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Showing papers on "Viremia published in 1981"


Journal ArticleDOI
TL;DR: Data suggest that some naturally occurring strains of dengue virus (endemic strains) are associated with low viremia and generally cause only mild illness in man.
Abstract: An outbreak of dengue type 3 was studied in Central Java, Indonesia, in 1978. In contrast to previous dengue 3 epidemics in Central and East Java, this outbreak was less explosive, associated with mild illness, and low viremia. The dengue virus isolation rate from serologically confirmed patients was only 32% compared to 65% for an epidemic in Bantul a year earlier. Neither dengue hemagglutination-inhibition antibody titers nor day of illness on which specimens were collected accounted for this difference. These data suggest that some naturally occurring strains of dengue virus (endemic strains) are associated with low viremia and generally cause only mild illness in man.

118 citations



Journal ArticleDOI
TL;DR: The ability of ndREVs to induce tolerant and non-tolerant infection, virus- and antigen-shedding into eggs, and chronic neoplastic disease resembled that of lymphoid leukosis virus, another common avian retrovirus.
Abstract: SUMMARY Chickens inoculated as embryos with non-defective reticuloendotheliosis viruses (ndREVs) generally developed a "tolerant" infection characterized by lack of immunofluorescent antibody and by a viremia that persisted through 93 weeks. Chickens inoculated at hatching generally developed a "non-tolerant" infection characterized by antibody development that gradually waned as the chickens aged and by a transient or intermittent viremia. Although chickens tolerantly infected with ndREV strain T were immunodepressed, tolerance to ndREVs did not depend on immunodepression, because 17-to-20-week-old chickens tolerantly infected with ndREV strain CS were normal in antibody response to sheep red blood cells and Brucella abortus and in mitogen-stimulated blastogenesis of blood lymphocytes. Tolerantly infected dams shed low levels of gs antigen and virus into eggs at high frequencies; however, in two trials, congenital transmission of virus by strain-CS-infected dams was documented in only 2 of 42 and 1 of 132 progeny chicks. Eggs and progeny chicks from non-tolerantly infected dams were always negative for virus and gs antigen. After long latent periods (17 to 93 weeks), ndREV-infected chickens developed lymphomas involving the bursa of Fabricius and other visceral organs at high frequency and developed sarcomas, carcinomas, and inflammatory nerve lesions at a lower frequency. The ability of ndREVs to induce tolerant and non-tolerant infection, virus- and antigen-shedding into eggs, and chronic neoplastic disease resembled that of lymphoid leukosis virus, another common avian retrovirus. Certain differences in epidemiological properties of these 2 viruses are discussed.

73 citations


Journal ArticleDOI
TL;DR: Six male volunteers were inoculated subcutaneously with a live, attenuated dengue-2 virus (PR-159/S-1) candidate vaccine and the vaccine virus genetically stable and immunogenic and seemed sufficiently attenuated for additional testing in humans.
Abstract: Six male volunteers, previously immunized with yellow fever vaccine, were inoculated subcutaneously with a live, attenuated dengue-2 virus (PR-159/S-1) candidate vaccine. Five recipients developed viremia 8 or 9 days after vaccination, which lasted 1 to 10 days. The onset of viremia was followed by fever in three people, transient leukopenia in four, and an erythematous rash in one. One volunteer developed an oral temperature of 38.8 degrees C with headache, myalgia, fatigue, and photophobia suggestive of mild dengue fever. All five viremic volunteers developed fourfold or greater rises in serum neutralizing antibody. The sixth volunteer, who had a low titer of preexisting dengue-2 neutralizing antibody, had no viremia, no symptoms, and a modest rise in hemagglutination inhibiting antibody. Virus isolates obtained from plasma retained the small-plaque and temperature-sensitive growth characteristics of the vaccine virus in vitro. In this study, the vaccine virus genetically stable and immunogenic and seemed sufficiently attenuated for additional testing in humans.

57 citations


Journal ArticleDOI
01 Sep 1981-Virology
TL;DR: The suppression of virus spread by antibody seems to be important for immunoprevention of this virus-induced leukemia.

57 citations


Journal ArticleDOI
TL;DR: It is indicated that measles virus may cause immunosuppression in the absence of detectable virus replication in mononuclear cells.

39 citations


Journal Article
TL;DR: During a 12-month period 80 children greater than 3 months of age seen at an emergency room with acute fevers greater than or equal to 39.7 C (103.5 F) and no localizing signs of infection were studied using blood and buffy coat cultures to isolate bacteria and viruses.
Abstract: During a 12-month period 80 children greater than 3 months of age seen at an emergency room with acute fevers greater than or equal to 39.7 C (103.5 F) and no localizing signs of infection were studied using blood and buffy coat cultures to isolate bacteria and viruses. Bacteremia was identified in three children (3.8%): two with Streptococcus pneumoniae and one with Neisseria meningitidis. Two children with viremia were identified: both isolates were ECHO virus, types 11 and 21, respectively. Fifty-eight of the study children (72%) were seen again in 24 to 48 hours and 27/58 (46%) were afebrile and completely well. No differences in sex, age, or initial WBC count existed among these children who returned afebrile and well and those with either localized disease or those persistently febrile.

32 citations


Journal ArticleDOI
TL;DR: The data demonstrate that the number of responsive lymphocytes is increased 30- to 100-fold in preleukemic mice and that such increases are dependent upon the induction of an immune response in viremic mice.
Abstract: In various mouse strains, inoculation with Moloney leukemia virus results in the establishment of an acute viremia which in most cases is followed by the induction of leukemia. Also associated with the viremia is the development of a chronic cellular immune response detectable in vitro by the ability of viral proteins to induce splenic lymphocyte proliferation. Previous studies have demonstrated that, in the absence of this cellular immune response, leukemia does not develop irrespective of whether viremia is present [Lee, J. C. & Ihle, J. N. (1981) Nature (London) 289, 407-409]. In vitro proliferative responses to antigens involve the nonspecific response of various subpopulations of lymphocytes to lymphokines produced by antigen-specific Thy 1+, Lyt 1+,2- lymphocytes. The studies presented here concern the effects of a chronic immune response in viremic mice on the frequency of lymphocytes capable of responding to lymphokines in vitro. The data demonstrate that the number of responsive lymphocytes is increased 30- to 100-fold in preleukemic mice and that such increases are dependent upon the induction of an immune response in viremic mice. The role of this altered immune response in leukemia is discussed.

26 citations



Journal ArticleDOI
TL;DR: Following intraperitoneal inoculation of measles (HBS) virus into newborn hamsters widespread but variable productive lymphoid tissue infection was detected by a sensitive viral isolation technique, and infection was thought to be macrophage-associated.

8 citations


Book ChapterDOI
TL;DR: The pathogenesis and mechanisms of virus persistency vary widely according to the type of model considered, andDiminution of the effectiveness of T cell-mediated responses, for example during immunosuppressive therapy, allows reactivation of the infection.
Abstract: Typical virus infections are short in incubation, acute in course, and rapid in their progress to either death or recovery. Some viruses, however, are able to escape host defense mechanisms and persist for long periods of time, often indefinitely. The pathogenesis and mechanisms of virus persistency vary widely according to the type of model considered. With scrapie, mink encephalopathy, kuru and Creutzfeld-Jacob disease, the infection elicits no inflammatory response. Apparently, immunological factors neither control nor complicate the disease. In other models, the virus persists in the face of an active host immune response. Two situations may be distinguished: the virus may be actively replicated by host cells, and viremia persists until the death of the host. This is true, for example, of lactic dehy-drogenase virus infection, Aleutian mink disease or equine infectious anemia. In these cases the virus circulates as infective immune complexes made of virus particles and specific antibody. Alternatively, like in herpes simplex and varicella-zoster infection, the virus remains latent and able to persist in cells of the nervous system. A permanent cell-mediated immune control is exerted on these infected cells, so that the virus is not actively replicated. Diminution of the effectiveness of T cell-mediated responses, for example during immunosuppressive therapy, allows reactivation of the infection.

Journal Article
TL;DR: A fatal adult respiratory distress syndrome occurred in a 15-month-old child who had suffered minor scalding during the febrile response to combined attenuated virus immunization (measles, mumps and rubella [MMR].
Abstract: A fatal adult respiratory distress syndrome (ARDS) occurred in a 15-month-old child who had suffered minor scalding during the febrile response to combined attenuated virus immunization (measles, mumps and rubella [MMR]). Despite vigorous efforts the child died 26 days after the accident. It is suggested that the scalding suppressed the normal immune response to the viremia and that the latter (i.e. most likely the measles viremia) caused the lung damage which, in turn, led to the ARDS. Histologically the lung presented a peculiar change with fibroblastic nodules, vessel wall inflammation and signs as observed in ARDS.


Journal Article
TL;DR: It can be concluded that Moloney virus-induced leukemia is a multistep process, viral production being necessary but not sufficient in and of itself to induce a malignant transformation.
Abstract: The incidence of leukemias was established in mice of different inbred strains inoculated with Moloney leukemia virus (M-MuLV), and a complex genetic control was found. To characterize the different steps of the host-virus relationship further, the degree of viremia, the appearance of leukemia, organ involvement, and the surface phenotype of leukemic cells were studied in individual mice. The results demonstrate that: a) The viremia was controlled by H-2 and non-H-2 genes. Three H-2 genes located in the I and D or T region of the MHC behave like immune-response genes controlling the specific antiviral immune response. Other gene(s) mapped outside the complex also affected the virus production. Both sets of genes influenced leukemia incidence, since leukemias were observed only in highly viremic strains. b) Additional non-H-2 genes, which were not involved in viremia control, were determinants in the induction of malignancies because some sensitive strains do not become leukemic despite high levels of viremia. c) The anatomical type of Moloney virus-induced leukemias varied according to the non-H-2 background. Most of the leukemias arising in B10 congeneic mice involved the thymus and were frequently limited to this organ, whereas BALB mice preferentially developed splenic leukemias. d) In a given inbred strain, the leukemias arising in different animals frequently expressed different phenotypes. It can be concluded that Moloney virus-induced leukemia is a multistep process, viral production being necessary but not sufficient in and of itself to induce a malignant transformation.


Journal ArticleDOI
TL;DR: These studies suggest that, in addition to physical removal of virus by the RES, inactivation of virus in the blood serum stream plays an important role in limiting viremia during infections with Sindbis virus.