Showing papers on "Viremia published in 1979"

Controlled clinical trial of prophylactic human-leukocyte interferon in renal transplantation. Effects on cytomegalovirus and herpes simplex virus infections.

Abstract: A double-blind, placebo-controlled trial of interferon prophylaxis against viral infections was conducted in renal-transplant recipients receiving standard immunosuppressive therapy with or without antithymocyte globulin. Interferon was administered for six weeks, beginning on the day of transplantation. Cytomegalovirus excretion began earlier and viremia was more frequent in placebo-treated than in interferon-treated patients. Cytomegalovirus viremia correlated with clinical syndromes and was more frequent in recipients of antithymocyte globulin. In contrast, neither interferon nor antithymocyte globulin altered excretion of herpes simplex virus. Reversible leukopenia and thrombocytopenia occurred in seven interferon recipients. Patient and graft survival were comparable in interferon and placebo groups. These preliminary results suggest that a six-week course of prophylactic interferon delays shedding of cytomegalovirus and decreases the incidence of viremia after transplantation. In contrast, ...

Identification of a non-H-2 gene (Rfv-3) influencing recovery from viremia and leukemia induced by Friend virus complex.

Abstract: The dominant C57BL/10 allele of a single autosomal, non-H-2 gene (Rfv-3) was found to be required for recovery from viremia and leukemia induced by Friend virus complex in H-2b/b mice. In H-2a/a mice, the Rfv-3 gene apparently influenced recovery from viremia in the presence of persistent leukemia because these mice lacked the appropriate H-2 genotype for recovery from leukemia. The Rfv-3 gene was distinct from the Fv-2 gene because recovery from viremia was seen in recombinant-inbred mice with the Fv-2s/s genotype. Furthermore, backcross studies indicated that Rfv-3 and Fv-2 were not linked. The Rfv-3 gene may act by influencing the specific anti-FV humoral antibody response.

Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production.

Abstract: A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies. 30--90 d after FV infection leukemic spleen cells from (B10.A X A)F1 and (B10.A X A.BY)F1 mice (Rfv-3r/s) were found to have low FV-induced cell-surface antigen expression compared to leukemic spleen cells from A and A.BY mice (Rfv-3s/s). In addition, these F1 mice recovered from viremia and generated cytotoxic anti-FV antibodies. A and A.BY mice did not recover from viremia and failed to generate anti-FV antibodies. Anti-FV leukemia cell antibody appeared to mediate FV-antigen loss because decrease of FV cell-surface antigens occurred at the same time as anti-FV antibody appeared in the plasma of F1 mice, and passive transfer of anti-FV antisera induced modulation of FV cell-surface antigens. Rfv-3 did not influence an intrinsic ability of FV antigens to be modulated from Rfv-3s/s leukemia cells because FV antigen loss from Rfv-3s/s spleen cells occurred after transfer of cells to an immune environment.

Pathogenesis of reactivated latent murine cytomegalovirus infection.

Abstract: Sixteen weeks after inoculation, murine cytomegalovirus (MCMV) can no longer be detected in the tissues of mice. However, a 2-week course of immunosuppression with antilymphocyte serum and cortisone acetate results in reactivation and dissemination of the latent virus in all animals. In this study of reactivation, MCMV was first detected in the liver, usually during the first week of immunosuppression, and virus replication was shown to be restricted to hepatocytes. Subsequently, a viremia occurred, with spread of infection to other organs. The highest titers of virus were reached in salivary glands in which replication occurred in serous acinar cells. In the lung, virus-specific abnormalities were difficult to detect because of superimposed bacterial and fungal infections. However, interstitial pneumonitis could be produced when cortisone acetate was deleted from the immunosuppressive regimen. Although the site of virus latency has not been defined, this model system will be useful for study of reactivation of latent cytomegalovirus infection.

Antibody-induced modulation of Friend virus cell surface antigens decreases virus production by persistent erythroleukemia cells: influence of the Rfv-3 gene.

Abstract: The Rfv-3 gene was found to influence the level of Friend leukemia virus production in spleens of leukemic mice later than 30 days after virus inoculation. Rfv-3r/s mice [(B10.A X A)F1 and (B10.A X A.BY)F1] had decreased spleen virus levels 30-90 days after virus inoculation compared to Rfv-3s/s mice [A.BY, A, BALB.B, and (BALB/c X A)F1)]. In (B10.A X A)F1 X A backcross mice the spleen virus titer segregated with the level of viremia. The Rfv-3 gene appeared to act by controlling anti-Friend virus antibody production. The interaction of antiviral antibody with infected cells led to a decrease in release of infectious virus by late leukemic spleen cells in Rfv-3r/s mice to 1/300th that in Rfv-3s/s mice. This decrease in virus release appeared to be due to interference with the virus budding process due to antibody-mediated modulation of virus-induced cell surface antigens.

Ribavirin Treatment of Toga-, Arena- and Bunyavirus Infections in Subhuman Primates and Other Laboratory Animal Species

Abstract: : Ribavirin was effective in reducing viremia and increasing the number of survivors compared to untreated monkeys infected with Rift Valley fever (a bunyavirus), Lassa or Machupo (both arenaviruses) viruses. Treatment was effective when given initially at the time of virus inoculation or later, after the onset of viremia and fever. Only minimal effect was evident against yellow fever virus (a flavivirus) infection in rhesus monkeys, even when treatment was initiated within 8 hours after virus inoculation. Ribavirin was ineffective against Chikungunya virus (an alphavirus) infection of monkeys. The apparent inability of ribavirin to achieve effective concentrations in the central nervous system may limit its usefulness against viruses causing primary encephalitis.

Genetic Control of Sensitivity to Moloney Leukemia Virus in Mice II. Mapping of Three Resistant Genes Within the H-2 Complex

Abstract: The level of viremia and the appearance of leukemias were studied after inoculation wtih Moloney leukemia virus (M-MuLV) in different H-2 congenic strains of mice. The viremia was regularly measured on individual mice with a radioimmunoassay of the major internal virion component p30. Three genes within the major histocompatibility complex controlled the level of circulating virus. Two of them, called Rmv.1 and Rmv.2, appear to be located in the I region, respectively, in the IA, and the IC-S or G regions. The third gene, Rmv.3, was mapped to the D end of the complex in the D or T region. Crosses between resistant and sensitive strans demonstrated that the H-2 associated resistance was inherited as a dominant or semi-dominant Mendelian trait. Rmv.1, Rmv.2, and Rmv.3 were shown to complement for resistance in trans when the hybrids between sensitive strains were examined. A good correlation was found between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. Nevertheless, additional non-H-2 genes must control viremia and/or the appearance of leukemia since, despite high levels of viremia, some sensitive strains do not become leukemic.

Pathogenesis of K virus infection in newborn mice.

Abstract: Newborn mice were inoculated with a murine papovavirus, K virus, by intracranial, intraperitoneal, oral, and intranasal routes, and the pathogenesis of infection was studied with immunofluorescence, virus assay, and histopathology. Inoculation by each route produced a fatal interstitial pneumonia. Pulmonary vascular endothelium and, to a lesser extent, cells lining hepatic sinusoids were the major sites of viral replication, but intranuclear antigen or inclusions or both were also found in extrapulmonary vascular endothelia, spleens, lymph nodes, and brains. Although K virus produced a predominantly respiratory illness, the virus was less infectious by intranasal than by oral inoculation and did not replicate in respiratory epithelial tissues. The earliest site of K virus replication was the jejunal submucosa, suggesting that in nature K virus may be transmitted by the oral route. Viral antigen was present in brains of animals inoculated by each route and correlated with the duration of viremia. Despite the presence of abundant viral antigen, however, the nervous system remained morphologically normal. The present study indicates that a member of the papovavirus group may produce clinically silent, noninflammatory involvement of the central nervous system during the initial infection of its natural host.

Characteristics of infection of b and t lymphocytes from mice after inoculation with cytomegalovirus.

Abstract: Viremia was produced by inoculating intravenously BALB/c mice with murine cytomegalovirus. Virus was detected in plasma and granulocytes only during the first 8 days after infection. Lymphocyte-associated viremia, detectable by cocultivation on syngeneic or allogeneic fibroblasts, persisted for at least 4 weeks. Eight to 10 days after infection, sonicated lymphocytes had no demonstrable free virus. When whole lymphocytes with no demonstrable free virus were enclosed in a Millipore chamber and placed on a fibroblastic feeder layer, T cells produced free virus but B cells did not. Compared to normal calf serum, specific hyperimmune serum reduced B cell-associated infectious centers by 74% and T cell-associated infectious centers by only 38%. Normal mouse sera reduced by 36% and 30% infectious center production by B cells and T cells, respectively. Lymphocytes enriched with Fc receptor-positive cells produced significantly more infectious centers than receptor-negative cells.

Mechanisms of C-Type Viral Leukemogenesis: I. Correlation of in Vitro Lymphocyte Blastogenesis to Viremia and Leukemia

Abstract: Various inbred strains of mice respond immunologically to genetically transmitted ecotropic C-type viruses. Part of this response is T cell blastogenesis with type specificity for the viral envelope glycoprotein gp71. Of those nonviremic, nonleukemic strains, and F1 crosses examined, in which virus expression occurs early in life, gp71-specific blastogenic T cells were detected within the first 2 months of age and temporally preceded the development of a humoral immune response. However, in the viremic, highly leukemic strain of AKR mice, gp71-specific T cell blastogenesis in vitro was readily detectable throughout the preleukemic phase, the first 5 months of age. In appropriate F1 crosses and backcrosses, the persistent in vitro blastogenic response segregated with viremia and leukemia. These data suggest that in vivo T cell stimulation by endogenous viral gp71, caused by viremia, may contribute to virus-induced leukemogenesis in mice.

Differences between Syrian Hamster Strains in Natural Killer Cell Activity Induced by Infection with Pichinde Virus

Abstract: Adult MHA hamsters are susceptible to a fatal Pichinde virus infection and are unable to limit viremia. Adult hamsters of other strains, such as LVG and LSH, limit viremia and do not develop fatal disease. Both survival and the ability to limit viremia are each controlled by a dominant gene. During studies to delineate the role of cytotoxic cells in Pichinde virus infection, it was observed that MHA hamsters exhibited appreciable levels of cytotoxic activity against syngeneic and allogeneic tumor cells and that this activity increased after Pichinde virus infection. In contrast, LSH hamsters showed lower endogenous cytotoxicity and less enhancement after virus infection. The cytotoxicity was primarily mediated by a cell with characteristics of natural killer (NK) cells. The separation of MHA hamster spleen cells by velocity sedimentation revealed that fractions of the gradient containing maximum NK activity also contained numerous infectious centers, whereas the corresponding fractions from gradients of LSH hamster spleen cells showed less cytotoxicity and contained one-tenth the number of infected cells. These observations suggest that a population of cells, defined by NK activity, may be a target for Pichinde virus replication, and that the activity of these cells is only minimally expressed in the resistant LSH strains.

Experimental infection of vertebrates of the Pocomoke Cypress Swamp, Maryland with Keystone and Jamestown Canyon viruses.

Abstract: Experimental studies were conducted to assess the susceptibility of white-tailed deer (Odocoileus virginianus), gray squirrels (Sciurus carolinensis), and cottontail rabbits (Sylvilagus floridanus) to Jamestown Canyon (JC) and/or Keystone (KEY) virus infection. Viremia occurred in 5 of 6 deer inoculated with JC virus; however, all deer developed KEY virus neutralizing antibody. Based on the observation that antibody elicited by primary infection of deer with either KEY or JC virus exhibited partial heterologous neutralization in vitro, cross-challenge experiments were performed in these animals. Keystone virus failed to infect deer 30 days post primary JC virus infection; however, deer became infected when challenged with KEY virus 80 days after the initial JC virus infection as indicated by a substantial increase in antibody titer. Similarly, JC virus failed to produce viremia in immune animals infected with KEY virus 80 days previously, although 2 of the 3 animals challenged had serological evidence of infection. Three field-collected cottontail rabbits with no evidence of KEY antibody were readily susceptible to KEY virus infection and developed viremias of 1-4 days' duration; rabbits with KEY virus antibody did not develop viremia upon KEY virus challenge. Eight antibody-negative field-collected gray squirrels became viremic following injection with KEY virus; however, a comparable group of squirrels did not become viremic when injected with JC virus.

Alterations of the thymus and peripheral lymphoid tissues in fatal measles. A review of 14 autopsy cases.

Abstract: As a result of re-examining 14 autopsy cases of fatal measles, neither aplastic nor hypoplastic thymuses were found even in a case with giant cell pneumonia, but there were degenerative and/or necrotic changes with giant cells mostly in the thymus and less in the peripheral lymphoid organs such as spleen, lymph nodes, Peyer's patches and tonsils. This damage of the lymphoid system was associated with the occurrence of complications, particularly of giant cell pneumonia and encephalitis. The lymphoid cell damage, which might be primarily due to virulence of the infected measles virus, seemed to prolong the viremia. Involvement of viremia in the process of complication is discussed.

Presence of viral particles in the salivary gland of Calomys musculinus infected with Junin virus by a natural route.

Abstract: Calomys musculinus, a wild cricetid rodent, is one of the main reservoirs of Junin virus. Six of these animals were infected by being placed in close contact with animals that had been experimentally infected with the virus. They were sacrificed at 10, 15 and 20 months after contact, and their salivary glands were studied by ultrastructural, immunohistochemical and virological methods. Two animals developed chronic viremia and low titers of complement-fixing antibodies. These animals were the only ones that had high viral titers in salivary glands and blood and viral antigen and particles in salivary glands. Although some of the other animals had viremia at the beginning of the experiment, it was absent 5 months later. Complement-fixing antibodies developed in all animals. On the basis of these findings, we assumed that the salivary gland is an important site of viral synthesis and excretion. This type of chronic infection, with persistent viremia and virus shedding, is possibly important for virus perpetuation in nature and transmission to man.

Infection and immunization of cats with the Kawakami-Theilen strain of feline leukemia virus.

Abstract: SummaryInjection of high doses of KT-FeLV feline leukemia virus produced both viremia and leukemia in a portion of 1- to 2-day-old kittens but not in 17- to 24-week-old animals. Contact of susceptible cats with infected cagemates did not result in viremia or disease. Development of cytotoxic antibody was coordinated with protection against viremia and disease in kittens challenged with FeL V virus. The rapid evolution of resistance to KT-FeLV virus precluded the development of a practical means for conventional vaccination and challenge experiments in cats. Killed vaccine given to pregnant queens did, however, afford protection against FeLV virus on challenge in the progeny.