ABSTRACT
The antiviral activity of alcoholic extracts of several species belonging to the Asteraceae, Labiatae, Plantaginaceae, Schizaceae, Umbelliferae, Usneaceae and Verbenaceae families has been studied. The tests were carried out in Vero celís-pseudorabies virus strain RC/79 (herpes suis virus) system. Eight plant extracts (Achyrocline satureioides, Ambrossia tenuifolia, Baccharis articulata, Eupatorium buniifolium, Mynthostachys verticillata, Plantago brasiliensis, Plantago mayor L and Verbascum thapsus) were able to inhibit at least 2 log, the viral infectivity.
Subject(s)
Antiviral Agents/isolation & purification , Herpesvirus 1, Suid/drug effects , Plant Extracts/pharmacology , Plants, Medicinal/chemistry , Animals , Antiviral Agents/pharmacology , Argentina , Chlorocebus aethiops , Herpesvirus 1, Suid/physiology , Vero Cells , Virus Replication/drug effectsABSTRACT
BACKGROUND: Most mucose-cutaneous infections can be diagnosed by clinical history with explorative technique. Nevertheless the definitive etiologic diagnostic can only be established with the help of the isolation and identification of the causal agent. PATIENT AND METHODS: We reported a case of generalized infection in a new born, with is clinical characteristics, virological diagnostic techniques and treatment of the disease. RESULTS: Herpes simplex virus was isolated in Vero cellular culture from CRL and vesiculose lesions of the child's thorax region and from the mothers endocervical scrapes. The agent was identified by seroneutralization test. This confirmed a perinatal transmission of Herpes simplex virus type 2. The tomographic studies revealed characteristic alterations of a viral encephalitis. An antiviral treatment was useful in this therapy. CONCLUSIONS: Our results demonstrate the importance of an early viral diagnostic which permits the applications of specific treatment and thus the prevention of severe complications.
Subject(s)
Herpes Simplex/congenital , Herpes Simplex/diagnosis , Herpes Simplex/drug therapy , Herpesvirus 2, Human/isolation & purification , Humans , Infant, Newborn , Neutralization TestsABSTRACT
The RC/79 strain of the Aujeszky's disease virus was able to induce reproductive failure of pregnant gilts intranasally inoculated at different gestation periods. Four gilts 40-46 days pregnant (group A) and 6 gilts 70-73 days pregnant (group B) were instilled with 0.2 ml x 10(5) tissue culture infectious dose 50 (TCID50/0.2 ml) of the RC/79 strain into each nostril. Two gilts 70-73 days pregnant (group C) were used as non exposed controls. The three groups were kept in separated boxes and they were observed for clinical signs of infections and samples were collected for determination of viral shedding every day. Viral isolation was attempted in Vero cells (figure 1). From the 2nd to 7th day after inoculation, groups A and B showed fever anorexia, sneezing, coughing and depression; and viral isolation from nasal swabs was possible in 7 gilts at days 4 to 11, 9 gilts developed neutralizing antibodies. The virus caused fetal reabsorption in swine during the first period of pregnancy (group A), while infection during late pregnancy resulted in still birth or normal pigs and one mummification (group B). The entire a live litter was composed of no more than 8 suckling pigs in both groups. At necropsy virus from turbinates, ovary , placenta, spleen and lung could be isolated only from 3 gilts (group B, table 1). In 5 of 35 stillbirth and alive fetuses virus could be isolated from spleen (100%), lung (80%), liver (60%) and brain (40%) indicating that the virus has the ability to cross the placental barrier thus producing lesions in porcine fetuses and causing reproductive failure in sows (table 2). Tissue specimens from these 35 fetuses were fixed in 10% formalin, included in paraffin sectioned and stained with hematoxylin and eosin. In 13 fetuses microscopic lesions i.e. necrotic foci were found in lung (60%), liver (40%) and spleen (20%), these alterations were coincident with gross lesions in most of them. Inclusion bodies were absent. The gilts organs did not present gross lesions.
Subject(s)
Fetal Death/veterinary , Fetal Diseases/veterinary , Herpesvirus 1, Suid/isolation & purification , Pregnancy Complications, Infectious/veterinary , Pseudorabies/transmission , Swine Diseases/transmission , Administration, Intranasal , Animals , Antibodies, Viral/biosynthesis , Brain/embryology , Brain/microbiology , Female , Fetal Death/etiology , Fetal Death/microbiology , Fetal Death/pathology , Fetal Diseases/etiology , Fetal Diseases/microbiology , Fetal Diseases/pathology , Fetal Resorption/etiology , Fetal Resorption/veterinary , Herpesvirus 1, Suid/classification , Herpesvirus 1, Suid/immunology , Maternal-Fetal Exchange , Pregnancy , Pregnancy Complications, Infectious/microbiology , Pseudorabies/microbiology , Swine , Swine Diseases/microbiology , Vero Cells , Viscera/embryology , Viscera/microbiologyABSTRACT
The RC/79 strain of the Aujeszkys disease virus was able to induce reproductive failure of pregnant gilts intranasally inoculated at different gestation periods. Four gilts 40-46 days pregnant (group A) and 6 gilts 70-73 days pregnant (group B) were instilled with 0.2 ml x 10(5) tissue culture infectious dose 50 (TCID50/0.2 ml) of the RC/79 strain into each nostril. Two gilts 70-73 days pregnant (group C) were used as non exposed controls. The three groups were kept in separated boxes and they were observed for clinical signs of infections and samples were collected for determination of viral shedding every day. Viral isolation was attempted in Vero cells (figure 1). From the 2nd to 7th day after inoculation, groups A and B showed fever anorexia, sneezing, coughing and depression; and viral isolation from nasal swabs was possible in 7 gilts at days 4 to 11, 9 gilts developed neutralizing antibodies. The virus caused fetal reabsorption in swine during the first period of pregnancy (group A), while infection during late pregnancy resulted in still birth or normal pigs and one mummification (group B). The entire a live litter was composed of no more than 8 suckling pigs in both groups. At necropsy virus from turbinates, ovary , placenta, spleen and lung could be isolated only from 3 gilts (group B, table 1). In 5 of 35 stillbirth and alive fetuses virus could be isolated from spleen (100
) and brain (40
) indicating that the virus has the ability to cross the placental barrier thus producing lesions in porcine fetuses and causing reproductive failure in sows (table 2). Tissue specimens from these 35 fetuses were fixed in 10
formalin, included in paraffin sectioned and stained with hematoxylin and eosin. In 13 fetuses microscopic lesions i.e. necrotic foci were found in lung (60
) and spleen (20
), these alterations were coincident with gross lesions in most of them. Inclusion bodies were absent. The gilts organs did not present gross lesions.
ABSTRACT
The RC/79 strain of the Aujeszkys disease virus was able to induce reproductive failure of pregnant gilts intranasally inoculated at different gestation periods. Four gilts 40-46 days pregnant (group A) and 6 gilts 70-73 days pregnant (group B) were instilled with 0.2 ml x 10(5) tissue culture infectious dose 50 (TCID50/0.2 ml) of the RC/79 strain into each nostril. Two gilts 70-73 days pregnant (group C) were used as non exposed controls. The three groups were kept in separated boxes and they were observed for clinical signs of infections and samples were collected for determination of viral shedding every day. Viral isolation was attempted in Vero cells (figure 1). From the 2nd to 7th day after inoculation, groups A and B showed fever anorexia, sneezing, coughing and depression; and viral isolation from nasal swabs was possible in 7 gilts at days 4 to 11, 9 gilts developed neutralizing antibodies. The virus caused fetal reabsorption in swine during the first period of pregnancy (group A), while infection during late pregnancy resulted in still birth or normal pigs and one mummification (group B). The entire a live litter was composed of no more than 8 suckling pigs in both groups. At necropsy virus from turbinates, ovary , placenta, spleen and lung could be isolated only from 3 gilts (group B, table 1). In 5 of 35 stillbirth and alive fetuses virus could be isolated from spleen (100
) and brain (40
) indicating that the virus has the ability to cross the placental barrier thus producing lesions in porcine fetuses and causing reproductive failure in sows (table 2). Tissue specimens from these 35 fetuses were fixed in 10
formalin, included in paraffin sectioned and stained with hematoxylin and eosin. In 13 fetuses microscopic lesions i.e. necrotic foci were found in lung (60
) and spleen (20
), these alterations were coincident with gross lesions in most of them. Inclusion bodies were absent. The gilts organs did not present gross lesions.
ABSTRACT
The RC/79 strain of the Aujeszkys disease virus was able to induce reproductive failure of pregnant gilts intranasally inoculated at different gestation periods. Four gilts 40-46 days pregnant (group A) and 6 gilts 70-73 days pregnant (group B) were instilled with 0.2 ml x 10(5) tissue culture infectious dose 50 (TCID50/0.2 ml) of the RC/79 strain into each nostril. Two gilts 70-73 days pregnant (group C) were used as non exposed controls. The three groups were kept in separated boxes and they were observed for clinical signs of infections and samples were collected for determination of viral shedding every day. Viral isolation was attempted in Vero cells (figure 1). From the 2nd to 7th day after inoculation, groups A and B showed fever anorexia, sneezing, coughing and depression; and viral isolation from nasal swabs was possible in 7 gilts at days 4 to 11, 9 gilts developed neutralizing antibodies. The virus caused fetal reabsorption in swine during the first period of pregnancy (group A), while infection during late pregnancy resulted in still birth or normal pigs and one mummification (group B). The entire a live litter was composed of no more than 8 suckling pigs in both groups. At necropsy virus from turbinates, ovary , placenta, spleen and lung could be isolated only from 3 gilts (group B, table 1). In 5 of 35 stillbirth and alive fetuses virus could be isolated from spleen (100
), lung (80
), liver (60
) and brain (40
) indicating that the virus has the ability to cross the placental barrier thus producing lesions in porcine fetuses and causing reproductive failure in sows (table 2). Tissue specimens from these 35 fetuses were fixed in 10
formalin, included in paraffin sectioned and stained with hematoxylin and eosin. In 13 fetuses microscopic lesions i.e. necrotic foci were found in lung (60
), liver (40
) and spleen (20
), these alterations were coincident with gross lesions in most of them. Inclusion bodies were absent. The gilts organs did not present gross lesions.
ABSTRACT
The RC/79 strain of the Aujeszkys disease virus was able to induce reproductive failure of pregnant gilts intranasally inoculated at different gestation periods. Four gilts 40-46 days pregnant (group A) and 6 gilts 70-73 days pregnant (group B) were instilled with 0.2 ml x 10(5) tissue culture infectious dose 50 (TCID50/0.2 ml) of the RC/79 strain into each nostril. Two gilts 70-73 days pregnant (group C) were used as non exposed controls. The three groups were kept in separated boxes and they were observed for clinical signs of infections and samples were collected for determination of viral shedding every day. Viral isolation was attempted in Vero cells (figure 1). From the 2nd to 7th day after inoculation, groups A and B showed fever anorexia, sneezing, coughing and depression; and viral isolation from nasal swabs was possible in 7 gilts at days 4 to 11, 9 gilts developed neutralizing antibodies. The virus caused fetal reabsorption in swine during the first period of pregnancy (group A), while infection during late pregnancy resulted in still birth or normal pigs and one mummification (group B). The entire a live litter was composed of no more than 8 suckling pigs in both groups. At necropsy virus from turbinates, ovary , placenta, spleen and lung could be isolated only from 3 gilts (group B, table 1). In 5 of 35 stillbirth and alive fetuses virus could be isolated from spleen (100
), lung (80
), liver (60
) and brain (40
) indicating that the virus has the ability to cross the placental barrier thus producing lesions in porcine fetuses and causing reproductive failure in sows (table 2). Tissue specimens from these 35 fetuses were fixed in 10
formalin, included in paraffin sectioned and stained with hematoxylin and eosin. In 13 fetuses microscopic lesions i.e. necrotic foci were found in lung (60
), liver (40
) and spleen (20
), these alterations were coincident with gross lesions in most of them. Inclusion bodies were absent. The gilts organs did not present gross lesions.
ABSTRACT
Two temperature sensitive (ts) mutants of Junin virus, a member of Arenaviridae, have been partially characterized. Both mutants, named ts-32 and ts-40, had a relative plating efficiency 40 degrees C/34 degrees C lower than 10(-3) an exhibited a leak yield below 10(-4). Standard growth curves showed that at 34 degrees C the viral mutants multiplied slower than wt virus and at high multiplicity did not display autointerference. No differences in thermolability were observed between wt and ts mutants. By contrast, when the pathogenic properties of the mutants were investigated they were significantly attenuated for mice. At the restrictive temperature both mutants were unable to synthesize viral-specific polypeptides, while at the permissive temperature the pattern was similar to wt virus. Shift-up and down experiments suggested that ts defect is expressed between 2 and 4 hours post-infection. It is concluded that ts-32 and ts-40 are early function mutants. The possible nature of their defect is discussed.
Subject(s)
Arenaviridae/genetics , Arenaviruses, New World/genetics , Animals , Animals, Newborn , Arenaviruses, New World/growth & development , Arenaviruses, New World/metabolism , Arenaviruses, New World/pathogenicity , Genes, Viral , Mice , Mutation , Temperature , Viral Plaque Assay , Viral Proteins/biosynthesisABSTRACT
This paper presents results concerning production, selection and isolation of conditionally lethal mutants of Junin virus. Two temperature sensitive (ts) mutants of Junin virus, XJCl3 strain, were isolated from a virus population that had been mutagenized with 5-Fluorouracil (5-FU). A study of the behaviour of wild-type virus over a range of temperature from 34 degrees C to 40 degrees C was done. In Vero cells, the initial cloned Junin virus stock gave very turbid plaques at 34 degrees C, more clear plaques at 37 degrees C and lytic pinpoint plaques at 40 degrees C. The efficiency of plaquing (ratio of plaques formed at 40 degrees C to plaques formed at 37 degrees C) in Vero cells was 0.86. Moreover, the wild-type virus had similar growth curves at 34, 37 or 40 degrees C in Vero cells. To study the 5-FU inhibition of Junin virus multiplication, Vero cell cultures were infected with approximately 0.6 PFU per cell and incubated in the presence of various doses of mutagen. After 24 hs of infection the yields were titrated. The mutagen inhibited virus multiplication in a dose-dependent manner. A concentration of 100 micrograms/ml, which reduced virus yields to 1% of that obtained in cultures lacking 5-FU, was chosen to select ts mutants. A rapid screening procedure based on the ability of Junin virus to develop cytopathic effects in Vero cells at 37 degrees C and 40 degrees C was used to identify potential ts mutants among 90 randomly picked plaque isolates obtained from virus grown at 34 degrees C during 24 hs in the presence of the mutagen.(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Arenaviridae/genetics , Arenaviruses, New World/genetics , Fluorouracil/pharmacology , Animals , Arenaviruses, New World/drug effects , Microbiological Techniques , Temperature , Vero CellsABSTRACT
This paper presents results concerning production, selection and isolation of conditionally lethal mutants of Junin virus. Two temperature sensitive (ts) mutants of Junin virus, XJCl3 strain, were isolated from a virus population that had been mutagenized with 5-Fluorouracil (5-FU). A study of the behaviour of wild-type virus over a range of temperature from 34 degrees C to 40 degrees C was done. In Vero cells, the initial cloned Junin virus stock gave very turbid plaques at 34 degrees C, more clear plaques at 37 degrees C and lytic pinpoint plaques at 40 degrees C. The efficiency of plaquing (ratio of plaques formed at 40 degrees C to plaques formed at 37 degrees C) in Vero cells was 0.86. Moreover, the wild-type virus had similar growth curves at 34, 37 or 40 degrees C in Vero cells. To study the 5-FU inhibition of Junin virus multiplication, Vero cell cultures were infected with approximately 0.6 PFU per cell and incubated in the presence of various doses of mutagen. After 24 hs of infection the yields were titrated. The mutagen inhibited virus multiplication in a dose-dependent manner. A concentration of 100 micrograms/ml, which reduced virus yields to 1
of that obtained in cultures lacking 5-FU, was chosen to select ts mutants. A rapid screening procedure based on the ability of Junin virus to develop cytopathic effects in Vero cells at 37 degrees C and 40 degrees C was used to identify potential ts mutants among 90 randomly picked plaque isolates obtained from virus grown at 34 degrees C during 24 hs in the presence of the mutagen.(ABSTRACT TRUNCATED AT 250 WORDS)
