Assuntos
Doenças por Vírus Lento , Vírus , Animais , Complexo Antígeno-Anticorpo , Doenças Autoimunes , Doenças do Sistema Nervoso Central/etiologia , Cricetinae , Humanos , Imunidade Celular , Leucoencefalopatia Multifocal Progressiva/etiologia , Coriomeningite Linfocítica/etiologia , Vírus da Coriomeningite Linfocítica , Vírus do Sarampo , Esclerose Múltipla , Degeneração Neural , Orthomyxoviridae , Papillomaviridae , Polyomaviridae , Vírus 40 dos Símios , Doenças por Vírus Lento/imunologia , Panencefalite Esclerosante Subaguda/etiologiaRESUMO
Several viral, fungal, and protozoal diseases of the eye are significantly associated with immunologic deficiencies. Of the viral agents, cytomegaly and herpes simplex and zoster cause a discrete necrotizing retinopathy that has the characteristics of vascular occlusion. Measles may result in a delayed retinopathy that is predominantly macular and associated with subacute progressive encephalopathy. Of the fungal agents, Candida and Aspergillus are apt to involve the eye, beginning as choroidal lesions with extension forward to involve the pigment epithelium and retina secondarily. Mucor and Cryptococcus are less common. Toxoplasmosis is the one ocular protozoal disease whose incidence is increased by immunosuppression, and, like the viral diseases, is characterized by a discrete necrotizing retinopathy and probably results from activation of dormant organisms in the retina. Autoimmunity undoubtedly plays an important role in eye disease but its ocular pathogenesis is obscure.
Assuntos
Oftalmopatias/etiologia , Terapia de Imunossupressão/efeitos adversos , Adulto , Animais , Formação de Anticorpos , Doenças Autoimunes/complicações , Criança , Pré-Escolar , Infecções por Citomegalovirus/complicações , Oftalmopatias/imunologia , Oftalmopatias/microbiologia , Humanos , Ceratite Dendrítica/etiologia , Ceratite Dendrítica/imunologia , Ceratite Dendrítica/microbiologia , Sarampo/complicações , Micoses/complicações , Doenças Retinianas/etiologia , Doenças Retinianas/imunologia , Doenças Retinianas/microbiologia , Doenças por Vírus Lento/etiologia , Doenças por Vírus Lento/imunologia , Doenças por Vírus Lento/microbiologia , Toxoplasmose Ocular/etiologiaRESUMO
The subacute spongiform encephalopathies include scrapie of sheep, transmissible mink encephalopathy, and kuru and Creutzfeldt-Jakob disease of man. These diseases are caused by filterable infectious agents with unique physical properties. The usual sources of infection in nature are not completely known. Epidemiological evidence suggests that the agents may enter the body through breaks in the skin and mucous membranes. Experimental studies of scrapie after subcutaneous inoculation demonstrated early replication of the agent in lymphoid tissues and later appearance in other organs; as the amount of agent in the central nervous system (CNS) increased, it decreased in or disappeared from lymphoid tissues. In preliminary studies of kuru and Creutzfeldt-Jakob disease, the infectious agents were regularly recovered from the brains of clinically-ill patients and experimental animals but only occasionally from organs outside the CNS. It remains to be seen if early events in the pathogenesis of the two human diseases, before the appearance of clinical signs, are similar to those in scrapie.
Assuntos
Síndrome de Creutzfeldt-Jakob/patologia , Doenças por Vírus Lento/patologia , Terminologia como Assunto , Adolescente , Adulto , Idoso , Animais , Encéfalo/patologia , Sistema Nervoso Central/microbiologia , Criança , Pré-Escolar , Síndrome de Creutzfeldt-Jakob/transmissão , Sistema Digestório/microbiologia , Feminino , Humanos , Lactente , Recém-Nascido , Rim/microbiologia , Kuru/patologia , Kuru/transmissão , Tecido Linfoide/patologia , Masculino , Pessoa de Meia-Idade , Príons , Scrapie/patologia , Scrapie/transmissão , Ovinos , Doenças dos Ovinos/patologia , Doenças dos Ovinos/transmissão , Doenças por Vírus Lento/imunologia , Doenças por Vírus Lento/transmissão , Baço/microbiologiaRESUMO
Based on personal experience with multiple sclerosis a hypothesis is set out concerning a possible viral origin for M.S, a protective immunological defense mechanism for sequestration of the virus, the processes involved in the occasional failure of this defense mechanism, thus permitting the onset of exacerbations, the avoidance of such exacerbations by blood-brain barrier protection with a phenothiazine during the prodromal pressor phase, and the probable site of action of the drug. The processes described may be general rather than specific to M.S. and may also occur in other encephalitides of viral or other slow agent origin.
Assuntos
Esclerose Múltipla/etiologia , Animais , Barreira Hematoencefálica , Humanos , Camundongos , Esclerose Múltipla/tratamento farmacológico , Esclerose Múltipla/imunologia , Fenotiazinas/uso terapêutico , Doenças por Vírus Lento/imunologia , Viroses/imunologiaRESUMO
In spite of the large number of theories advanced to clarify the etiology of Paget's disease, its cause is still being discussed, and no satisfactory conclusion has been reached. The possibility of a viral origin was raised by the discovery of inclusion bodies, detectable by electron microscopy, in the nuclei and cytoplasm of the osteoclasts in the affected bone tissue, in 1974. In fact, the microcylindrical structures described by various authors, and visible only in osteoclasts and only in Paget's disease, if one excepts certain giant-cell bone tumors, have a close analogy, morphologically, with the nucleocapsids of paramyxovirus of the measles group, described in experimental infections or human diseases (subacute sclerosing panencephalitis). Various morphological arguments, drawn from studies of inclusions in richly nucleated giant osteoclasts found in Paget's disease, are in favor of the viral nature of these formations. Immunocytological methods have constituted another approach to the problem raised by the discovery of inclusions. They have demonstrated the existence of an antigenic material in the osteoclasts found in Paget's disease which reacts positively with antiserums containing anti-measles antibodies or with produce a crossed reaction with them. Controlled tests have confirmed these findings. Biological arguments are presently sufficient, therefore, for the possibility of a viral etiology of Paget's disease to be validly accepted from among the pathogenic hypotheses proposed for a disease that was first described a century ago.
Assuntos
Osteíte Deformante/etiologia , Viroses , Antígenos Virais/análise , Imunofluorescência , Humanos , Técnicas Imunoenzimáticas , Corpos de Inclusão Viral/ultraestrutura , Vírus do Sarampo/imunologia , Osteíte Deformante/patologia , Osteoclastos/ultraestrutura , Doenças por Vírus Lento/imunologia , Viroses/patologiaRESUMO
In order to describe the complex virus-host relationship the authors review the viral mechanisms of infection and viral replication as well as the basic pattern of the immune responses. The delicate balance of the infection-immunity equation is complicated by the instability of both entities. The better understanding of these factors provides a rationale for the therapeutic counteraction of virus infections, reducing the likelihood of viral exposure becoming clinical viral infection.
Assuntos
Viroses/imunologia , Animais , Formação de Anticorpos , Linfócitos B/imunologia , Proteínas do Sistema Complemento/imunologia , Citocinas/imunologia , Humanos , Imunidade Inata , Recém-Nascido , Infecções por Lentivirus/imunologia , Macrófagos/imunologia , Vírus Oncogênicos/genética , Doenças por Vírus Lento/imunologia , Linfócitos T/imunologia , Viroses/microbiologia , Replicação ViralRESUMO
It had previously been shown that intrauterine infection of mice with influenza virus resulted in growth retardation and significant immunosuppression to various nonspecific agents and influenza virus. The present study demonstrated that such mice also had lower production of specific antibody and reduced capacity to form the delayed hypersensitivity to influenza virus. Despite the lack of specific immune response, such mice had high levels of response to influenza virus in adoptive transfer. The reasons for which lymphocytes of mice with slow influenza infection fail to manifest their immunological potentials in situ require further study.
Assuntos
Reações Antígeno-Anticorpo/imunologia , Vírus da Influenza A/imunologia , Infecções por Orthomyxoviridae/imunologia , Doenças por Vírus Lento/imunologia , Animais , Anticorpos Antivirais/análise , Especificidade de Anticorpos/imunologia , Células Produtoras de Anticorpos/imunologia , Feminino , Hipersensibilidade Tardia/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , GravidezRESUMO
The status of the interferon system and level of immunoglobulins were studied in C57BL6 mice with slow influenza infection. These mice showed signs of immunosuppression: low endogenous interferon production, synthesis of alpha- and gamma-interferon by splenocytes of these mice in vitro 4-8 times lower than by those of the controls, lower levels of IgG in the blood serum. These data indicate general suppression of humoral immunity.
Assuntos
Infecções por Orthomyxoviridae/imunologia , Doenças por Vírus Lento/imunologia , Envelhecimento/imunologia , Animais , Formação de Anticorpos/imunologia , Feminino , Tolerância Imunológica/imunologia , Imunoglobulinas/análise , Interferons/análise , Interferons/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Gravidez , Efeitos Tardios da Exposição Pré-NatalRESUMO
The progency of C57BL/6 mice consisting of three groups: with signs of slow influenza infection ("dwarf"), "nude-like" resembling nude mice, and "nude-like" with spontaneous fur growth, was examined. The slow influenza infection in "dwarf" mice was found to be characterized by marked immunosuppression manifested by a sharp reduction of the number of antibody- and rosette-forming cells and blasttransformation of spleen lymphocytes into T- and B-mitogens. The most marked immuno-suppression was found in the "dwarfs" born to the females infected with the virus enriched with standard virions. "Nude-like" animals also had marked immunosuppression (particularly with regard to the rosette-formation), however, the "dwarfs" appeared to have more marked affection of B-cells as compared with "nude-like" mice. Gradual restoration of fur in a portion of "nude-like" animals (spontaneous growth) was due to sharp stimulation of immune responsiveness in them as manifested by a two-fold (as compared with the controls) increase in the number of antibody- and rosette-forming cells and normalization of spleen cell response to T- and B-mitogens. Differences between nude and "nude-like" mice consisting in the latter in the affection of not only T- but also B-link of immunity are discussed.
Assuntos
Doenças Fetais/imunologia , Infecções por Orthomyxoviridae/imunologia , Complicações Infecciosas na Gravidez/imunologia , Doenças por Vírus Lento/imunologia , Animais , Formação de Anticorpos , Células Produtoras de Anticorpos/imunologia , Vírus Defeituosos/patogenicidade , Nanismo/imunologia , Feminino , Imunidade Celular , Vírus da Influenza A/patogenicidade , Ativação Linfocitária , Camundongos , Camundongos Endogâmicos C57BL , Gravidez , Formação de RosetaRESUMO
Pathogenesis of amyotrophic leukospongiosis (ALSP) with a short incubation period induced in guinea pigs was studied. After retrobulbar inoculation, the unconventional ALSP virus disseminated both neurogenically (along the optic nerve) and hematogenically. At early stages of the disease the spleen appeared to play the leading role in multiplication and/or accumulation of the agent. The earliest morphological sign of the CNS involvement was vacuolation of motoneuron cytoplasm. The ALSP agent first affected the spinal motoneurons, then an ascending pathological process developed. In the terminal stage of the disease, the unconventional ALSP virus was also detected in visceral tissue, besides the CNS, spleen, and peripheral blood lymphocytes.
Assuntos
Encefalopatias/etiologia , Modelos Animais de Doenças , Cobaias , Doenças por Vírus Lento/etiologia , Animais , Anticorpos/análise , Encefalopatias/imunologia , Encefalopatias/microbiologia , Encefalopatias/patologia , Olho , Imunidade Celular , Injeções , Linfócitos/imunologia , Fibras Nervosas/imunologia , Proteínas do Tecido Nervoso/imunologia , Doenças por Vírus Lento/imunologia , Doenças por Vírus Lento/microbiologia , Doenças por Vírus Lento/patologia , Fatores de TempoRESUMO
Young mice with congenital influenza infection have lower immune responsiveness of lymphocytes to nonspecific mitogens and influenza virus antigens. Lymphocytes of such animals inhibit proliferation of normal lymphoid cells activated with concanavalin A and immune lymphocytes activated with influenza virus antigens. It is assumed that in congenital influenza infection one of the possible mechanisms of immunosuppression in mice is the activation of suppressor T-cells.
Assuntos
Infecções por Orthomyxoviridae/congênito , Linfócitos T Reguladores/imunologia , Animais , Reações Antígeno-Anticorpo , Antígenos Virais/imunologia , Concanavalina A/farmacologia , Vírus da Influenza A/imunologia , Ativação Linfocitária/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos C57BL , Infecções por Orthomyxoviridae/imunologia , Doenças por Vírus Lento/congênito , Doenças por Vírus Lento/imunologia , Linfócitos T Reguladores/efeitos dos fármacosRESUMO
Using 51Cr isotope label it was demonstrated that a very low per cent of syngeneic lymphocytes derived from healthy donors and inoculated in the blood stream of uninfected or influenza virus-infected pregnant mice is found in fetuses before delivery. Similar results were obtained after inoculation of virus-specific cytotoxic lymphocytes (CTL) into uninfected pregnant mice. After inoculation into the blood stream of infected pregnant mice of virus-specific CTL their migration into fetuses before delivery increases, being most marked in 25-30% of mice. Intravenous inoculation of excess CTL (10(6) cells) to infected pregnant mice resulted in rapid development of signs of slow influenza infection in the progeny with typical clinical picture and histopathological lesions in organs and tissues. Large doses (10(7)-10(8) cells) of CTL inoculated into the blood stream cause higher reduction and death of fetuses and increase the rate of stillbirths. The role of maternal virus-specific CTL in the pathogenesis of experimental congenital and especially slow influenza infection is discussed.
Assuntos
Doenças do Sistema Imunitário/imunologia , Vírus da Influenza A/imunologia , Infecções por Orthomyxoviridae/imunologia , Linfócitos T Citotóxicos/imunologia , Animais , Radioisótopos de Cromo , Feminino , Feto/imunologia , Doenças do Sistema Imunitário/etiologia , Doenças do Sistema Imunitário/patologia , Troca Materno-Fetal/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Infecções por Orthomyxoviridae/complicações , Infecções por Orthomyxoviridae/congênito , Infecções por Orthomyxoviridae/patologia , Gravidez , Doenças por Vírus Lento/complicações , Doenças por Vírus Lento/congênito , Doenças por Vírus Lento/imunologia , Doenças por Vírus Lento/patologia , Linfócitos T Citotóxicos/transplanteRESUMO
Twenty-six patients including 12 with lateral amyotrophic sclerosis, 7 with multiple sclerosis, 5 with the Creutzfeld-Jakob disease and 2 with Alzheimer's disease were examined. Antibodies to neurofilaments in the blood serum were detected in all cases of the Creutzfeld-Jakob disease and Alzheimer's disease and in 8 patients with lateral amyotrophic sclerosis with clinical evidence of supranuclear structure involvement. A conclusion is drawn about a certain similarity of pathogenic mechanisms of these diseases, as well as about heterogeneity of the cytoskeleton of neurons in the brain and the spinal cord.