RESUMO
Se investigó la eolución virológica, hematológica y de los nveles de glucemia de Calomys musculinus neonatos infectados con virus Junin, cepa XJCi3 por vía intraperitoneal. Como controles se utilizaron animales sanos y cricétidos inoculados con un homogeneizado de cerebro de ratón blanco no infectado. Los cricétidos que recibieron virus Junin desarrollaron el cuadro característico de la infección aguda, muriendo entre 50-70%. Se aisló virus del cerebro de los animales infectados, durante la fase aguda de la enfemedad, a partir del 6ª día post infectión, siendo el título de alrededor de 10***8 DL50/ml a los 12 días post infección. A partir del día 11 pi. todos los animales infectados presentaron anticuerpos neutralizantes que perduiraron durante el estado crónico de la infección, iniciado después del día 24 pi. Del análisis de los valores hematolóficos obtendos durante la fase aguda, se concluye que aproximadamente el 40% de los animales inoculados presentan linfopenia y neutrofilia, mientras que en la fase crónica nose encontraron modificaciones. Los estudios de glucemia realizados durante la infección aguda demostraron hipoglucemia (X=3,52mmol/VI) en el lote de animales infectados respecto del grupo control (X = 6,15 mmol/l) con una p < 0,01)
Assuntos
Camundongos , Animais , Arvicolinae/sangue , Febre Hemorrágica Americana/sangue , Análise de Variância , Arenavirus do Novo Mundo/isolamento & purificação , Arvicolinae/microbiologia , Glicemia , Febre Hemorrágica Americana/microbiologia , Testes de NeutralizaçãoRESUMO
Se investigó la eolución virológica, hematológica y de los nveles de glucemia de Calomys musculinus neonatos infectados con virus Junin, cepa XJCi3 por vía intraperitoneal. Como controles se utilizaron animales sanos y cricétidos inoculados con un homogeneizado de cerebro de ratón blanco no infectado. Los cricétidos que recibieron virus Junin desarrollaron el cuadro característico de la infección aguda, muriendo entre 50-70%. Se aisló virus del cerebro de los animales infectados, durante la fase aguda de la enfemedad, a partir del 6¬ día post infectión, siendo el título de alrededor de 10***8 DL50/ml a los 12 días post infección. A partir del día 11 pi. todos los animales infectados presentaron anticuerpos neutralizantes que perduiraron durante el estado crónico de la infección, iniciado después del día 24 pi. Del análisis de los valores hematolóficos obtendos durante la fase aguda, se concluye que aproximadamente el 40% de los animales inoculados presentan linfopenia y neutrofilia, mientras que en la fase crónica nose encontraron modificaciones. Los estudios de glucemia realizados durante la infección aguda demostraron hipoglucemia (X=3,52mmol/VI) en el lote de animales infectados respecto del grupo control (X = 6,15 mmol/l) con una p < 0,01) (AU)
Assuntos
Camundongos , Animais , Arvicolinae/sangue , Febre Hemorrágica Americana/sangue , Arvicolinae/microbiologia , Febre Hemorrágica Americana/microbiologia , Glicemia , Arenavirus do Novo Mundo/isolamento & purificação , Testes de Neutralização , Análise de VariânciaRESUMO
The aim of this study was to analyze the alterations in homeostasis induced by Junin virus during acute and persistent infection of C. musculinus. Virus presence in brain, hematological response and glycemia levels were evaluated. Newborn C. musculinus inoculated with 4000 DL50 of Junin virus, strain XJCl3 by intraperitoneal route developed a typical acute disease, with 50-70% mortality. Virus was isolated from brain starting day 6 post-infection (Fig. 1) and the peak titer (10(8) DL50/ml) was reached at 12 days post-infection. Neutralizing anti-Junin virus antibodies were detected from day 11 post-infection and all chronically infected animals developed persistent levels of neutralizing antibodies. In the acute stage of infection, 40% of the animals developed lymphopenia and neutrophilia (Fig. 2) while a slight variation was observed in the monocyte population. An important hypoglycemia was also seen in the acute infection (mean = 3.52 mmol/l) in comparison with control values (mean = 6.21 mmol/l), p less than 0.01 (Fig. 3). By contrast during the chronic stage of infection, neither hematological parameters (Table 2) varied between infected and control animals.
Assuntos
Arvicolinae/sangue , Febre Hemorrágica Americana/sangue , Análise de Variância , Animais , Arenavirus do Novo Mundo/isolamento & purificação , Arvicolinae/microbiologia , Glicemia , Febre Hemorrágica Americana/microbiologia , Camundongos , Testes de NeutralizaçãoRESUMO
The aim of this study was to analyze the alterations in homeostasis induced by Junin virus during acute and persistent infection of C. musculinus. Virus presence in brain, hematological response and glycemia levels were evaluated. Newborn C. musculinus inoculated with 4000 DL50 of Junin virus, strain XJCl3 by intraperitoneal route developed a typical acute disease, with 50-70
mortality. Virus was isolated from brain starting day 6 post-infection (Fig. 1) and the peak titer (10(8) DL50/ml) was reached at 12 days post-infection. Neutralizing anti-Junin virus antibodies were detected from day 11 post-infection and all chronically infected animals developed persistent levels of neutralizing antibodies. In the acute stage of infection, 40
of the animals developed lymphopenia and neutrophilia (Fig. 2) while a slight variation was observed in the monocyte population. An important hypoglycemia was also seen in the acute infection (mean = 3.52 mmol/l) in comparison with control values (mean = 6.21 mmol/l), p less than 0.01 (Fig. 3). By contrast during the chronic stage of infection, neither hematological parameters (Table 2) varied between infected and control animals.
RESUMO
Treatment of neonatal mice with an antiviral factor, (AVF), obtained from the leaves of Melia azedarach L. protected them against lethal encephalitis caused by Tacaribe virus inoculation. The degree of protection obtained varied from 66% to 100% depending on the virus dose. Similarly, administration of AVF to nursing mothers protected their offspring from developing virus encephalitis. AVF does not directly inactivate Tacaribe virus; it inhibits an early step (s) in the replication process in cell cultures.
Assuntos
Antivirais/uso terapêutico , Encefalite/prevenção & controle , Febre Hemorrágica Americana , Extratos Vegetais/uso terapêutico , Animais , Animais Recém-Nascidos , Antivirais/farmacologia , Arenavirus do Novo Mundo/fisiologia , Encefalite/etiologia , Feminino , Lactação , Camundongos , Gravidez , Replicação Viral/efeitos dos fármacosRESUMO
In nature, the cricetid Calomys musculinus is the principal host of Junin virus, the etiological agent of Argentine hemorrhagic fever. In the experimental infection, adult C. musculinus survived whereas newborns died after intraperitoneal inoculation with the XJ.Cl3 strain of Junin virus. The role of peritoneal macrophages in this age-related resistance was studied. Junin virus multiplied in cultivated macrophages from either neonatal or adult animals and, therefore, it was not possible to correlate the susceptibility of peritoneal macrophages to Junin virus infection with the age-dependent resistance. When adult and neonatal animals were treated with silica prior to Junin virus infection, deaths occurred in the adults, while a delay and decrease in the mortality rate were observed in neonatals. These results suggest that in neonatal C. musculinus macrophages could be permissive cells for Junin virus multiplication, whereas in adult cricetids, these cells would act as a barrier against viral infection by means of an extrinsic antiviral activity.
Assuntos
Envelhecimento , Macrófagos/imunologia , Animais , Arenavirus do Novo Mundo/imunologia , Arvicolinae , Células Cultivadas , Febre Hemorrágica Americana/imunologia , Febre Hemorrágica Americana/mortalidade , Macrófagos/citologia , Macrófagos/efeitos dos fármacos , Cavidade Peritoneal/citologia , Dióxido de Silício/efeitos adversos , Dióxido de Silício/farmacologiaRESUMO
Mouse peritoneal macrophages were successfully infected with two strains of Junin virus producing high titers with no apparent cell damage. Infected cultures survived longer than noninfected cultures. The pattern of virus release suggested a persistent infection. Virus replication was delayed in macrophages from mice previously immunized with Junin virus. These results support the opinion that macrophages are targets for virus replication in vivo infections.