Showing papers on "Virus published in 1974"
TL;DR: The results suggest that the lack of hemagglutinating activity of mutant virus grown at 39.5° is a consequence of the formation of aggregates of virus particles carrying neuraminic acid on their surface, and that the ts defect is in the neuraminidase but not the hemagGLutinin molecule.
810 citations
TL;DR: The human origin of the virus strains was confirmed by the reisolation from the original clinical specimens and the demonstration of increases in neutralizing antibody in patients from whom virus was isolated, and cross-neutralization and immunodiffusion tests indicated that the virus was distinct from the currently recognized enteroviruses of man.
Abstract: An apparently new enterovirus was isolated in California from more than 20 patients with central nervous system (CNS) disease during the past four years; one strain was isolated from the brain of a fatal case of encephalitis. The representative BrCr strain had the physicochemical properties of an enterovirus. The human origin of the virus strains was confirmed by the reisolation from the original clinical specimens and the demonstration of increases in neutralizing antibody in patients from whom virus was isolated. Cross-neutralization and immunodiffusion tests indicated that the virus was distinct from the currently recognized enteroviruses of man. A few strains in the group were weakly pathogenic in suckling mice and produced symptoms similar to those produced by group A coxsackieviruses. A number of the strains required treatment with sodium deoxycholate to disaggregate the virus before neutralization could be demonstrated with homologous antiserum.
739 citations
TL;DR: The results suggest that it is possible to prepare a live varicella vaccine which may be safely and effectively used for high-risk children as well as normal children.
663 citations
TL;DR: Persistence of the viral DNA from preimplantation stages to adult life may provide a new tool for experimental investigation of vertical transmission and expression of tumor viruses.
Abstract: Explanted mouse blastocysts were microinjected in the blastocoel cavity with simian virus 40 (SV40) viral DNA. After surgical transfer to the uteri of pseudopregnant surrogate mothers, approximately 40% of the blastocysts developed to term and became healthy adults without apparent tumors at 1 year of age. Molecular hybridization tests for the presence of SV40-specific DNA sequences were conducted on DNA extracted from various organs of these animals. Between 0.5 and 13 SV40 genome equivalents per diploid mouse DNA value were found in some organs of approximately 40% of the adult survivors; this represents a substantial augmentation of the amount administered per embryo. The results are consistent with the working hypothesis that the SV40 DNA may have been integrated into the host genome; alternatively, the viral DNA may have replicated as an extrachromosomal entity or by lytic infection in a few permissive cells. Persistence of the viral DNA from preimplantation stages to adult life may thus provide a new tool for experimental investigation of vertical transmission and expression of tumor viruses.
406 citations
TL;DR: It is suggested that a large proportion of long-incubation post-transfusion hepatitis is unrelated to hepatitis B and that control of post- transfusion hepatitis will require identification of a hepatitis virus(es) type C.
384 citations
TL;DR: It is concluded that the Epstein-Barr virus DNA found in biopsies of human nasopharyngeal carcinomas is localized in the neoplastic cells.
Abstract: A well-differentiated squamous cell carcinoma and three poorly differentiated carcinomas of the nasopharynx were analyzed for the presence of Epstein-Barr virus DNA by hybridization with radioactive complementary RNA. The well-differentiated carcinoma contained no detectable Epstein-Barr virus DNA, whereas the three anaplastic carcinomas contained 41, 16, and 14 viral genome equivalents per cell. The anaplastic carcinomas were heavily infiltrated with lymphocytes and other non-neoplastic cells. All four tumors were successfully passaged in nude (thymusless) mice. Mouse cell admixture in the heterotransplanted tumors was estimated by analysis of glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and varied between 25% and 80%. After two passages in nude mice, the carcinoma that was negative for Epstein-Barr virus DNA remained negative, while the three anaplastic carcinomas retained their viral DNA. After correction for mouse cell admixture, the latter tumors were found to contain about 80, 55, and 160 Epstein-Barr virus genome equivalents per human cell. The virus-determined nuclear antigen was localized in the large carcinoma cell clusters in all three mouse-passaged tumors positive for the viral DNA, but other virus-determined antigens were not detected, indicating the absence of virus induction. In contrast to the original tumor biopsies, the nude-mouse-passaged tumors showed virtually no lymphocytic infiltration. It is concluded that the Epstein-Barr virus DNA found in biopsies of human nasopharyngeal carcinomas is localized in the neoplastic cells.
334 citations
312 citations
TL;DR: Three exceptional cell lines have been tested for the presence of the Epstein-Barr virus genome by nucleic acid hybridization (complementary RNA) and virus-determined nuclear antigen tests and two clearly had characteristics of B-cells (bone-marrow-derived).
Abstract: Three exceptional cell lines have been tested for the presence of the Epstein-Barr virus genome by nucleic acid hybridization (complementary RNA·DNA) and Epstein-Barr virus-determined nuclear antigen tests. Two lines were derived from Swedish lymphoma cases and one from an African Burkitt-like lymphoma biopsy that was negative for Epstein-Barr virus DNA and the virus-determined nuclear antigen. All three lines apparently lacked the viral genome. Two of the three lines clearly had characteristics of B-cells (bone-marrow-derived).
303 citations
Journal Article•
TL;DR: Administration of ATS greatly suppressed the production of inflammation and tissue injury in infected hearts of CD-1 mice and T cell deprivation protected BALB/c mice against lethal infection, implying that antiviral antibody synthesis during the 1st week of infection was not T cell dependent.
Abstract: Coxsackie virus B 3 , inoculated i.p., replicated to high titer in the hearts of adult CD-1 and BALB/c mice but virus growth was completely suppressed 6 to 8 days after infection. On day 6 histologic examination showed that the hearts were infiltrated with mononuclear inflammatory cells which surrounded foci of necrotic myofibers. CD-1 animals survived the infection but most BALB/c mice died 8 to 14 days after virus challenge. CD-1 mice pretreated with rabbit anti-thymocyte serum (ATS) and T lymphocyte-deprived BALB/c mice (thymectomized, lethally irradiated, and bone marrow reconstituted) exhibited no reduction in their capacity to terminate viral replication suggesting that the development of effective anti-Coxsackie viral resistance occurred independently of T cell function. In addition, evidence was obtained implying that antiviral antibody synthesis during the 1st week of infection was not T cell dependent. However, observations in ATS-treated mice suggested that at later intervals T cells were required for optimal serum antibody production. T cell dependent reactions were also found to play an important role in the pathogenesis of the heart disease induced by the virus. Thus administration of ATS greatly suppressed the production of inflammation and tissue injury in infected hearts of CD-1 mice. Similarly, T cell deprivation protected BALB/c mice against lethal infection. Moreover, the degree of cardiac inflammation and necrosis in virus-infected T cell-deprived BALB/c mice was significantly less than that found after infection of both intact mice and thymectomized irradiated mice which had been reconstituted with both bone marrow and thymus cells.
297 citations
TL;DR: 2-Deoxy-2,3-dehydro-N-trifluoroacetylneuraminic acid inhibits hemagglutination by NDV and SV5 but does not inhibit agglutination of red cells by Sendai virus or influenza A and B viruses.
285 citations
TL;DR: Genetical and biochemical evidence indicates that herpes simplex virus (types 1 and 2) specifies a unique kinase activity which is able to phosphorylate both thymidine and deoxycytidine, which is indispensable for virus growth in serum starved cells but not important for virus replication in actively growing culture cells.
Abstract: Summary
Genetical and biochemical evidence indicates that herpes simplex virus (types 1 and 2) specifies a unique kinase activity which is able to phosphorylate both thymidine and deoxycytidine. Pseudorabies virus specifies an enzyme which has only thymidine kinase activity and so does vaccinia virus, while equine abortion virus does not induce either activity.
It is shown that the HSV specified deoxypyrimidine kinase is indispensable for virus growth in serum starved cells but not important for virus replication in actively growing culture cells.
TL;DR: A large number of clinical observations have suggested that in the interval between ovaryctomavirus infections in man, the immune defences of the immune system are weakened and mucosal infections are more likely to occur.
Abstract: HERPES simplex virus is well known for its propensity to cause recurrent oral or genital mucosal infections in man. A variety of clinical observations have suggested that in the interval between overt infections, the virus may reside in neural tissue.1 These circumstances include the frequent occurrence of numbness or tingling before the mucosal eruption, the reliable provocation of oral lesions by surgical manipulation of the trigeminal sensory root,2 and the absence of such lesions in areas previously denervated by section of one or more divisions of the trigeminal nerve.3 Recently, the virus has been recovered from trigeminal ganglions of unselected . . .
TL;DR: The reovirus-like particles present in faeces of young children with acute gastroenteritis and the virus causing acute diarrhœa in newborn calves were found to be indistinguishable from each other in size and shape.
TL;DR: In this paper, the authors compared the biologic activities of extracellular Epstein-Barr virus (EB virus) from two laboratory strains, namely, P(3)J-HR-1 (P-H) from Burkitt lymphoma and B95-8 (B95) from infectious mononucleosis, were compared.
Abstract: Biologic activities of extracellular Epstein-Barr virus (EB virus) from two laboratory strains, namely, P(3)J-HR-1 (P-H) from Burkitt lymphoma and B95-8 (B95) from infectious mononucleosis, were compared. Virus stocks from both sources contained approximately the same number of virions. Virus from the P-H line induced "early antigen" in six nonproducer EB virus genome carrier cell lines; virus from B95 did not induce "early antigen." Extracellular virus from B95 regularly caused lymphocytes from human umbilical cords to form continuous lines (immortalization); P-H virus did not cause primary cultures of human lymphocytes to grow continuously. B95 virus stimulated DNA synthesis as determined by rate of incorporation of [(3)H]thymidine into acid-insoluble material; P-H virus did not stimulate DNA synthesis. Pretreatment of lymphocytes with undiluted P-H virus inhibited immortalization and stimulation of DNA synthesis by B95 virus. The inhibitory properties of the P-H virus were sedimented at 100,000 x g and inactivated by heat and UV irradiation; interference by the P-H virus was neutralized by human serum with antibody to EB virus and not by antibody-negative human serum. The hypothesis most consistent with these results is that the P-H virus is defective in gene(s) needed for initiation of immortalization. We speculate that the absence of this gene allows early antigen to be expressed upon super-infection of nonproducer cell lines. The availability of two laboratory strains of EB virus which differ in biologic behavior provides starting material for analysis of the mechanism of lymphocyte immortalization by EB virus and of virus structural differences which affect immortalization.
TL;DR: Human wart virus was isolated from plantar warts and component I was transcribed into radioactive complementary RNA (cRNA) with the aid of Escherichia coli RNA polymerase, and used as a probe for the detection of wart viral DNA in human warts, condylomata acuminata, laryngeal papillomas and some malignant human tumors.
Abstract: Human wart virus was isolated from plantar warts. After extraction of its DNA, component I was transcribed into radioactive complementary RNA (cRNA) with the aid of Escherichia coli RNA polymerase. The resulting cRNA annealed specifically to wart viral DNA and was used as a probe for the detection of wart viral DNA in human warts, condylomata acuminata, laryngeal papillomas and some malignant human tumors. High concentrations of hybridizing DNA were found in plantar warts. Verrucae vulgares annealed to a considerably lower extent only, indicating that very few genome equivalents were present in those papilloma cells. Some verrucae vulgares were found to be completely negative in this test. Condylomata acuminata, as well as laryngeal papillomas and all malignant tumors tested, did not hybridize with wart viral cRNA.
TL;DR: It is concluded that the virus does not really travel along with malignant lymphomas as a passenger in the seropositive patients, and the EBNA antigen test appears a relatively simple way of testing for the presence of the virus genome, provided it is carried out with appropriate controls.
Abstract: Twenty-six of 27 African Burkitt lymphomas with histologically confirmed diagnosis contained relatively large amounts of EBV DNA (10–101 viral genomes per cell), as determined by nucleic acid hybridization. Twenty-five of the 26 EBV DNA-positive lymphomas contained the EBV-determined nuclear antigen, EBNA, in the majority of the nuclei. Technical reasons may have accounted for the apparent EBNA-negativity of one EBV DNA-positive biopsy. Four African lymphoma biopsies, one with a definite diagnosis of Burkitt's lymphoma and three with a questionable diagnosis of the same disease, were all EBV DNA- and EBNA-negative. The same was true for a collection of Swedish cases of Hodgkin's disease, lymphocytic lymphoma, chronic lymphatic leukemia and some other lymphoproliferative malignancies. Thus, there is excellent agreement between the presence of EBV DNA and of EBNA in tumor biopsies. The EBNA antigen test therefore appears a relatively simple way of testing for the presence of the virus genome, provided it is carried out with appropriate controls. Several of the EBV-genome and EBNA-negative cases came from patients with high serum titers of EBV antibodies. It is concluded that the virus does not really travel along with malignant lymphomas as a passenger in the seropositive patients. In comparison with other lymphomas, African Burkitt's lymphoma of the high endemic areas is unique in that the tumors (with rare exceptions) represent the proliferation of an EBV-genome carrying clone. These findings stress the necessity to distinguish between EBV-seropositive status and evidence for EBV-genome-carrying neoplastic cells.
TL;DR: Nucleic acid hybridisation with a 3H-DNA transcript of the viral genome demonstrates that this virus is genetically different from previously studied mammalian C-type viruses, and suggests that M7 is an endogenous baboon virus.
Abstract: A C-type virus (“M7”) has been isolated from a specimen of baboon placenta cocultivated with various mammalian host cell lines. Nucleic acid hybridisation with a 3H-DNA transcript of the viral genome demonstrates that this virus is genetically different from previously studied mammalian C-type viruses, and suggests that M7 is an endogenous baboon virus.
TL;DR: The pathogenesis of immune complex glomerulonephritis in mice is related to the expression of this specific viral envelope glycoprotein and to the host immune response to this protein.
Abstract: The use of monospecific antisera for the analysis by radioimmunoassay and immunofluorescence study of two major viral proteins, gp69/71 and p30 of murine leukemia virus, that could be of significance in the pathogenesis of immune complex glomerulonephritis of mice, particularly NZB and B/WF1 hybrid mice, yielded the following conclusions. A remarkably high concentration of viral envelope glycoprotein, gp69/71, was detected in the spleen and serum of New Zealand mice (NZB, NZW, B/WF1, and W/BF1); the concentration in the spleen was 10-fold greater than that found in AKR mice and 30-fold greater than that present in C57BL/6 mice. The gp69/71 was deposited along with bound immunoglobulins, apparently as an immune complex, in the diseased kidneys of mice, and the glomerular site and extent of deposition of gp69/71 was related to the severity of the glomerulonephritis. This study suggests that the pathogenesis of immune complex glomerulonephritis (and vasculitis) in mice is related to the expression of this specific viral envelope glycoprotein and to the host immune response to this protein.
TL;DR: The nature of the neuropathologic changes suggests that this disease may share pathogenic mechanisms with postinfectious encephalitis of man, and the causative agent is a virus, which thus far appears to be serologically unrelated to other animal viruses.
Abstract: A previously unreported afebrile, infectious leukoencephalomyelitis of oneto four-month-old dairy goats was studied. The disease was characterized by pleocytosis and posterior ataxia that progressed to complete paralysis within two weeks of onset. Dense perivenous accumulations of lymphoreticular cells in white matter and variable myelinoclasis were the essential neuropathologic lesions. These were accompanied by mild interstitial pneumonia and hyperplasia of pulmonary lymphoid tissue. Epizootiologic observations suggest that goats become infected either in utero or immediately after birth. The disease was transmitted to newborn goats by intracerebral and intraperitoneal inoculation of a 220-nm millipore filtrate of nervous tissue from a naturally infected goat. This observation and the failure to isolate bacteria or mycoplasma suggest that the causative agent is a virus, which thus far appears to be serologically unrelated to other animal viruses. The nature of the neuropathologic changes suggests that this disease may share pathogenic mechanisms with postinfectious encephalitis of man.
Book•
01 Jan 1974
TL;DR: A definition of a virus and some methods for studying animal viruses, as well as the classification and nomenclature of viruses, are presented.
Abstract: Preface Towards a definition of a virus How to handle animal viruses The structure of viruses Viral nucleic acids The process of infection I: Attachment and penetration The process of infection IIA: The Baltimore classification The process of infection IIB: The replication of viral DNA The process of infection IIC: RNA synthesis by RNA viruses The process of infection IID: RNA viruses with a DNA intermediate and vice versa The process of infection III: The regulation of gene expression The process of infection IV: The assembly of viruses Lysogeny Interactions between viruses and eukaryotic cells The immune system and interferon Virus-host interactions Vaccines and chemotherapy: the prevention and treatment of virus diseases Carcinogens and tumour viruses The evolution of viruses HIV and AIDS Trends in virology The classification and nomenclature of viruses
TL;DR: Cross-neutralization studies on 42 flaviviruses and their respective antisera were performed by a plaque assay in a line of pig kidney cells, finding four mosquito-borne, one tick-borne and one bat virus showed no relationship to any other flavivirus.
Abstract: Summary Cross-neutralization studies on 42 flaviviruses and their respective antisera were performed by a plaque assay in a line of pig kidney cells. Six tick-borne viruses fell into one subgroup; seven viruses associated with bats and small rodents and a further tick-borne virus fell into a second subgroup. Twenty-two mosquito-borne viruses fell into one major and four minor subgroups. Four mosquito-borne, one tick-borne and one bat virus showed no relationship to any other flavivirus.
TL;DR: These isolants support the theories that wild birds play an important role in the dissemination of type-A influenza viruses and may provide optimum conditions for genetic interaction of type of A influenza viruses, resulting in new hybrid strains.
Abstract: From 6 October 1972 to 3 December 1972, 41 type-A influenza virus isolants were recovered from free-flying wild ducks, and 7 isolants from domestic ducks in southern California. The typespecific antigen (ribonucleoprotein) was identified by the agar-geldiffusion test, and tentative identification of one strain-specific antigen (hemagglutinin) was attempted by the hemagglutinationinhibition test. These isolants support the theories that wild birds play an important role in the dissemination of type-A influenza viruses and may provide optimum conditions for genetic interaction of type-A influenza viruses, resulting in new hybrid strains.
TL;DR: The initial antineoplastic effect of the mumps virus therapy seemed to occur rapidly and strongly in proportion to swiftness in proliferation of cancer cells, indicating a possible participation of tumor immunity in the present virus therapy.
Abstract: Based on confirmation that slightly toxic mumps virus having a strong affinity with mankind has a carcinostatic effect, it was used in cancer. As priority was put not on healing but on reconfirmation of its effectiveness against human cancer and on its mode of administration, patients mostly received only small amounts of the virus. Of 90 patients with terminal cancer of various kinds, treatment was assessed as very good in 37, and good in 42, excluding 11 patients who had been near death. Administration of mumps virus produced few side-effects. The initial antineoplastic effect of the mumps virus therapy seemed to occur rapidly and strongly in proportion to swiftness in proliferation of cancer cells. Patients retaining physical strength often showed continuously suppressed growth of remaining tumors even after the disappearance of the initial effect, indicating a possible participation of tumor immunity in the present virus therapy.
TL;DR: A cat cell line carrying the genome of a murine sarcoma virus developed discrete foci in linear response to infection with feline leukemia virus or xenotropic murine C-type virus.
Abstract: A cat cell line carrying the genome of a murine sarcoma virus developed discrete foci in linear response to infection with feline leukemia virus or xenotropic murine C-type virus.
TL;DR: The clear-cut association between virus infection and rejection episodes suggests a pathogenic relationship and the two mechanisms which seem to best explain the relationship are (1) the virus infection acting as an adjuvant and triggering the rejection of the allograft or (2) theAllograft rejection activating a latent virus infection.
TL;DR: The hypothesis that immunosuppressive drugs (azathioprine and prednisone) are associated with reactivation of latent E.B. virus infections is supported.
TL;DR: Examination of the protein components of highly purified polyoma virions by electrophoretic separation in SDS-polyacrylamide gels has revealed the presence of three previously undetected protein bands, designated P3a and P4a, which may represent modified products of their respective doublet partners, P3b and P 4b.
TL;DR: The production of viral dsRNA in response to infection could bring about a general inhibition of protein synthesis in the interferon-treated cell, as is indeed observed in interferons-treated, vaccinia virus-infected mouse fibroblast L cells.
Abstract: NATURALLY occurring and synthetic double-stranded RNAs (dsRNAs) are interferon inducers1. They inhibit protein synthesis in animal cells2 and cell-free systems3–5. It is intriguing, therefore, that interferon treatment renders cells more sensitive to the toxic effects of dsRNA6, particularly as viral dsRNA may be involved in the replication of RNA viruses and has been isolated from DNA virus-infected cells7. Accordingly, the production of viral dsRNA in response to infection could bring about a general inhibition of protein synthesis in the interferon-treated cell, as is indeed observed in interferon-treated, vaccinia virus-infected mouse fibroblast L cells8,9. The cell dies but little virus is produced: an effective way of limiting a natural infection.