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At least 1,153 records · Page 64Linked to original sources
PubMed2003

Reinfection, rather than persistent infection, in patients with chronic granulomatous disease.

Chronic granulomatous disease (CGD) is characterized by severe recurrent infections with Staphylococcus aureus, certain gram-negative rods, Nocardia species, and fungi. When infections with the same species recur, they may represent relapses or new infections. We collected organisms from infections that occurred between 1992 and 2000 in patients with CGD and determined the biochemical phenotypes, in vitro antibiotic susceptibility patterns, and pulsed-field gel electrophoresis (PFGE) patterns of the organisms causing the initial and recurrent infections. Recurrence of infection with Burkholderia cepacia or Serratia marcescens was caused by a new strain in 9 of 10 cases (P=.001). Recurrent S. aureus infections were caused by new strains in 7 of 8 cases (P=.006). In patients with CGD, recurrence of infection with the same bacterial species after appropriate antibiotic therapy usually represents new infection.

Adolescent↗
PubMed1998

Persistent infection by Helicobacter pylori down-modulates virus-specific CD8+ cytotoxic T cell response and prolongs viral infection.

To determine whether Helicobacter pylori infection affects clearance of a concomitant viral infection and cytotoxic T lymphocyte (CTL) and cytokine response to that infection, H. pylori-infected BALB/c mice were challenged with a recombinant vaccinia virus expressing human immunodeficiency virus type 1 gp160. Two H. pylori strains, a colonizing clinical isolate (KS612) and an established standard noncolonizing strain (NCTC11637), were compared. Clearance of recombinant vaccinia virus was reduced in KS612-infected mice compared with NCTC11637-infected and control mice. As a potential mechanism, in contrast to control or NCTC11637-infected mice, the H. pylori clinical isolate KS612 diminished gp160-specific and vaccinia virus-specific CTL activity, even in the presence of exogenous interleukin-2. Furthermore, KS612-infected mice had reduced Th1 cytokine responses to gp120 in vitro compared with control or NCTC11637-infected mice. These results have implications for possible effects of prevalent H. pylori infection on other human diseases.

Animals↗
PubMed1997

Transmission and establishment of a persistent infection of Enterocytozoon bieneusi, derived from a human with AIDS, in simian immunodeficiency virus-infected rhesus monkeys.

Enterocytozoon bieneusi is closely linked with chronic diarrhea and wasting in AIDS. Although reported >10 years ago, little is known about the infection and the disease it induces in humans. Duodenal E. bieneusi spores from an AIDS patient were orally transmitted to 2 simian immunodeficiency virus-infected rhesus monkeys. Both animals began shedding spores within a week of inoculation, as confirmed by microscopy and polymerase chain reaction, and continued until euthanatized 7 and 8 months later. E. bieneusi infection in the gut was sparse, either because of moderate numbers of circulating CD4 cells or because monkeys are less susceptible than humans to this infection. This is apparently the first documented transmission of E. bieneusi infection between hosts.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Increased neoplasm development due to immunosuppressive treatment with FK-506 in BALB/C mice persistently infected with the mouse herpesvirus (MHV-72).

BALB/c mice were infected with the lymphotropic mouse gammaherpesvirus (MHV-72). At late (7-12 months) post-infection intervals the latent virus was detected in the cells of lymphatic system (peripheral blood, lymphocytes and macrophages, thymocytes, lymph nodes, bone marrow, and peritoneal macrophages,) and in the spleen, lungs, liver, and kidney by cocultivation as well as by explantation. The MHV-72 infected mice, in which latency had been established, were treated with the immunosuppressive (IS) drug FK-506 (2 mg/kg/mouse for 30 days). This treatment increased the probability of virus reactivation by over two-fold. During the post-treatment observation period of 19 months, the incidence of lymphomas and the development of MHV-related lymphoproliferative and hemoblastic disorders raised to nearly five-fold in the drug treated mice as compared to untreated animals.

Animals↗
PubMedDate not supplied

Taeniasis unresponsive to a single dose of niclosamide: case report of persistent infection with Taenia saginata and a review of therapy.

A patient infected in Ethiopia with the beef tapeworm Taenia saginata was unsuccessfully treated with 2 g of niclosamide on four separate occasions over four months. clinical and parasitologic cures were effected by a regimen of 2 g of niclosamide given on three consecutive days. Niclosamide is the drug of choice for treatment of T. saginata and Taenia solium (pork tapeworm) infection; cure rates are approximately 90%. It is not absorbable and thus is nontoxic. Alternative treatments of taeniasis vary in the degree of safety; tin compounds and Aspidium extracts often are toxic. Paromomycin sulfate, which is also nonabsorbable, is effective, although adverse gastrointestinal effects are common with multiple-dose regimens. A relatively safe therapy is with mebendazole, a broad-spectrum anthelmintic agent, although efficacy has varied in different trials. A number of benzimidazoles, as well as nitazoxamide, have been effective against tapeworms. Praziquantel is the best alternative to niclosamide in terms of cost, efficacy, availability, and safety.

Adult↗
PubMed1990

Aerosol vaccination with a sendai virus temperature-sensitive mutant (HVJ-pB) derived from persistently infected cells.

Experimental infections of mice with a Sendai virus temperature-sensitive (ts) mutant (HVJ-pB) were studied. Infection with the ts mutant induced the priming effect of interferon production and both humoral and cellular immune responses, although the ts mutant virus neither multiplied satisfactorily in the respiratory tracts of mice nor caused appreciable histopathologic lesions. Inoculation with the ts mutant protected mice from subsequent challenge with a parental wild-type virus. The efficacy of this protection began as little as 1 day after vaccination and continued for at least 12 weeks. It is suggested that serum antibodies were efficacious in the nasal turbinates, while specific immune spleen cells act more protectively in the lungs.

Aerosols↗
PubMed1991

Borna disease virus replicates in astrocytes, Schwann cells and ependymal cells in persistently infected rats: location of viral genomic and messenger RNAs by in situ hybridization.

Borna disease (BD) is an immune-mediated neurological disease caused by infection of the nervous system with a negative strand RNA virus, Borna disease virus (BDV). The host range for BDV is broad and extends from birds to primates. A BDV-like agent may cause disease in humans. Until recently, BDV-infected neural cells could only be identified immunocytochemically using serum from BDV-infected animals. The advent of BDV cDNA clones allowed definition of the relationship between viral nucleic acids and viral proteins in vivo. In situ hybridization with strand-specific RNA probes from a BDV cDNA clone, pAF4, identified BDV genomic RNA and BDV mRNAs in neurons, astrocytes, Schwann cells and ependymal cells in an anatomic distribution consistent with that of BDV proteins. Genomic RNA was contained primarily within the nucleus, whereas mRNAs were found in both the nuclear and cytoplasmic compartments. Viral RNAs were demonstrated in neurons expressing BDV proteins and in glial cells by combined techniques of immunocytochemistry and in situ hybridization.

Animals↗
PubMed1980

Persistent infection of a cell line of mouse origin after cell fusion by u.v.-inactivated Sendai virus.

A cell line derived from Sendai virus-induced fusion of human adenocarcinoma and CBA mouse embryo cells had Sendai virus antigen (detected by immunofluorescence), together with bi-armed marker chromosomes, in 100% of the cells. After repeated passage, antigen-free cells carrying the same marker chromosomes appeared in the culture. Acrylamide gel analysis showed that all the Sendai virus antigens of antigen-positive cells were normal with the exception of the M protein. Antigen-negative cells contained no virus proteins and could be superinfected with wild-type virus, when all virus proteins appeared.

Adenocarcinoma↗