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PubMed2002

Role of persistent infection in the control and severity of asthma: focus on Chlamydia pneumoniae.

Conventional risk factors have been unable to explain most of the substantial increase in the prevalence of asthma observed in many countries during the last few decades. Much attention has been directed at the "hygiene hypothesis", the apparent inverse relationship between intense systemic childhood infections and the subsequent development of asthma and atopy. However, it is not only the absence or scarcity of infections, but the prolonged presence of certain microorganisms in the lungs that may be involved in the development of asthma. Accumulating evidence suggests that Chlamydia pneumoniae, an intracellular ubiquitous pathogen with an innate propensity to persist and cause chronic infections, may be associated with asthma. This microorganism can achieve a state of "latency" in which it is viable but dormant and does not multiply. During this state, however, chlamydia continues to synthesize the "stress" protein, a 60-kDa heat shock protein (hsp60). This protein is able to elicit a strong host inflammatory response at sites of its production and appears to be involved in tissue injury and scarring processes. As inflammation has been found to be present in almost all asthmatics, whatever the severity and aetiology of the disease, inhaled glucocorticoids now have an established position in the treatment of early stages. However, corticosteroids negatively affect many aspects of cell-mediated immunity and favour the shift from a T-helper-1-type response towards a T-helper-2-type response. Corticosteroids may thus severely deteriorate the host's ability to eradicate an intracellular pathogen, such as Chlamydia pneumoniae, which requires a properly functioning cell-mediated (T-helper-1-type) immune response to be cleared. These drugs are also able to reactivate persistent Chlamydia to an active growth phase, which, by increasing the production of pro-inflammatory cytokines at the site of infection, can further amplify inflammation in the airways of patients with asthma.

Asthma↗
PubMed1998

A role for herpesvirus saimiri orf14 in transformation and persistent infection.

The product of open reading frame 14 (orf14) of herpesvirus saimiri (HVS) exhibits significant homology with mouse mammary tumor virus superantigen. orf14 encodes a 50-kDa secreted glycoprotein, as shown previously (Z. Yao, E. Maraskovsky, M. K. Spriggs, J. I. Cohen, R. J. Armitage, and M. R. Alderson, J. Immunol. 156:3260-3266, 1996). orf14 expressed from recombinant baculovirus powerfully induces proliferation of CD4-positive cells originating from several different species. To study the role of orf14 in transformation, a mutant form of HVS (HVS Deltaorf14) was constructed with a deletion in the orf14 gene. The transforming potential of HVS Deltaorf14 was tested in cell culture and in common marmosets. Parental HVS subgroup C strain 488 immortalized common marmoset T lymphocytes in vitro to interleukin-2-independent growth, while the HVS Deltaorf14 mutant did not produce such a growth transformation. In addition, HVS Deltaorf14 was nononcogenic in common marmosets. In contrast to other nononcogenic HVS mutant viruses which were repeatedly isolated from peripheral blood mononuclear cells of infected marmosets for more than 5 months, HVS Deltaorf14 did not persist at a high level in vivo. These results demonstrate that orf14 of HVS is not required for replication but is required for transformation and for high-level persistence in vivo.

Animals↗
PubMed1980

Antigen-specific detection of HBsAg-containing immune-complexes in sera from chronic active hepatitis patients with hepatitis B virus persistent infection by enzyme-immunoassay (EIA).

Clq levels in immune complexes (IC) were determined by a new enzyme-immunoassay (EIA) method to estimate serum antigen-specific HBsAg-containing immune complexes (specific HBsAg-IC). Serum was used from 15 hepatitis patients with persistent hepatitis B virus infection, 2 patients with non-B type chronic active hepatitis (CAH) and 5 healthy persons. This EIA technique detected and assayed HBsAg-IC in patients with hepatitis. Clq levels in specific HBsAg-IC were higher than optical density (OD) 5.00 in 10 of 15 patients, and all 10 patients had CAH and were positive Fc reactive antibody to liver cell membrane. In the other 5 patients Clq levels in specific HBsAg-IC were lower than OD 5.00, and 3 of them had asymptomatic carrier with non-specific reactive hepatitis and 2 had inactive liver cirrhosis.

Antigen-Antibody Complex↗
PubMedDate not supplied

[Cytomorphologic study of a line of hybrid somatic cells persistently infected with the scrapie agent].

Virological, cytological and electron microscopic methods were used to study the peculiarities of the scrapie agent persistence in the tissue culture of the mouse and human hybrid cells. A long-term persistence of the scrapie agents in the cells (658 days) has been obtained. The fact of persistence is confirmed by the results of biotest and electron microscopic studies of the mouse CNS. The agent persistence promotes a decrease in the mitotic activity of the infected cells and development of the ultramicroscopic changes in cells similar to the picture of the specific changes in the CNS of mice inoculated by scrapie agent.

Animals↗
PubMed1994

Suppression of development of glomerulonephritis in NZB x NZWF1 mice by persistent infection with lactic dehydrogenase virus: relations between intercellular adhesion molecule-1 expression on endothelial cells and leucocyte accumulation in glomeruli.

The development of glomerulonephritis (GN) in autoimmune NZB x NZWF1 mice was suppressed by persistent lactic dehydrogenase virus (LDV) infection. In this study the expression of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells in glomeruli was examined during the development of GN. ICAM-1 expression on endothelial cells preceded the accumulation of leucocytes within glomeruli. The uninfected mice exhibited an age-related and profound increase in ICAM-1 expression associated with the development of a GN as evidenced by deposits of IgG and C3. Uninfected mice also showed increased accumulation of leucocytes, such as polymorphonuclear leucocytes (PMNs), macrophages, T and CD4+ cells, which express the lymphocyte function-associated antigen-1 (LFA-1) within glomeruli during the development of GN. These changes were strongly suppressed by LDV infection. Our findings suggest that the expression of ICAM-1 in glomerular endothelial cells may, at least in part, contribute to the development of GN. Suppressed expression of ICAM-1 in LDV-infected mice may be responsible for the suppression of GN seen in these animals. Thus there may be a pathogenetic role for ICAM-1 expression and for intraglomerular accumulation of leucocytes, especially PMNs, which express LFA-1 in the development of GN.

Animals↗
PubMed1993

Suppression of development of anti-nuclear antibody and glomerulonephritis in NZB x NZWF1 mice by persistent infection with lactic dehydrogenase virus: possible involvement of superoxide anion as a progressive effector.

The development of anti-nuclear antibody (ANA) and glomerulonephritis (GN) in autoimmune NZB x NZWF1 mice was suppressed by persistent lactic dehydrogenase virus (LDV) infection. This observation was used to study a possible pathogenetic role for the toxic oxygen radical, superoxide anion (O2-), in the progression of ANA and GN. Compared to macrophages from NZB x NZWF1 mice with LDV infection, macrophages from uninfected NZB x NZWF1 mice exhibited an age-related and drastic increase in O2- production in association with the development of the ANA and GN (representing the late stage of disease). NZB x NZWF1 mice with or without LDV infection were then given the O2- scavenger superoxide dismutase (SOD) during the late stage of the disease. Treatment of uninfected NZB x NZWF1 mice with SOD (10,000 units/mouse/day for 3 weeks) protected animals from the development of ANA and GN. SOD treatment also suppressed the development of the lesions in NZB x NZWF1 mice with LDV infection. Our findings suggest that O2- may, at least in part, contribute to the development of ANA and GN in the late stage of disease, and that decreased O2- production in NZB x NZWF1 mice with LDV infection may be responsible for the suppression of the development of ANA and GN in the late stage of the disease.

Aging↗
PubMed2006

Molecular mimicry, bystander activation, or viral persistence: infections and autoimmune disease.

Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistence. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-medicated diseases often linked with virus infections.

Animals↗
PubMed1981

Simian virus 40 causes persistent infection of muntjac cells in the absence of virus transformation.

SV40 infection of Muntiacus muntjak cells (ATCC, CCL: 157) resulted in abortive transformation with formation of T antigen and induction of cellular DNA replication in the absence of virus production. These cells were resistant to stable transformation by SV40 regardless of the route of infection, including microinjection of virus into cell nuclei. The present studies show that T antigen-containing cells persist and that the number of T antigen-positive cells remains constant in infected cultures, which is reflected in the nearly constant fraction of T antigen-positive cells in stationary cultures and a decrease of the fraction of T antigen-positive cells in proliferating cultures. These data suggest that following cell division only one daughter cell on the average can maintain a detectable level of T antigen. The cell cycle kinetics of proliferating muntjac cultures were not altered by the abortively transforming infection, and infectious progeny was made following cell fusion with permissive CV-1 cells. It is suggested that the few copies of viral DNA that do persist are present in a "plasmid-like' state as non-integrated DNA. In this way SV40 can appear to be lost from the majority of the cells in a culture but actually be conserved in a small population of cells for a long time. In such a state a papovavirus might go undetected in vitro as well as in vitro by even the most sensitive immunological and molecular techniques.

Animals↗
PubMed2000

Persistent infection of human pancreatic islets by coxsackievirus B is associated with alpha interferon synthesis in beta cells.

The interactions of coxsackievirus B3 (CVB3), CVB4E2 (diabetogenic), and CVB4JBV (nondiabetogenic) strains with human pancreatic islets from eight adult brain-dead donors were investigated. Persistent replication of viruses in human islets was proved by detection of viral RNA by in situ hybridization, VP1 capsid protein by immunofluorescence (IF) staining, negative-strand viral RNA by reverse transcription-PCR in extracted RNA from islets, and release of infectious particles up to 30 days after infection without obvious cytolysis. By double IF staining, glucagon-containing alpha cells and insulin-containing beta cells were shown to be susceptible to CVB. The persistence of CVB3 and CVB4 in islet cells was associated with the chronic synthesis of alpha interferon (IFN-alpha), as evidenced by the detection of IFN-alpha mRNA and immunoreactive IFN-alpha with antiviral activity. By double IF staining, IFN-alpha was detected in insulin-producing beta cells only. Experiments with neutralizing anti-coxsackievirus and adenovirus receptor (CAR) antibodies provided evidence that CAR was expressed by alpha and beta cells and that it played a role in the infection of these cells with CVB and the consecutive IFN-alpha expression in beta cells. The viral replication and the expression of IFN-alpha in islets were not restricted to the CVB4E2 diabetogenic strain and did not depend on the genetic background of the host. The neutralization of endogenous IFN-alpha significantly enhanced the CVB replication in islet cells and resulted in rapid destruction of islets. Thus, human beta cells can harbor a persistent CVB infection, and CVB-induced IFN-alpha plays a role in the initiation and/or maintenance of chronic CVB infection in human islets.

Adult↗
PubMed1982

A mutant standard virus isolated from vesicular stomatitis virus persistent infection interferes specifically with wild-type virus replication.

A clone of vesicular stomatitis virus (VSV) isolated after 76 months of persistence exerts specific homologous interference with replication of wild-type or tsG31 (temperature-sensitive) virus in a mixed infection at 37 degrees C in the absence of defective-interfering particles. Other VSV ts mutants showed little or no specific interfering ability.

Animals↗
PubMed1979

Persistent infection of human lymphoid and myeloid cell lines with herpes simplex virus.

Herpes simplex virus (HSV) type 1 replicated and persisted in human T, B, and myeloid cell lines with different patterns of viral replication and various effects on cell growth. T cell line CEM supported the replication of HSV for over 400 days without detectable differences in cell growth as compared with uninfected cells. HSV persisted in B cell line NC37 and myeloid cell line K562 for up to 222 and 374 days, respectively, but led to a significant decrease in the number of viable cells by 7 weeks of infection. The average number of cells producing infectious virus was very low in these cell lines (range, 0.5 to 2.7+) compared with a larger proportion of cells exhibiting HSV antigens by immunofluorescence (range, 24 to 58%). In contrast, null cell line LAZ 221 failed to replicate HSV even though the viral infection led to a cessation of cell growth.

B-Lymphocytes↗
PubMed1986

Transmission of bovine leukemia virus (BLV) to immunocompromised monkeys: evidence for persistent infection.

Splenectomized or irradiated adult and untreated baby macacques were infected with bovine leukemia virus from continuously virus producing fetal lamb kidney cell cultures. Persisting high antibody titers were followed for 4 years in the adult and 16 months in the baby monkeys, using an ELISA technique. With the exception of a persistent leukocytosis in one adult monkey, the animals remained healthy throughout the observation period. Transfer of lymphocytes from this animal to a seronegative recipient led to anti-BLV seroconversion with a lag of 5 months. All other transfer experiments showed a negative result. Virus could be recovered from the newly infected baby macacques by means of lymphocyte/fetal lamb kidney cell cocultivation for up to 4 weeks after inoculation. All other attempts to recover virus from the infected animals at a later point were unsuccessful.

Animals↗
PubMed1989

Persistent infection of mice by lactate dehydrogenase-elevating virus: effects of immunosuppression on virus replication and antiviral immune responses.

Maximum plasma titers (10(9)-10(10) ID50/ml) of lactate dehydrogenase-elevating virus (LDV) in mice are observed one day after infection, but then decrease 4-5 log during the next 5 weeks to attain a persistent steady-state level for the remainder of the life of the animal. The decrease in plasma LDV level during the first 5 weeks after infection and long-term viremia were not affected by lethal X-irradiation of the mice, daily injections of cyclosporin A or depletion of the mice of T cells by treatment with anti-CD4, anti-CD8, or anti-Thy1.2 monoclonal antibodies, although these treatments inhibited the formation of anti-LDV antibodies. LDV viremia was also the same in nu/nu and nu/+ Swiss mice, though the former did not mount an anti-LDV immune response, while the latter did. The appearance of anti-LDV neutralizing antibodies in infected mice 1-2 months after infection or the injection of infected mice with high doses of anti-LDV neutralizing monoclonal antibodies also did not affect the level of LDV viremia. Repeated treatments of infected mice with either cyclophosphamide or dexamethasone caused 1-2 log increases in plasma LDV titers. Although cyclophosphamide treatment prevented the formation of anti-LDV antibodies, dexamethasone caused an increase in plasma LDV levels without affecting anti-LDV antibody formation. We conclude that an anti-LDV immune response does not play a significant role in controlling LDV replication in mice. The data support the view that within 1 day after infection of a mouse, all LDV-permissive macrophages, which appear to be the only cells supporting LDV replication in the mouse, are destroyed as a result of a cytocidal infection by LDV. Subsequently, LDV replication is limited by the rate of generation of new permissive macrophages. The steady-state viremia attained about 5 weeks after infection reflects a balance between LDV replication in permissive macrophages as they arise and LDV inactivation and clearance.

Animals↗
PubMed2002

Persistent infection with human papillomavirus following the successful treatment of high grade cervical intraepithelial neoplasia.

In a need case-control study, we identified women who were successfully treated for CIN 3. Cases had biopsy proven recurrence, whilst controls remained disease free for at least five years. One hundred and seventy-two women were beta-globin positive at diagnostic and at six-month post-treatment smear (90 controls and 82 cases). Thirty-nine cases (47.6%) were HPV16/18 positive at biopsy or follow up smear and 14 (17.1%) of 82 were positive at both. Of the controls, 37 (41.1%) were HPV positive at biopsy or smear with (3.3%) positive at both. The unadjusted OR associated with being HPV positive at both points compared to being HPV negative at both was 8.0 (95% CI 2.13-30.37). The persistence of HPV 16/18 infection following the confirmed eradication of CIN is a highly significant risk factor for recurrence.

Adult↗
PubMed1993

Experimental Lyme disease in dogs produces arthritis and persistent infection.

Lyme disease was reproduced in specific pathogen-free beagle dogs by exposure to Borrelia burgdorferi-infected ticks (Ixodes dammini). Seroconversion and disease frequency were higher after exposure to infected adult ticks than to infected nymphs. Young pups developed clinical disease more readily than older dogs. The incubation period lasted 2-5 months. Acute recurrent lameness with fibrinopurulent arthritis was the dominant clinical sign. Dogs recovered but developed persistent mild polyarthritis. B. burgdorferi persisted in recovered dogs for at least 1 year. Isolation of B. burgdorferi and detection by polymerase chain reaction was most successful from skin biopsies at the site of the tick bite. Antibody to B. burgdorferi antigens was first detected by ELISA and Western blots by 4-6 weeks after exposure. High serum levels persisted during 17 months of observation. In contrast to infection from ticks, inoculation of dogs with cultured B. burgdorferi resulted in seroconversion with a shorter duration of antibody persistence and no clinical disease.

Age Factors↗
PubMed1999

Persistent infection of rhesus macaques by the rev-independent Nef(-) simian immunodeficiency virus SIVmac239: replication kinetics and genomic stability.

We generated previously a Nef(-), replication-competent clone of SIVmac239 in which the Rev protein and the Rev-responsive element were replaced by the constitutive transport element (CTE) of simian retrovirus type 1 (A. S. von Gegerfelt and B. K. Felber, Virology 232:291-299, 1997). In the present report, we show that this virus was able to infect and replicate in rhesus macaques. The Rev-independent Nef(-) simian immunodeficiency virus induced a persistent humoral immune response in all monkeys, although viral loads were very low. Upon propagation in the monkeys, the genotype remained stable and the virus retained its in vitro growth characteristics. The infected monkeys showed normal hematological values and no signs of disease at more than 18 months post-virus exposure. Therefore, replacement of the essential Rev regulation by the CTE generated a virus variant that retained its replicative capacity both in vitro and in vivo, albeit at low levels.

Animals↗
PubMed2001

Validation of a test for dams carrying foetuses persistently infected with bovine viral-diarrhoea virus based on determination of antibody levels in late pregnancy.

Our objective was to estimate, using a generalised linear mixed-model approach, the sensitivity and specificity of an indirect ELISA when used to identify dams pregnant with persistently bovine viral-diarrhoea virus (BVDV)-infected foetuses. Cows that had been tested for antibodies to BVDV with a positive result during their pregnancy and where the offspring had been tested for both antibody and virus were identified by accessing the Swedish BVD database and the official pedigree records. The resulting data set consisted of 2162 cow-calf pairs in 126 herds, of which 281 included virus-positive calves. The sensitivities and specificities at 12 different decision thresholds (corresponding to optical densities (ODs) between 0.5 and 1.6) were estimated using generalised linear mixed models (binomial error, logit link), in which the gold standard (the BVDV status of the calf) was included as a covariate. In each model, the dependent variable was the dichotomous test result at the decision threshold in question. There was a significant positive interaction between the calf's status and gestational stage in all 12 models--indicating that the sensitivity and specificity at any given decision threshold was improved when the the test was performed later in pregnancy. The test should be applied only when samples have been taken in late gestation--not before the seventh month in pregnancy. If applied during the last months of pregnancy, the point estimate of the sensitivity ranges between 0.94 and 1.0 as the decision threshold is moved from 1.0 and downwards to 0.7. Similarly, the specificity ranges between 0.39 and 0.67 as the decision threshold is moved from 0.8 and upwards to 1.1.

Animals↗