However, HIV-infected patients in need of treatment are currently committed to lifelong suppressive therapy. The persistence of integrated HIV DNA genomes capable of producing virus is a fundamental obstacle to the eradication or cure of HIV infection. Rational molecular or pharmacologic strategies to eliminate persistent HIV proviral genomes are an unaddressed therapeutic need. Coupled with potent antiretroviral therapy, treatments that could efficiently deplete the persistent DNA reservoir of HIV could radically alter treatment paradigms. Prior attempts to target persistent proviral infection deployed intensive antiretroviral therapy (ART) in combination with global inducers of T-cell activation. Initial trials of this approach were unsuccessful. Non-specific T-cell activation may induce high-level viral replication above a level that can be fully contained by ART, while increasing the susceptibility of uninfected cells. Selective targeting of HIV provirus via agents that induce the expression of quiescent HIV, but have limited effects on the uninfected host cell is an alternate approach to attack latent HIV. Recent studies define the role of repressive chromatin structure in maintaining HIV quiescence, and suggest that mechanisms that remodel chromatin about the HIV promoter are a possible therapeutic target. Other studies have uncovered specific factors that may act to induce or maintain latency by limiting the efficiency of HIV gene expression. Attempts to deplete latent HIV using drugs that alter chromatin structure have entered clinical study.

Anti-HIV Agents↗
PubMed1991

Prolonged CD4+ lymphocytopenia and thrombocytopenia in a chimpanzee persistently infected with human immunodeficiency virus type 1.

The immunologic and virologic status of a chimpanzee inoculated with multiple isolates of the human immunodeficiency virus type 1 (HIV-1) were assessed over 57 months to determine whether prolonged thrombocytopenia and CD4+ lymphocytopenia observed in the animal might be associated with long-term HIV infection. Although the chimpanzee showed no signs of disease, it lost both CD4+ (as low as 134 cells/microliter) and CD8+ lymphocytes approximately 30 months after initial infection, followed by thrombocytopenia that has persisted for greater than 2 years. Lymphopenia and thrombocytopenia were preceded by or coincided with the appearance of antibodies cross-reactive with histone H2B and decreased levels of complement component C4; an eightfold decrease in HIV-specific antibody titers; the inability of CD8+ lymphocytes to suppress virus replication; impaired proliferative responses to T cell mitogens; and the isolation of cell-free HIV from plasma. These data suggest that, given sufficient time, HIV-infected chimpanzees may develop disease.

Animals↗