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CNS Infection

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17041. Multiple determinants contribute to the virulence of HSV ocular and CNS infection and identification of serine 34 of the US1 gene as an ocular disease determinant. (PubMed)

Multiple determinants contribute to the virulence of HSV ocular and CNS infection and identification of serine 34 of the US1 gene as an ocular disease determinant. The virulence of any given strain of herpes simplex virus (HSV) is probably due to the effects of the constellation of genes in that strain and how they act in concert to promote disease. The goal of this work was to develop a system to identify and study the role of multiple genes in HSV disease.Mixed ocular infection with HSV-1 (...) strains CJ394 and OD4 yield recombinants with increased ocular and central nervous system (CNS) virulence. Clones and subclones of the CJ394 genome were cotransfected with intact OD4 DNA into Vero cells, the transfection pools were inoculated into BALB/c mouse eyes, and disease severity was scored. Fragments transferring increased ocular or CNS disease were sequenced. Site-directed mutagenesis was used to revert one mutation to wild type.Five of the determinants (UL9, -33, -41, and -42 and US1

2003 Investigative Ophthalmology & Visual Science

17042. Sequential Polymicrobial Infections Lead to CNS Inflammatory Disease: Possible Involvement of Bystander Activation in Heterologous Immunity (PubMed)

Sequential Polymicrobial Infections Lead to CNS Inflammatory Disease: Possible Involvement of Bystander Activation in Heterologous Immunity VV(PLP) is a recombinant vaccinia virus (VV) encoding myelin proteolipid protein (PLP) that has been used to investigate molecular mimicry and autoimmunity. Since virus infections can cause bystander activation, mice were first infected with VV(PLP), and later challenged with wild-type VV, lymphocytic choriomeningitis virus (LCMV), or murine cytomegalovirus (...) (MCMV). Among the VV(PLP)-primed mice, only MCMV challenge induced significant Ki-67(+), CD3(+)T cell infiltration into the central nervous system (CNS) with a mild PLP antibody response. While MCMV alone caused no CNS disease, control VV-infected mice followed with MCMV developed mild CNS inflammation. Thus, heterologous virus infections can induce CNS pathology.

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2007 Journal of Neuroimmunology

17043. Infections in the CNS During Childhood and the Risk of Subsequent Psychotic Illness: A Cohort Study of More Than One Million Swedish Subjects. (PubMed)

Infections in the CNS During Childhood and the Risk of Subsequent Psychotic Illness: A Cohort Study of More Than One Million Swedish Subjects. Infections during early life have been suggested to play a role in the etiology of schizophrenia. Most studies have focused on fetal life; few have explored risk associated with infection during childhood. The results of these have been inconsistent. The present study aims to investigate whether there is an increased risk of schizophrenia and other (...) nonaffective psychoses associated with viral or bacterial CNS infections during childhood and, if so, which specific agents are involved.A national cohort consisting of 1.2 million children born between 1973 and 1985 was followed up by using Swedish national registers to retrieve data on hospital admissions for CNS infections at 0-12 years of age (bacterial: N=2,435, viral: N=6,550) as well as admissions for nonaffective psychotic illnesses from the 14th birthday (N=2,269).There was a slightly increased

2007 American Journal of Psychiatry

17044. Ultrastructural localization of viral antigens in the CNS of mice persistently infected with lymphocytic choriomeningitis virus (LCMV). (PubMed)

Ultrastructural localization of viral antigens in the CNS of mice persistently infected with lymphocytic choriomeningitis virus (LCMV). Lymphocytic choriomeningitis virus (LCMV) produces a persistent infection of the nervous system in susceptible mice. To map the localization of viral antigens in the central nervous system (CNS), the authors studied, by means of ultrastructural immune peroxidase techniques, 4-6-month-old mice persistently infected with LCMV following an intracerebral (...) of LCMV. Glycopeptide antigens were minimally expressed. Electron-microscopic examination of selected individual infected neurons showed viral antigens exclusively associated with ribosomes. No staining was seen on cell surfaces. Glutaraldehyde-fixed CNS tissue studied by electron microscopy did not reveal morphologic abnormalities or mature viral particles. This study demonstrates that LCMV persistently infects specific neuronal populations. Infected neurons express viral antigens in association

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1983 The American journal of pathology

17045. Pathogenesis of mouse scrapie: patterns of agent replication in different parts of CNS following intraperitoneal infection (PubMed)

Pathogenesis of mouse scrapie: patterns of agent replication in different parts of CNS following intraperitoneal infection The dynamics of agent replication were studied at 8 levels of spinal cord and in 9 areas of brain of mice infected intraperitoneally with the 139A strain of scrapie agent. Replication in the CNS was first detectable at 2 levels of spinal cord between thoracic vertebrae 4 and 9. The onset of replication was progressively delayed by up to 4 weeks at increasingly lower levels (...) until the whole CNS is infected. However, experiments involving sympathectomy gave inconclusive results and the evidence for neural spread of scrapie in the peripheral nervous system is circumstantial.

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1982 Journal of the Royal Society of Medicine

17046. Infected splenic dendritic cells are sufficient for prion transmission to the CNS in mouse scrapie (PubMed)

Infected splenic dendritic cells are sufficient for prion transmission to the CNS in mouse scrapie Transmissible spongiform encephalopathies display long incubation periods at the beginning of which the titer of infectious agents (prions) increases in peripheral lymphoid organs. This "replication" leads to a progressive invasion of the CNS. Follicular dendritic cells appear to support prion replication in lymphoid follicles. However, the subsequent steps of neuroinvasion remain obscure. CD11c (...) (+) dendritic cells, an unrelated cell type, are candidate vectors for prion propagation. We found a high infectivity titer in splenic dendritic cells from prion-infected mice, suggesting that dendritic cells carry infection. To test this hypothesis, we injected RAG-1(0/0) mice intravenously with live spleen cell subsets from scrapie-infected donors. Injection of infected dendritic cells induced scrapie without accumulation of prions in the spleen. These results suggest that CD11c(+) dendritic cells can

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2001 Journal of Clinical Investigation

17047. A Phase III Study to Evaluate the Safety and Efficacy of Ganciclovir (Dihydroxypropoxymethyl Guanine [DHPG]) Treatment of Symptomatic Central Nervous System (CNS) Congenital Cytomegalovirus (CMV) Infections.

A Phase III Study to Evaluate the Safety and Efficacy of Ganciclovir (Dihydroxypropoxymethyl Guanine [DHPG]) Treatment of Symptomatic Central Nervous System (CNS) Congenital Cytomegalovirus (CMV) Infections. A Phase III Study to Evaluate the Safety and Efficacy of Ganciclovir (Dihydroxypropoxymethyl Guanine [DHPG]) Treatment of Symptomatic Central Nervous System (CNS) Congenital Cytomegalovirus (CMV) Infections. - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers (...) : refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. A Phase III Study to Evaluate the Safety and Efficacy of Ganciclovir (Dihydroxypropoxymethyl Guanine [DHPG]) Treatment of Symptomatic Central Nervous System (CNS) Congenital Cytomegalovirus (CMV) Infections. The safety and scientific validity

1999 Clinical Trials

17048. A Multicenter Placebo-Controlled Double-Blind Trial to Evaluate Azidothymidine (AZT) Treatment of the AIDS Dementia Complex and Central Nervous System (CNS) Human Immunodeficiency Virus (HIV) Infection

A Multicenter Placebo-Controlled Double-Blind Trial to Evaluate Azidothymidine (AZT) Treatment of the AIDS Dementia Complex and Central Nervous System (CNS) Human Immunodeficiency Virus (HIV) Infection A Multicenter Placebo-Controlled Double-Blind Trial to Evaluate Azidothymidine (AZT) Treatment of the AIDS Dementia Complex and Central Nervous System (CNS) Human Immunodeficiency Virus (HIV) Infection - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer (...) to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. A Multicenter Placebo-Controlled Double-Blind Trial to Evaluate Azidothymidine (AZT) Treatment of the AIDS Dementia Complex and Central Nervous System (CNS) Human Immunodeficiency Virus (HIV) Infection The safety and scientific validity of this study

1999 Clinical Trials

17049. Endogenous presentation of self myelin epitopes by CNS-resident APCs in Theiler’s virus–infected mice (PubMed)

Endogenous presentation of self myelin epitopes by CNS-resident APCs in Theiler’s virus–infected mice The mechanisms underlying the initiation of virus-induced autoimmune disease are not well understood. Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD), a mouse model of multiple sclerosis, is initiated by TMEV-specific CD4(+) T cells targeting virally infected central nervous system-resident (CNS-resident) antigen-presenting cells (APCs), leading to chronic (...) activation of myelin epitope-specific CD4(+) T cells via epitope spreading. Here we show that F4/80(+), I-A(s+), CD45(+) macrophages/microglia isolated from the CNS of TMEV-infected SJL mice have the ability to endogenously process and present virus epitopes at both acute and chronic stages of the disease. Relevant to the initiation of virus-induced autoimmune disease, only CNS APCs isolated from TMEV-infected mice with preexisting myelin damage, not those isolated from naive mice or mice with acute

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1999 Journal of Clinical Investigation

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