Showing papers on "Viremia published in 1976"
TL;DR: Observations that HVT protects against productive MDV infection in the thymus and against cell-associated viremia are evidence for an anti-viral immune response and a limited oncogenic (transforming) potential of HVT would provide the basis to assume that at least one component of H VT-induced immunity may be directed against tumor-specific antigens.
Abstract: SUMMARY Chickens vaccinated at hatching with high doses of turkey herpesvirus (HVT) developed viremia that peaked in titer around the 12th day and gradually declined. HVT infection also induced mild microscopic lymphoproliferative lesions in the nerves and gonads. These lesions were most prominent around the 12th day and then regressed. The fact that such lesions were also induced by HVT in cyclophosphamide-treated chicks suggests that they were T-cell-dependent. Some of the cells in early HVT lesions appeared to have morphologic properties of neoplastic cells. HVT viremia and lesions were both dose-dependent and were less in chickens with maternal antibodies against Marek's disease virus (MDV). Sequential studies on chickens vaccinated with HVT and challenged with MDV showed that chickens were protected against the earliest detectable MD viremia and lymphoproliferative lesion response attributed to MD. Also, the transient necrobiotic lesions associated with productive infection of thymic lymphocytes by MDV were totally absent in vaccinated chickens. These data provide further insight on the mechanisms by which HVT protects against MD lymphoma induction. A limited oncogenic (transforming) potential of HVT as suggested by our data would provide the basis to assume that at least one component of HVT-induced immunity may be directed against tumor-specific antigens. On the other hand, our observations that HVT protects against productive MDV infection in the thymus and against cell-associated viremia are evidence for an anti-viral immune response. These hypotheses are not mutually exclusive.
79 citations
TL;DR: There was no evidence for a primary role of humoral or cellular immune responses in the age-dependent resistance of mice to infection with Sindbis virus.
Abstract: One- to eight-week-old mice were studied after subcutaneous inoculation of Sindbis virus. Local replication at the site of inoculation, transient viremia, and invasion of the brain were found in mice of all ages, although the quantities of virus were greater in younger mice. Death occurred in 100% of one-week-old mice, 28% of two-week-old mice, and none of the mice four weeks old or older. Pathologic examination of the brains on day 7 after infection revealed a mononuclear inflammatory infiltrate in all mice, with evidence of necrosis in the youngest. Neutralizing antibody was present by day 3 and reached high titers by day 6 in all age groups. Specific stimulation of cells from the draining lymph node by Sindbis virus antigen was also demonstrable by day 6 in all groups. There was no evidence for a primary role of humoral or cellular immune responses in the age-dependent resistance of mice to infection with Sindbis virus.
76 citations
TL;DR: The humoral immune response to Friend virus leukemia was studied in congenic F1 mice differing in their incidence of recovery from leukemia, and mice of both high and low recovery genotypes produced antibodies in equal titer and recovered from viral infection in spite of striking differences in recovery from leukemic splenomegaly.
Abstract: The humoral immune response to Friend virus leukemia was studied in congenic F1 mice differing in their incidence of recovery from leukemia. Antiviral neutralizing antibodies rose in titer in vivo concurrently with disappearance of viremia and fall in spleen virus levels. Cytotoxic antileukemia cell antibodies also appeared at this time. Passive transfer of these antibodies could inactivate low numbers of leukemia cells in vivo; however, mice of both high and low recovery genotypes produced antibodies in equal titer and recovered from viral infection in spite of striking differences in recovery from leukemic splenomegaly. Mice lacking C57BL genes did not produce antibodies or recover from viremia except in rare instances. Recovery from splenomegaly was found to be influenced by three or more C57BL genes independent of the H-2 complex.
75 citations
TL;DR: Peristence of virus in both brain and kidney is demonstrated late in this infection, and the development of neutralizing and hemagglutination-inhibiting antibodies in serum correlates with the clearance of virus from most systemic sites.
Abstract: Neuroadapted mumps virus produces systemic infection in newborn hamsters after intraperitoneal inoculation. Virus is disseminated via a low-level viremia and appears to enter the central nervous system by passage through the choroid plexus. At such sites, choroidal and ependymal epithelial cells are productively infected and become a source for further viral spread throughout the brain parenchyma. The development of neutralizing and hemagglutination-inhibiting antibodies in serum correlates with the clearance of virus from most systemic sites. However, persistence of virus in both brain and kidney is demonstrated late in this infection.
64 citations
TL;DR: In this paper, the recovery of herpes simplex virus (HSV) Type 1 from the blood buffy coat of four adults is reported for the first time, all of the patients had vesicular stomatitis and facial vesicles; two also had either keratoconjunctivitis or disseminated skin lesions.
Abstract: Recovery of herpes simplex virus (HSV) Type 1 from the blood buffy coat of four adults is reported for the first time. All of the patients had vesicular stomatitis and facial vesicles; two also had either keratoconjunctivitis or disseminated skin lesions. The infection was not the primary one with HSV in any of them. Two of three patients who had renal failure were receiving immunosuppressive drugs; one patient was normal except for alcoholism and diabetes. None developed signs of visceral organ infection and all recovered within 2 to 4 weeks. The findings demonstrate the occurrence of heretofore unrecognized nonfatal HSV Type 1 viremia in both healthy and immunosuppressed leukocytes, can occur regardless of the presence of serum antibody, and may or may not be associated with the disseminated lesions.
59 citations
TL;DR: The results of these tests suggest that serologically the three serum viruses were similar to one another, but that the fecal virus was distinct.
Abstract: Parvovirus-like particles found in the sera of two blood donors had the size and appearance on electron microscopy of a virus (B19) found in the serum of a blood donor by Cossart et al. (1975), and those of a virus found in the feces of a normal subject. Antibody to these viruses was detected by immune electron microscopy and immunoelectro-osmophoresis in the sera of 50 children aged 10 to 15 years. Of these, 36% had antibody to the fecal virus, 36% had antibody to B19, and 54% had antibody to the two other serum viruses. The results of these tests suggest that serologically the three serum viruses were similar to one another, but that the fecal virus was distinct. The two blood donors had nonspecific symptoms at the time of viremia. Both donors had developed immunoglobulin M antibody to the virus when tested 3.5 and 4.5 weeks later, but no viruses were detected in the feces or urine.
54 citations
TL;DR: Human leukocyte interferon was injected into nine patients with cytomegalovirus infections; four of these patients were congenitally infected, and five had acquired infections.
Abstract: Human leukocyte interferon was injected into nine patients with cytomegalovirus infections; four of these patients were congenitally infected, and five had acquired infections. In three patients viruria was completely inhibited. In five patients viral excretion in the urine was only transiently inhibited. Viremia was not significantly suppressed. The lymphocyte response to phytohemagglutinin was suppressed in two patients.
48 citations
TL;DR: The prolonged urinary excretion of large amounts of lymphocytic choriomeningitis virus by asymptomatic, chronically infected hamsters is an important public health consideration when dealing with potential human infection.
Abstract: The pathogenesis of lymphocytic choriomeningitis virus infection in fetal, newborn, and young adult hamsters was studied. Infected newborn hamsters initially developed a persistent viremia and viruria with titers often in excess of 10(4.0) mean infectious doses/0.03 ml of blood or urine. After week 12 two different patterns of infection became evident. Approximately one-half of the hamsters eventually cleared the infection, whereas the others developed a chronic progressive and ultimalely fatal disease characterized by continuous high-titered viremia and viruria and high titers of virus in their tissues. Complement-fixing antibody and, to a lesser degree, virus-neutralizing antibody coexisted with the viremia. Hamsters with persistently high levels of viremia and viruria developed chronic glomerulonephritis and widespread vasculitis, whereas hamsters that cleared their infections did not develop these lesions. Litters of hamsters born to viremic mothers were invariably infected. Litter sizes were small and breeding effectiveness was reduce; however, vertical, congenital infection was successfully passed through three generations. The course of infection in the congenitally infected hamsters was similar to that in newborn infected hamsters, with all animals producing complement-fixing antibody, some animals being capable of clearing the viremia and remaining healthy, and other animals having persistent viremia and fatal disease. Inoculated young adult hamsters did not become diseased, developed viremia and viruria which persisted up to 3 and 6 months, respectively, and developed complement-fixing antibody by 10 days after infection. The prolonged urinary excretion of large amounts of lymphocytic choriomeningitis virus by asymptomatic, chronically infected hamsters is an important public health consideration when dealing with potential human infection.
38 citations
Journal Article•
TL;DR: Specific pathogen-free cats were immunized with an inactivated feline oncornavirus tumor cell vaccine and were protected from oncogenic feline sarcoma virus challenge, but immunization did not produce virus-neutralizing antibody nor did it prevent viremia.
Abstract: Specific pathogen-free cats were immunized with an inactivated feline oncornavirus tumor cell vaccine. Immunized cats produced high antibody titers to the feline oncornavirus-associated cell membrane antigen and were protected from oncogenic feline sarcoma virus challenge. However, immunization did not produce virus-neutralizing antibody nor did it prevent viremia.
30 citations
Journal Article•
TL;DR: An essential role for humoral passive antibody, but not for cellular immunity, is suggested in protection from primary systemic bovine viral diarrhea virus infection in calves.
Abstract: A series of investigations was designed to study the role of cellular immunity and passive antibody in protecting neonatal calves from primary bovine viral diarrhea virus infection. Administration of corticosteroids (dexamethasone) in doses capable of suppressing cellular immunity markedly potentiated systemic bovine viral diarrhea virus infection in calves which lacked bovine viral diarrhea passive neutralizing antibody. Immunosuppressed calves did not form neutralizing antibody to bovine viral diarrhea virus and developed a fatal viremia. Calves with high levels of passive bovine viral diarrhea neutralizing antibodies were protected from the effect of corticosteroids. The results suggest an essential role for humoral passive antibody, but not for cellular immunity, in protection from primary systemic bovine viral diarrhea virus infection in calves.
28 citations
TL;DR: The results suggest an association between HVT viremia and protection against MD development in chickens experiencing "vaccine breaks" following vaccination with HVT vaccine against MD.
Abstract: Viremia with turkey herpesvirus (HVT) and/or Marek's disease (MD) herpesvirus (MDHV) was examined in chickens from three different commercial flocks experiencing "vaccine breaks" following vaccination with HVT vaccine against MD. In all groups of sample chickens from the flocks, the incidence of detectable HVT viremia was significantly less in the MD-affected than in the healthy penmates, and incidence of MD was significantly higher in the birds without detectable HVT viremia than in the viremic penmates. The results suggest an association between HVT viremia and protection against MD development.
TL;DR: The pathogenesis of experimental vaccinia virus infection in weanling mice after intracerebral inoculation was followed with virological, histological, and immunohistological methods and rise of neutralizing antibody correlated with disappearance of cell-free virus in blood, brain, and viscera.
Abstract: The pathogenesis of experimental vaccinia virus infection in weanling mice after intracerebral inoculation was followed with virological, histological, and immunohistological methods. High-dose inoculation, virus spread from brain to thoracic and abdominal viscera probably by an undetected early viremia. Virus did rise to detectable levels in blood by day 5 and was found to be associated with the mononuclear cell fraction. By day 12, 30% of the animals had died and no further deaths occurred. Rise of neutralizing antibody correlated with disappearance of cell-free virus in blood, brain, and viscera. Virus was present in the brains of animals for 20 days after inoculation. This animal model may be useful to study mechanisms of persistent central nervous system virus disease relevant to man.
TL;DR: By virus neutralization and cytotoxicity tests and by immunoelectron microscopy, antibodies against virus and cell-surface antigens of transplanted AKR leukemia were not detectable in sera of nonleukemic mice of any group.
Abstract: An inactivated and lyophilized preparation of a low virulence strain (Su) of Streptococcus pyogenes (group A) was designated OK-432. When 2- and 5-month-old AKR mice were inoculated im with OK-432 twice weekly throughout their life-spans, spontaneous leukemias occurred later and at a lower incidence than in control groups. By virus neutralization and cytotoxicity tests and by immunoelectron microscopy, antibodies against virus and cell-surface antigens of transplanted AKR leukemia were not detectable in sera of nonleukemic mice of any group. Whereas sera from mice treated with OK-432 were the only positive for interferon, viremia was clearly demonstrated in control groups by reverse transcriptase assays of the plasma.
TL;DR: Two contrasting immunological phenomena are examined as contributing factors responsible for the enhancement by this virus of asparaginase (EC 3.5.1.1; L-asparagine amidolydrolase) therapy against leukemia in mice, and for the alteration of the susceptibility of mice to various neoplastic processes.
Abstract: Spleen antibody-forming cells of mice yield a 3- to 10-fold increase in their response to sheep erythrocyte antigen if they are acutely infected by lactate dehydrogenase-elevating virus. This early stimulation is replaced by a long-term inhibition of the antibody-forming cells as the viremia goes into its persisting chronic stage. These contrasting immunological phenomena are examined as contributing factors responsible for the enhancement by this virus of asparaginase (EC 3.5.1.1; L-asparagine amidolydrolase) therapy against leukemia in mice, and for the alteration of the susceptibility of mice to various neoplastic processes.