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Biomedical subjects

C E Coto

Publications and source records attributed to C E Coto.

At least 55 records · Page 3Linked to original sources
PubMed1982

In vitro infection of murine macrophages with Junin virus.

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.

Animals↗
PubMed1982

Cross-protection in nonhuman primates against Argentine hemorrhagic fever.

The susceptibility of the marmoset Callithrix jacchus to Tacaribe virus infection was investigated to perform cross-protection studies between Junin and Tacaribe viruses. Five marmosets inoculated with Tacaribe virus failed to show any signs of disease, any alterations in erythrocyte, leukocyte, reticulocyte, and platelet counts or any changes in hematocrit or hemoglobin values. No Tacaribe virus could be recovered from blood at any time postinfection. Anti-Tacaribe neutralizing antibodies appeared 3 weeks postinfection. The five Tacaribe-infected marmosets and four noninfected controls were challenged with the pathogenic strain of Junin virus on day 60 post-Tacaribe infection. The former group showed no signs of disease, no viremia, and no challenge virus replication, whereas the control group exhibited the typical symptoms of Argentine hemorrhagic fever, high viremia, and viral titers in organs. Soon after challenge, the Tacaribe-protected marmosets synthesized neutralizing antibodies against Junin virus. These results indicate that the marmoset C. jacchus can be considered an experimental model for protection studies with arenaviruses and that the Tacaribe virus could be considered as a potential vaccine against Junin virus.

Animals↗
PubMed1982

[Inhibition of the production of infectious particles in cells infected with Junín virus in the presence of tunicamycin].

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.

Animals↗
PubMed1981

Persistent infection of Vero cells with Tacaribe virus.

Persistently infected cultures have been established from Vero cells surviving primary infection with Tacaribe virus (Vero-T). The growth rate and morphological characteristics of the persistently infected cells were indistinguishable from normal Vero cells. Virus release declined during the first 6 passages, a cyclical pattern was observed between passages 6 and 16, and subsequently no virus infectivity could be detected. Co-cultivation with normal RK-13 or Vero cells enhanced virus yield from virus-producing cultures of Vero-T cells (passage 15), but the addition of susceptible cells had no effect on non-producer Vero-T cultures (passage 19). Only a small proportion (less than 1%) of the persistently infected cells tested during the first 16 passages produced infectious virus. The virus released during the early stages of persistence was temperature-sensitive if grown at 40 degree C, more thermolabile at 50 degree C than parental virus, and unable to initiate a persistent infection in Vero cells. Vero-T cells consistently showed refractoriness to homotypic Tacaribe virus superinfection and a selective graded resistance to other arenavirus replication. The possible use of viral susceptibility of persistently infected cultures as marker of antigenic relationship among Tacaribe complex viruses if considered.

Animals↗
PubMed1981

Induction of RNA polymerase II activity in Junin virus-infected cells.

Nuclear involvement of the host cell in Junin virus (JV) replication was studied. alpha-Amanitin was shown to inhibit JV yield, and RNA synthesis in cell nuclei was found to be augmented during the eclipse period. JV infection exerted a selective effect on cellular RNA polymerase activities, when measured in purified infected nuclei. RNA polymerase I was inhibited, but RNA polymerase II was stimulated. These data support the hypothesis that RNA polymerase II is involved in arenavirus replication.

Amanitins↗
PubMed1980

Serological survey to detect subclinical Junín virus infection in laboratory personnel.

Serological survey for detecting subclinical infections with Junín virus, the etiological agent of Argentine hemorrhage fever, was carried out in a group of 107 individuals working in laboratories where this virus was handled. The group was divided into high risk and low risk personnel according to the degree of exposure to the virus. Neutralizing tests were performed in Vero cell cultures to detect circulating antibodies. Results were evaluated comparatively with those obtained in a previous survey. This study shows that among high risk personnel three out of 52 developed neutralizing antibodies (NA) against Junín virus; one of them had a mild clinical illness, and the other two showed no overt disease during this period. No one among the low risk group developed NA against Junín virus.

Antibodies, Viral↗
PubMed1980

Protection of guinea pigs inoculated with Tacaribe virus against lethal doses of Junin virus.

Guinea pigs were protected against lethal doses of Junin virus by a previous inoculation with Tacaribe virus. Fourteen guinea pigs were infected with 10(6) 50% lethal doses (LD50) of Tacaribe virus and superinfected 45 days later with 10(3) LD50 of Junin virus. Appropriate control groups for both infections were also studied. The replication of Junin virus was impaired, as no virus was isolated from blood and organs of animals killed on days 9 and 11 after infection. High levels of neutralizing antibodies to Tacaribe virus were present by day 45, and no cross-reacting neutralizing antibodies to Junin virus were detected. However, three days after challenge with Junin virus, a typical secondary immune response to this virus was established. From these results it was concluded that the protection observed was mainly due to a specific immune response that was triggered by the Junin virus but primed by Tacaribe virus, which is antigenically similar to Junin virus.

Animals↗
PubMed1979

Temperature sensitivity of the arenavirus junin isolated from persistently infected Vero cells.

A persistently infected cell culture was established from Vero cells surviving primary infection with wild-type Junin virus (JVwt). The cells were refractory to superinfection by both Junin virus and the related Tacaribe virus. Replication of virus released from the persistently infected cells (JVpi) was inhibited at 39 degrees. JVpi did not interfere with JVwt at 37 degrees, and it was inactivated at 37, 40, 43, 46 and 50 degrees much more rapidly than was JVwt.

Arenaviridae↗
PubMed1974

Junín virus.

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Animals↗