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Results for “VIRAL INTERFERENCE”

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At least 487 records · Page 27Linked to original sources
PubMed1981

Mechanisms of persistence in arenavirus infections: a brief review.

A characteristic of the arenaviruses is persistent infections in their natural host. Age at infection is an important factor in the establishment of persistence. Infections early in life regularly result in persistence and this appears to be related to the immaturity of the immune system. Persistently infected animals make antibodies to the viral antigens, which indicates that the animals are not tolerant with respect to B cell functions. However, cytotoxic T cells cannot be demonstrated in persistently infected animals, suggesting a defect in effector T cell functions. The mechanisms leading to this defect in cytotoxic T cells have not been resolved. Persistence of arenaviruses in cell cultures is also regularly observed but the molecular basis for survival of the virus and cell in long-term cultures has yet to be clarified.

Animals↗
PubMed1999

Co-infection of acyclovir-resistant and acyclovir-sensitive herpes simplex type 2 virus strains in BS-C-1 cells.

Co-infection of BS-C-1 cells by the herpes simplex virus type 2 (HSV-2) Curtis strain with its acyclovir (ACV)-resistant mutant (HSV-2-ACV(R)), resulted in a severalfold increase in virus yield, as compared to a single infection. On the other hand, when two viruses (G strain and HSV-2-ACV(R)) belonging to different strains of HSV-2 were involved, their growth was significantly inhibited; the decrease in the titer of the second virus to infect the cells was greater when its infection took place at later times following infection by the first. This inhibition was not due to the shut-off of host cell protein synthesis caused by the first virus, since an HSV-2 mutant which is unable to inhibit the protein synthesis of the host cell was still capable of efficiently inhibiting the growth of the superinfecting virus.

Acyclovir↗
PubMed1982

Persistent infection of a nonvector mosquito cell line (TRA-171) with dengue viruses.

Dengue viruses often caused an apparent, persistent infection in a cell line derived from a nonvector mosquito, Toxorhynchites amboinensis. The characteristics of the viruses were modified during the course of persistent infection, as demonstrated by the changes in neutralizing titers of hyperimmune ascitic fluids against dengue serotypes, increased ability to induce syncytia, and increased temperature sensitivity. Although neurovirulence in suckling mice was reduced for all serotypes, considerable levels of neurovirulence were detected for DEN-1, DEN-2, and DEN-4, after 1 year in culture. Replication of the original viruses was not significantly inhibited when the cell cultures were treated with virus-free supernatant fluids from persistently infected cultures.

Animals↗
PubMed1975

Cyclic appearance of defective interfering particles of herpes simplex virus and the concomitant accumulation of early polypeptide VP175.

Serial passage of undiluted herpes simplex virus types 1 and 2 resulted in cyclic production of infectious and defective virions. Defective virus production was characterized by the appearance of a new species of viral DNA with a higher bouyant density in CsCl than standard viral DNA. Measurement of the infectivity titer and DNA synthesis revealed that the defective particles interfered with the replication of standard virions and stimulated the overproduction of a large molecular weight (175,000 daltons) polypeptide.

Cell Line↗
PubMed2006

CD1 antigen presentation by human dendritic cells as a target for herpes simplex virus immune evasion.

In contrast to MHC molecules, which present peptides, the CD1 molecules have been discovered to present lipid Ags to T cells. CD1-restricted T lymphocytes have been recently associated with resistance to virus infection. The mechanisms underlying activation of CD1-restricted T cells in the course of virus infection are not defined. In this study, we wanted to investigate the interaction of HSV with the antiviral CD1 Ag presentation system in human dendritic cells (DC). In response to low titers of HSV, the surface expression of CD1b and CD1d on human DC was up-regulated. These phenotypic changes enhanced the capacity of infected DC to stimulate proliferation of CD1-restricted T lymphocytes. High titers of HSV, however, lead to strong down-regulation of all surface CD1 molecules. This modulation of surface expression was associated with intracellular accumulation, colocalization with viral proteins, and disruption of the CD1 recycling machinery. Finally, even at low titers HSV interfered with the capacity of infected DC to stimulate the release of important cytokines by CD1d-restricted NKT cells. Thus, we demonstrate both the existence of a CD1 pathway allowing human DC to react to viral infection, as well as its blockage by a human herpesvirus.

Antigen Presentation↗
PubMedDate not supplied

Involvement of protein-DNA interaction in adeno-associated virus Rep78-mediated inhibition of HIV-1.

OBJECTIVE: It has been well documented by several laboratories that adeno-associated virus (AAV) is able to inhibit HIV-1 replication and gene expression. This effect has been mapped to the AAV-encoded Rep78 protein. However, the mechanism by which Rep78 is able to inhibit HIV-1 is unclear. As Rep78 is a DNA binding transcription factor, the objective of this study was to investigate where Rep78 might bind within the HIV-1 long terminal repeat (LTR) sequences and to judge the importance of this protein-DNA interaction. STUDY DESIGN/METHODS: Rep78's binding to HIV-LTR DNA was analyzed by electrophoretic mobility shift assay (EMSA). The importance of this protein-DNA interaction was analyzed using a Rep78 mutant defective for binding HIV-LTR DNA in an assay for monitoring gene expression (chloramphenicol acetyltransferase [CAT] assay). RESULTS: The preferred site for Rep78 binding was found to be adjacent to the HIV-LTR TATA box, within nt -54 to -34 relative to the site of transcription initiation. Furthermore, a Rep78 mutant with substitutions at amino acid residues 64 and 65 which was found defective for binding HIV-LTR DNA, was also found to be defective for inhibition of tat transactivated HIV-LTR gene expression. CONCLUSION: These data strongly suggest that Rep78's DNA binding ability is important for its mechanism of inhibition. Furthermore, the TATA box region of the HIV-LTR, to which Rep78 preferentially binds, is a likely target through which the inhibition takes place.

DNA, Viral↗
PubMedDate not supplied

[Virus-specific syntheses in cells infected with the virions from standard and "defective" populations of the influenza virus (author's transl)].

The structure of influenza virus virions from the standard and "Magnus" populations as well as intracellular syntheses induced by them were studied. Virions of influenza virus were shown to be heterogeneous with respect to the set of fragments in them. This heterogeneity was more marked in virions of the "Magnus" population and consisted in a relatively greater deficiency of large fragments. A marked induction of light RNA fractions in the cell by defective influenza virus was demonstrated. Synthesis of protein and the polypeptide composition of virions were found to be similiar in standard and "Magnus" viruses.

Animals↗
PubMed1992

Multiple HPV infection: microanatomy by in situ hybridization and immunohistochemistry.

Specific human papillomavirus (HPV) types have been shown to be associated with proliferative epithelial lesions with variable biological consequences in infected patients. Simultaneous infection by more than one HPV type has been infrequently reported, and its clinical significance is unknown. We have examined four biopsies of cervical and vulvar tissue, each with evidence of infection by two different HPVs. Using both in situ hybridization and immunohistochemical techniques, we determined the cellular distribution of the viral infections. Using biotinylated type-specific probes and stringent conditions we were able to demonstrate that in each case the two HPVs occupied distinct, non-overlapping foci within the lesions. The condylomatous tissues contained DNA from HPV types that are associated with high-grade neoplasia and invasive cancer (16 and 18), as well as types commonly associated with benign proliferative lesions. Immunohistochemical analysis of the lesions with antibody to bovine papillomavirus capsid antigen failed to detect HPV in regions shown by in situ hybridization to contain HPV 16 and 18 DNA, whereas type 6 and 11 infected areas were readily identified. These results provide indirect evidence of viral interference between HPV types and indicate that interference may limit the number of HPV types that produce active infections within a single cell.

Cervix Uteri↗