摘要:

The genus Enterovirus is a large group of viruses belonging to the family Picornaviridae. They have a worldwide distribution, cause a wide spectrum of disease, and are a common cause of central nervous system disease. Included among the sixty-six enterovirus serotypes known to infect humans are the three poliovirus (PV) serotypes, the cause of paralytic poliomyelitis (PPM). PPM has been controlled in many parts of the world by vaccination. Molecular and functional comparison of PV vaccine strain and wild neurovirulent PV strains has provided an insight into mechanisms of neurovirulence. Enteroviruses are also the most commonly implicated viral agents of aseptic meningitis. Less commonly they cause a more serious encephalitis. Specific antiviral treatment for enterovirus infections is not currently available. Virological diagnosis is nonetheless important to distinguish between enterovirus-induced meningitis or encephalitis and other treatable causes of disease with a similar clinical picture.

ISSN:0300-5526    

DOI:10.1159/000150542

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

Rubella virus is a single-stranded, plus-sense RNA virus belonging to the Togaviridae family. Rubella virus infection causes a benign disease known as rubella or German measles, however infection during early pregnancy can lead to severe birth defects known as congenital rubella syndrome (CRS). Sequelae of rubella virus infection include three distinct neurological syndromes: a postinfectious encephalitis following acute infection, a spectrum of neurological manifestations following congenital infection, and an extremely rare neuodegenerative disorder, progressive rubella panencephalitis (PRP), that can follow either congenital or postnatal infection. The pathogenesis of all three of these syndromes is incompletely understood. Virus invasion and replication in the brain has only been definitively demonstrated in CRS and appears to account for the majority of neurological lesions observed in this disease. Immune-mediated pathology is particularly evident in PRP and may be autoimmune in nature, possibly triggered by molecular mimicry between viral and host epitopes, considering the apparent lack of virus in the brain. The pathogenesis of rubella encephalitis following acute infection has not been determined.

ISSN:0300-5526    

DOI:10.1159/000150543

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

Acute measles is a classic infectious disease of childhood with worldwide distribution. Its causative agent, measles virus (MV), is an efficent pathogen, persisting in nature in populations large enough to support it, even though it is able to cause an acute infection in any individual only once in his lifetime. The characteristic clinical hallmarks of measles, fever and rash, coincide with antiviral immune response. MV-specific T lymphocyte and antibody responses contribute to virus clearance and protection from reinfection, respectively. Concomitant with immune activation immunologic abnormalities arise during MV infection. The ensuing suppression of cellular immune responses is presumably responsible for increased susceptibility to other infections. Additionally, central nervous system (CNS) complications of MV infection with different pathogenesis occur. Autoimmune disease may appear in the form of acute measles encephalomyelitis. Furthermore, MV may persist in the CNS in rare cases without periodic shedding of infectious virus. Measles inclusion body encephalitis can develop on the basis of inadequate virus-specific cell-mediated immune responses and subacute sclerosing panencephalitis occurs many years after primary measles as a slow virus infection. Host cell factors operating in cells of the CNS together with mutations particularly in genes coding for viral envelope proteins initiate and maintain the persistent state of infection with a viral replication cycle that is attenuated at the transcriptional and translational level.

ISSN:0300-5526    

DOI:10.1159/000150544

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

The unique genetic and biological properties of this small enveloped RNA virus indicate that Borna disease virus (BDV) is an evolutionary old pathogen. It appears perfectly adapted to persist inside the limbic system, a most delicate and sensitive old area of the mammalian brain involved in the control of mood, behavior, and memory. In many infected individuals, BDV remains a commensal during their lifetime. In a minority of vulnerable subjects, BDV becomes frequently activated, leading to episodes of distinct, more or less severe disturbances of information processing, behavioral and mood alterations. BDV research in humans is anticipated to initiate new insights into the interplay of exogenous and endogenous factors governing mood disorders. In nature BDV preferentially behaves as a neurotropic virus, but may latently and/or persistently infect cells of the reticuloendothelial system. This has been shown to be of great diagnostic importance, because now BDV ‘footprints’ can be followed in vivo in animals and man. BDV, which has long been considered as a classical animal virus, is present in humans, and has been found to be associated with some defined psychiatric disorders in particularly vulnerable individuals. An interaction of BDV proteins with neurotransmitter activities is plausible in the light of experimental animal data. Interference with normal behavior and the influence on mood and cognitive functions as demonstrated in animals and assumed in humans require extensive future research on the molecular etiopathogenesis. Aside from these clinical aspects, BDV is an unusual agent with outstanding features, namely replication in the nucleus of its target cells by an elusive, partially unknown mechanism, showing no cytopathogenicity or disturbance of vital cell functions, but altering luxury functions, and with a lifelong persistence giving rise to periods of long latency and short activat

ISSN:0300-5526    

DOI:10.1159/000150545

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

Since the first description by A.M. Jakob and H.G. Creutzfeldt, five human diseases have been identified as transmissible spongiform encephalopathies (TSE). The disease bearing these authors’ name, Creutzfeldt-Jakob disease (CJD) occurs sporadically, may be transmitted and has a genetic basis in 10-15% of all cases. Genetic diseases are the Gerstmann-Sträussler-Scheinker syndrome and fatal familial insomnia. The latest form of CJD in humans, variant CJD (vCJD), was first described in 1996 and may be considered as evidence for a link between human TSEs and those in the animal kingdom. The putative agent of all TSEs is a proteinaceous infectious agent or prion. The gene for the physiological isoform of this protein (prion related protein or PrPc) is encoded on the short arm of chromosome 20 in humans. The role of the physiological isoform of PrPc is unknown. The physiological isoform PrPc is protease-sensitive and thus designated as PrP-sen, while the pathological isoform is protease-resistant and thus called PrP-res. The pathological isoform PrP-res is invariably associated with TSEs and has given rise to the term prion diseases. PrP-sen and PrP-res have an identical amino acid sequence and have identical posttranslational modifications as assessed by currently available methodology but differ in their tertiary and quaternary structure. These structural differences are thought to be propagated by interaction of PrP-res with PrP-sen, appear to be governed by the polymorphism of PrPc and have been shown to be invariably associated with disease. PrP-sen has a high content of α-helical structures, PrP-res consists predominantly of β-pleated sheets. These physicochemical characteristics of PrP-res cause it to behave like amyloid. The neuropathological hallmarks of TSEs or prion diseases are spongiform change, astrocytic gliosis, neuronal loss and PrP-positive plaques. A nucleic acid has never consistently been shown in any TSE. Diagnosis of TSE can be reliably made only postmo

ISSN:0300-5526    

DOI:10.1159/000150546

出版商:S. Karger AG    

年代:1997

数据来源: Karger

ISSN:0300-5526    

DOI:10.1159/000150547

出版商:S. Karger AG    

年代:1997

数据来源: Karger

ISSN:0300-5526    

DOI:10.1159/000150548

出版商:S. Karger AG    

年代:1997

数据来源: Karger