Showing papers on "Viremia published in 1978"

Viremia in experimental Creutzfeldt-Jakob disease

Abstract: Inoculation of the buffy coat of blood from guinea pigs infected with Creutzfeldt-Jakob disease resulted in passage of this disease to recipient animals. This demonstrates that there is a viremia in experimental Creutzfeldt-Jakob disease. These findings suggest that the hematogenous route may be implicated in the human infection and that the disease may possibly be transmitted by blood transfusions.

Cytomegalovirus infection in guinea pigs. I. Viremia during acute primary and chronic persistent infection.

Abstract: Studies on the pathogenesis of cytomegalovirus (CMV) infection in guinea pigs have revealed two distinct phases of infection, without any signs of clinical disease. During acute primary infection, viremia was easily demonstrated and infectious virus was recovered from various tissues, including lung, spleen, and kidney, of the infected animal two to 10 days after inoculation. Chronic persistent infection was readily established thereafter. In animals with chronic persistent infection with high levels of circulating antibody, infectious virus was consistently isolated from the salivary gland and pancreas. Evidence of CMV in the blood of the persistently infected animals was detected only occasionally and only when a highly sensitive method and/or a large inoculum was used. However, the anticoagulant heparin was found to inactivate CMV significantly during collection of blood. These data suggest that CMV was indeed circulating in the blood of apparently healthy but persistently infected animals for prolonged periods. Such infected blood could conceivably be the source of CMV infection when large quantities of blood are given to susceptible recipients.

Genetic control of sensitivity to Moloney-virus-induced leukemias in mice. I. Demonstration of multigenic control.

Abstract: The appearance of hematopoietic malignancies and the level of viremia were studied in mice of different inbred strains and their F1 or F2 hybrids inoculated with the Moloney leukemia virus (MLV) The viremia was regularly measured in individual mice by radioimmunoassay of the major internal virion component p30. A complex genetic control was found. (1) The level of circulating virus was controlled by at least two genes. An H-2 linked gene, tentatively called Rmv-1, displayed a dominant sensitivity. Alleles for resistance existed in H-2b and H-2r haplotypes and alleles for sensitivity in H-2a, H-2d and H-2f. Another gene with dominant resistance mapped outside the H-2 complex and probably interacted with Rmv-1. (2) A good correlation existed between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. (3) Nevertheless, additional genes which were not involved in the viremia control could be determinant in the induction of malignancies. One of them with a resistant allele in DBA/2 mice seemed to inhibit the appearance of leukemia despite a high level of viremia. Another gene controlled the spleen involvement resulting in generalized leukemias in sensitive lines contrasting with mainly thymus-localized tumors in resistant animals.

The Effect of Complement Depletion on the Course of Sindbis Virus Infection in Mice

Abstract: The course of Sindbis virus infection in 12-day-old BALB/c mice was altered significantly in animals depleted of the third component of complement (C3) by treatment with purified cobra venom factor (CoVF). Although the same percentage of C3-depleted and normal animals died (30%) after the subcutaneous inoculation of 1000 PFU Sindbis virus, the mean day of death was later in C3-depleted mice (8.4 days) than in controls (6.5 days). In addition, morbidity was prolonged in C3-depleted mice. Growth of virus at the inoculation site in the foot was not different; however, viremia was prolonged and the amount of virus in the brain was 1000-fold greater 6 days after infection in C3-depleted animals. These studies demonstrated that complement plays an important role in the host's response to Sindbis virus infection by participating in both beneficial and immunopathologic responses to the infection.

Spring viremia of carp virus RNA and virion-associated transcriptase activity.

Abstract: An RNA-dependent RNA polymerase activity has been demonstrated for spring viremia of carp virus (SVCV). The optimal temperature for in vitro synthesis of RNA was 20 to 25 degrees C. The SVCV enzyme activity was stimulated when the methyl donor S-adenosyl-L-methionine was included in the reaction mixture. S-adenosyl-L-methionine was not particularly effective in stimulating the virion RNA polymerase activity of vesicular stomatitis virus or pike fry rhabdovirus. The 5' nucleotide of the SVCV viral RNA is pppAp.

Influence of Transplacentally Acquired Antibody on Neonatal Susceptibility to Canine Distemper Virus in Gnotobiotic Dogs

Abstract: In utero acquisition of protective levels of neutralizing antibody to canine distemper virus (CDV) was observed in four litters of colostrum-deprived gnotobiotic and specific-pathogen-free puppies. Pregnant bitches with high antibody titers passively transferred antibody to these pups transplacentally in average titers of 1:7 to 1:16 per litter. Maternally derived antibody protected neonatal pups from otherwise fatal infection with virulent CDV. Protection was associated with a transient lymphopenia and viremia and temporary suppression of lymphocyte responses to phytohemagglutinin-P. The precise mechanisms involved in the resolution of infection with canine distemper virus (CDV) in dogs have not been delineated. Susceptible dogs, when challenged with virulent virus, experience a generalized infection of lymphoid organs initially and subsequently show involvement of epithelial cells (particularly respiratory) and the central nervous system. Recovery is correlated with development of virusspecific cell-mediated [1] and humoral antibody [2, 3] responses beginning five to nine days after infection.

Duration of vaccinal immunity against Marek's disease.

Abstract: Specific vaccinal immunity against Marek's disease (MD) virus was measured by a short-term challenge test in which chickens vaccinated with turkey herpesvirus (HVT) and control chickens at various ages up to 40 weeks were inoculated with virulent MD virus and evaluated 2 weeks later for microscopic lesions and MD viremia. Vaccinal immunity induced by high (2,900 PFU) and low (29 PFU) doses of HVT persisted without detectable reduction through the 40th week in line 151 chickens, thus indicating that resistance of older vaccinated chickens to MD may not be based solely on general age resistance (immunocompetence) or on subsequent exposure to field MD virus. The HVT viremia titers (number of buffy-coat cells inducing virus plaques in vitro) decreased with increasing age, but even chickens from which no HVT was isolated were usually immune to MD. The dose of vaccine appeared to influence, at least slightly, the magnitude of MD immunity and vaccine virus viremia.

Potentiation of coxsackievirus B3 infection in adult mice pretreated with a gold salt.

Abstract: In mice treated with sodium aurothiomalate (myocrisin), prior to infection with Coxsackievirus B3, 90% of the animals died by the 11th day postinfection (p.i.). A mortality of 10% was noted in mice receiving myocrisin only, and no deaths occurred in animals infected with virus alone. The highest amount of virus was recovered from the pancreas of myocrisin-treated mice on day 3 p.i. This was over 500-fold higher than the virus titer found in the pancreas of mice infected with virus only. Generally the titer of virus present in different organs was higher at every point in drug-treated animals as compared to intact mice infected with the virus. A high and persistent viremia was present in myocrisin-treated mice; in contrast a low viremia followed by virus clearance from the blood was observed in intact mice infected with the virus. The antibody response was studied in intact and myocrisin-treated mice infected with the virus. In both groups, no neutralizing antibodies were detected on days 1, 2, and 3 p.i. On day 7 after infection, the titers of antibodies were 1:16 and 1:12 in intact and myocrisin-treated mice, respectively. Administration of hyperimmune anti-Coxsackievirus B3 serum 6 hours after infection protrected in myocrisin-treated group of mice against lethal disease. The results of these studies suggest that (1) antibodies alone may not be sufficient to limit the spread and persistence of virus in natural infections and (2) in the absence of any apparent histopathological differences the increased multiplication of Coxsackievirus B3 could be the cause of death in myocrisin-treated mice.

Pathogenesis of a Venezuelan Encephalitis Virus Strain Lethal for Adult White Rats

Abstract: The pathogenesis for adult rats of a Venezuelan encephalitis virus (VEE) strain, V-198, was studied. This virus strain was chosen following virulence-testing of 12 prototype alphavirus strains, selected from the Semliki Forest, Venezuelan, Eastern, and Western encephalitis virus complexes; only VEE strain V-198 killed all adult rats when inoculated subcutaneously (sc) with 6.0–6.5 log10 plaque-forming units (PFU). Lower doses of strain V-198 by the same route were also lethal: 5.0 and 3.0 log10 PFU killed 100%, and 1.0 log10 PFU killed 70% of rats. Viral infectivity titrations of tissues obtained from V-198 straininfected rats demonstrated that virus replicated early in thymus and spleen, but did not replicate in bone marrow or liver. Following a brief viremia, virus infectivity titers peaked in brain, but did not persist there. A biphasic neutrophilia also occurred. Lower doses of inoculum virus affected the timing but not the degree of neutrophil fluctuations, virus replication, and clinical disease. Rats, moribund seven days after inoculation of 4.3 log10 PFU, exhibited central nervous system signs and histologic evidence of encephalomyelitis. Significant proportions of rats, otherwise lethally infected with V-198 virus, were protected by a single intraperitoneal inoculation of hyperimmune V-198 antiserum, administered 3 or 4, but not 5 days after virus. Since the rat has been well characterized with respect to metabolic alterations following other infectious diseases, it is anticipated that this model for lethal virus-induced disease will be useful for defining more precisely the functional relationships between viral growth, tissue destruction, metabolic alterations, and clinical course of disease, and that it may suggest specific approaches for effective treatment of viral diseases in general.

Field experiments on live attenuated Japanese encephalitis virus vaccine for swine.

Abstract: The efficacy of a live attenuated Japanese encephalitis virus (JEV) vaccine was examined in swine under conditions where natural infection could occur. The pigs immunized with the vaccine produced antibodies within one week after vaccination, and the antibody was retained until the end of the experiment, i.e. 36 days. However, the antibody titers in this group were lower than that in control group naturally infected with JEV. No virus was isolated from the five vaccinated pigs, but virus was isolated from all four untreated control pigs after natural infection, i.e., viremia was detected in all these animals. The duration of viremia in control pigs varied from one to four days. From these findings, it is concluded that immunization of swine with live attentuated JEV vaccine is useful in control of Japanese encephalitis (JE) in humans and some susceptible domestic animals.

CNS disease following dissemination of SSPE measles virus from intraperitoneal inoculation of suckling hamsters.

Abstract: Acute encephalitis was observed in suckling Golden Syrian hamsters following intraperitoneal (ip) inoculation of a hamster brain adapted strain of subacute sclerosing panencephalitis (SSPE) measles virus (HBS). Virus was isolated from the brains of all encephalitic animals by cocultivation of tissue with Vero cells. The histopathology of the encephalitis was characterized by perivascular mononuclear infiltrates, necrosis, eosinophilic inclusion bodies, and rare giant cells. Association of encephalitis with systemic viral infection was observed with virus present in lung and a kidney-spleen pool in addition to brain. Viral dissemination in asymptomatic animals was documented with virus being isolated from multiple non-neural tissues (spleen, lung, liver) of animals having no recoverable virus in their brains and no signs of encephalitis. Treatment of animals with cyclophosphamide prior to ip virus inoculation did not increase dissemination to brain. Absence of encephalitis in asymptomatic animals with proven viral dissemination to parenchymal organs indicates that neither viremia alone, nor viremia in conjunction with dissemination are sufficient conditions to establish central nervous system disease. The association of encephalitis with systemic viral infection and the dissemination to brain establish this model's potential value for the study of the pathogenesis of measles encephalitis.

Cytomegalovirus infection in malignant blood diseases:clinical and laboratory data in 29 patients.

Abstract: Twenty-nine patients treated for malignant blood diseases developped CMV infection. Their clinical and laboratory features were studied. The results indicated that this infection apparently did not influence the prognisis of the underlying disease. The main hematological feature was pancytopenia. The data of viremia suggested active infection. A marked increase of CMV CF antibodies were observed in 27/29 patients, and the peak titers of 42% of our cases were greater than 1:1024. Homogenous Ig were detected in 7/29 patient's serum.

Pancreas-passaged avian encephalomyelitis virus and its immunogenicity.

Abstract: A serial 34-chicken pancreas passage of avian encephalomyelitis virus by oral administration was successful. Oral inoculation test with 4 passaged viruses showed rapid infection of the duodenal wall and unchangeable infection of pancreas diminishing the viral invasiveness to other organs. The passaged virus caused neither detectable viremia nor clinical avian encephalomyelitis signs and produced neutralizing antibody of high titers.

Intranasal exposure of the Richardson's ground squirrel to Western equine encephalomyelitis virus.

Abstract: Adult Richardson's ground squirrels were infected with western equine encephalomyelitis virus by intranasal instillation. Mortality followed the instillation of a minimum threshold of 4.7 logs of virus while infection was produced by a dosage of 2.3 logs. The incubation period was from four to seven days, being preceded by a viremic phase. Signs were depression, ataxia and paralysis of the limbs. Highest titres of virus were recovered from the brain and histopathological changes involving the central nervous system included meningitis, vasculitis, perivascular cuffing, gliosis, neuronophagia and neuronal degeneration. The virus was also found in a variety of extraneural tissues. Lesions in extraneural tissues included necrosis of brown fat and an apparent increase in number of Kupffer's cells in the liver. The lymphoid tissue was involved indicating a possible source for viremia. The duration and magnitude of viremia were ample enough to provide virus source for arthropods. The potential for transmission of the virus independent of arthropods was discussed in view of the pathogenesis demonstrated in the experimental infections.

[Host-virus relationship during experimental spring viremia in carp].

Abstract: One-summer-old virus-free carps produce both circulating interferon and neutralizing antibodies when stored at +20 degrees C and injected intraperitonealy with 10(5), 10(6), 10(7) p. f. u. of Spring Viremia of Carp virus per fish: Kinetics and intensity of interferon production are maximum for the highest virus imput (Fig.) and neutralizing antibodies are present in most of the fish 2 1/2 months post infection (Table).