RESUMO
Administration of cyclophosphamide (CY) to guinea pigs infected with a lethal strain of Junin virus (JV) delayed the time of death, with survival of a small number of animals. Virological studies showed a temporary decrease of virus concentration in blood and viscera shortly after the CY injection. In the pathological study no differences were found in the organic lesions present in CY-treated and nontreated animals, with the exception of the pulmonary alterations. In CY-treated guinea pigs the lungs appeared almost normal, but in the control, nontreated animals severe alterations with the pattern of the "respiratory distress syndrome of the adult" were consistently present. In in vitro experiments, incorporation of serum collected from guinea pigs injected 30 minutes before exsanguination with CY to cell cultures, infected with JV, prevented virus replication. On the basis of these results it is suggested that the delay of time of death and eventual survival of CY-treated guinea pigs after JV infection depends on a direct antiviral effect of the drug rather than on its known immunosuppressive action. In addition, the absence of pulmonary alterations in CY-treated animals was tentatively considered to be dependent on the marked polymorphonuclear leukocyte depletion induced by the drug.
Assuntos
Arenaviridae/efeitos dos fármacos , Arenavirus do Novo Mundo/efeitos dos fármacos , Ciclofosfamida/uso terapêutico , Febre Hemorrágica Americana/tratamento farmacológico , Animais , Arenavirus do Novo Mundo/crescimento & desenvolvimento , Sobrevivência Celular , Células Cultivadas , Relação Dose-Resposta a Droga , Cobaias , Febre Hemorrágica Americana/patologia , Masculino , Especificidade de Órgãos , Ensaio de Placa ViralRESUMO
The antibiotic tunicamycin, an inhibitor of glycoprotein synthesis, suppressed Junin virus multiplication in Vero cells. No infectious virus was formed if tunicamycin was added, at a concentration of 1 microgram/ml, immediately after virus adsorption and remained up to the end of the replicative cycle. Tunicamycin added at 24,48 or 72 hours p.i. immediately stopped virus synthesis. The effect was irreversible. Virus grown in the presence or absence of tunicamycin and labelled with 3H-uridine was purified and layered on a (20-60%) sucrose gradient. The radioactive profile of both gradients was coincident. The total number of cpm associated to the peak gradient of virus grown with tunicamycin represented 70% of the cpm from control virus. Since viral infectivity was 99.4% inhibited in the presence of TM it can be assumed that most of the radioactive particles formed are not infectious. Therefore, in the presence of tunicamycin Junin virus buds normally. From these results we can conclude that carbohydrates are important for viral infectivity but play no role in the transport of viral proteins through cellular membranes.
Assuntos
Arenaviridae/efeitos dos fármacos , Arenavirus do Novo Mundo/efeitos dos fármacos , Tunicamicina/farmacologia , Replicação Viral/efeitos dos fármacos , Animais , Arenavirus do Novo Mundo/fisiologia , Glicoproteínas/biossíntese , Glicoproteínas/fisiologia , Glicosilação , Processamento de Proteína Pós-Traducional , Células Vero , Proteínas Virais/biossíntese , Proteínas Virais/fisiologiaAssuntos
Arenaviridae/efeitos dos fármacos , Arenavirus do Novo Mundo/efeitos dos fármacos , Febre Hemorrágica Americana/tratamento farmacológico , Interferons/farmacologia , Animais , Encéfalo/microbiologia , Camundongos , Interferência Viral/efeitos dos fármacos , Replicação Viral/efeitos dos fármacosRESUMO
The multiplication of arenaviruses Tacaribe, Pichinde and Junin was inhibited by 16 mM of glucosamine and by 10 mM of 2-deoxi-D-glucose.