Detection of non-A, non-B hepatitis antigen by immunocytochemical staining.

Burk, Kenneth H.; Oefinger, Paul E.; Dreesman, Gordon R.

doi:10.1073/pnas.81.10.3195

Cited by 7 publications

(3 citation statements)

References 34 publications

(44 reference statements)

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“…By using strand-specific probes, we know now that the block in gene expression in preterminal SSPE applies to the synthesis of both plus-and minus-strand RNA. We also confirmed the rarity of cells that contain detectible NP or M polypeptides using an immunoperoxidase technique that is 40 times more sensitive than immunofluorescence (20 …”

supporting

confidence: 51%

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Natural history of restricted synthesis and expression of measles virus genes in subacute sclerosing panencephalitis.

Haase¹,

Gantz²,

Eble³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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Subacute sclerosing panencephalitis (SSPE) is a slow infection caused by measles virus in which several years separate recovery from typical acute measles and the development of a slowly progressive neurological disease. We have investigated replication of measles virus in brain tissue obtained after the onset of neurological disease and in the terminal phase. With a hybridization tomographic technique that combines in situ hybridization with macroradioautographic screening of large areas of tissue, we analyzed the spatial and temporal distribution of virus genes in vivo, using region-and strand-specific probes for the nucleocapsid and matrix genes. We show that early in the course of SSPE there is a global repression in the synthesis and expression of the genome. In the final stage of SSPE most infected cells still have depressed levels of plus-and minus-strand viral RNA and contain nucleocapsid protein but lack matrix protein. These findings provide further evidence for a unified view of slow infections of the nervous system, where the general constraints on virus gene expression provide an explanation for persistence of virus in the face of the host's immune response, and the slow evolution of pathological change. In the final phases of SSPE the more specific block in virus replication accounts for the cell-associated state of the virus and the difficulty in virus isolation.In slow infections caused by conventional viruses, periods often of years separate acquisition of virus and overt symptoms, and, during the long incubation period, virus persists in the face of the host's immune response. Subacute sclerosing panencephalitis (SSPE), for example, is a rare complication of measles infections in which the afflicted child ostensibly recovers from measles, develops normally for several years, and then slowly succumbs to a neurological disorder. The neurological disease reflects destruction of cells in the brain harboring measles virus despite high levels of virusspecific antibody in serum and cerebrospinal fluid (1-3).We have attributed the slow evolution of SSPE and the persistence of measles virus in this disease to restricted synthesis and expression of virus genes in the nervous system (4). These global constraints result in decreased levels of viral antigens in the cell and, pari passu, diminished effectiveness of immune surveillance in eradication of infected cells.Restricted gene expression also mitigates cellular injury accompanying virus replication, and tissue damage therefore accumulates slowly.This interpretation of the pathogenesis of SSPE emerged from investigations of tissues obtained for diagnosis relatively early in the disease (4). In the terminal state a more specific block in virus replication has been identified (5-9). The viral matrix (M) protein required for maturation of measles virus is markedly decreased in brain and in cell cultures derived from a patient with SSPE. In the latter case, mRNA for the M protein is present but is not translated effectively in vitro (9).In this arti...

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confidence: 51%

“…2 Middle). We used monoclonal antibodies to NP and M and the most sensitive of current methods for detection of antigens in individual cells (20) to evaluate synthesis of measles gene products in terminal SSPE. Cells in the subjacent sections to those that had both NP and M plus-strand RNA contained NP antigen (Fig.…”

Section: Resultsmentioning

confidence: 99%

Natural history of restricted synthesis and expression of measles virus genes in subacute sclerosing panencephalitis.

Haase¹,

Gantz²,

Eble³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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“…Consequently, the identification of the NANB hepatitis virus still remains an open subject and awaits further clarification. We have recently described an avidin-biotin immunoperoxidase tissue-staining procedure which has been used to identify specific NANB hepatitis virus antigen in infected chimpanzee liver (25). This method and others will be necessary to fully characterize the NANB hepatitis virus.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Sequelae of Non-A, Non-B Hepatitis in Experimentally Infected Chimpanzees

et al. 1984

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We have observed the development of long-term sequelae in four cases of experimentally induced non-A, non-B (NANB) hepatitis in chimpanzees. These sequelae were characterized by the following manifestations: nonprotection against challenge with autologous infectious plasma following acute disease and subtle histopathological alterations typical of long-lasting viral hepatitis. These manifestations were observed in animals infected with either of two human inocula. Whether or not these inocula represent sources of single or multiple etiologic agents is not known. However, our studies suggest that these inocula share at least one common etiologic agent. Further, these results may represent an atypical chronology of convalescence from viral hepatitis infection. For example, the convalescent stage of a type B hepatitis infection may be expected to occur within 6 to 8 months following exposure, whereas true convalescence in NANB hepatitis may be protracted over several months to several years. Thus, future efforts to identify the causative agent(s) of NANB hepatitis, and efforts to define the immune response in NANB, must take into consideration these studies.

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Detection of hepatitis C virus (HCV) RNA in paraffin embedded tissue sections of human liver of non‐A, non‐B hepatitis patients by in situ hybridization

Yamada

Koji

Nozawa

et al. 1992

Clinical Laboratory Analysis

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Localization of hepatitis C virus (HCV) RNA was investigated by non-radioactive in situ hybridization in human liver specimens of chronic non-A, non-B (NANB) hepatitis patients who were seropositive for antibodies to HCV (anti-HCV). For in situ hybridization, T-T dimerized synthetic oligodeoxynucleotide probes were used and DNAs hybridized in situ were detected immunohistochemically using specific antibodies against T-T dimer. The data demonstrates that HCV-RNA was localized in the cytoplasm of hepatocytes in human liver biopsies obtained from the patients with chronic NANB hepatitis seropositive for anti-HCV.

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Detection of non-A, non-B hepatitis antigen by immunocytochemical staining.

Cited by 7 publications

References 34 publications

Natural history of restricted synthesis and expression of measles virus genes in subacute sclerosing panencephalitis.

Natural history of restricted synthesis and expression of measles virus genes in subacute sclerosing panencephalitis.

Long-Term Sequelae of Non-A, Non-B Hepatitis in Experimentally Infected Chimpanzees

Detection of hepatitis C virus (HCV) RNA in paraffin embedded tissue sections of human liver of non‐A, non‐B hepatitis patients by in situ hybridization

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