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Results for “VIRAL INTERFERENCE”

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At least 793 records · Page 44Linked to original sources
PubMed1985

[Immunomorphological research on the changes in the focal contacts of cultured cells transformed by Kirsten sarcoma virus].

Alterations of focal contacts (FC) of NRK cultured cells transformed by Kirsten's sarcoma virus and by ts-mutant of this virus were examined immunomorphologically using a new antibody-exclusion method. In nontransformed NRK cells the FC are arranged in the form of a network near the cell edges; numerous single contacts are seen in the center. The FC are always present in both KNRK and tsKNRK cells at permissive temperature. However, their quantity is drastically reduced, especially in the center of the cells, as is often their size. It is suggested that expression of the product of viral oncogene interferes with maturation of the FC continuously formed at the cell edge.

Animals↗
PubMed1993

Papillomaviruses in head and neck disease: pathophysiology and possible regulation.

Human papillomaviruses (HPVs) are etiologic agents of both benign and malignant epithelial tumors. More than 60 different types of viruses are known, each associated with tissue site and lesion type specificities and differing probabilities of malignant progression. HPVs type 6 and type 11 cause benign papillomas of mucosal squamous epithelium in the aerodigestive tract, with only rare conversion to malignancy. HPV 16 is the most frequently detected HPV in the genital tract, inducing flat lesions with a significant risk of malignant conversion. In the aerodigestive tract, HPV 16 is found only rarely in benign lesions but is detected in 5-20% of squamous carcinomas. In the aerodigestive tract, HPVs frequently cause latent infection, i.e., viral DNA present in tissue but no evidence of clinical or histologic disease. Approximately 10% of the general population may have latent infections. Regulation and activation of latent infections are not well understood, although it is clear that viral functions are tightly regulated by the state of differentiation of the squamous host cell. Control of viral transcription may be the key to prevention of viral activation, and thus control of disease. Among the possible agents under investigation are retinoids, growth factors, anti-sense RNA which interferes with viral expression, and estrogen metabolites. All of these agents modulate either viral expression or cell differentiation or both. It is hoped that in the near future one or more of these agents will be useful in preventing HPV-associated disease.

Animals↗
PubMed2003

Cytopathogenicity of pestiviruses: cleavage of bovine viral diarrhea virus NS2-3 has to occur at a defined position to allow viral replication.

Despite of highly divergent genome organizations, the N terminus of nonstructural protein 3 (NS3) is highly conserved between cytopathogenic (cp) bovine viral diarrhea virus (BVDV) strains. Generation of NS3, often by NS2-3 cleavage, is a marker of cp BVDV. The significance of the cleavage site within NS2-3 for viral replication was addressed by the use of BVDV replicons. Our results demonstrate that elongation as well as truncation of NS3 strongly interfere with viral RNA replication. This finding strongly suggests that the observed conservation of the N terminus of NS3 between cp BVDV is caused by functional selection and not by the presence of a hotspot of recombination.

Amino Acid Sequence↗
PubMed2003

Adenosine kinase is inactivated by geminivirus AL2 and L2 proteins.

AL2 and L2 are related proteins encoded by geminiviruses of the Begomovirus and Curtovirus genera, respectively. Both are pathogenicity determinants that cause enhanced susceptibility when expressed in transgenic plants. To understand how geminiviruses defeat host mechanisms that limit infectivity, we searched for cellular proteins that interact with AL2 and L2. Here, we present evidence that the viral proteins interact with and inactivate adenosine kinase (ADK), a nucleoside kinase that catalyzes the salvage synthesis of 5'-AMP from adenosine and ATP. We show that the AL2 and L2 proteins inactivate ADK in vitro and after coexpression in Escherichia coli and yeast. We also demonstrate that ADK activity is reduced in transgenic plants expressing the viral proteins and in geminivirus-infected plant tissues. By contrast, ADK activity is increased after inoculation of plants with diverse RNA viruses or a geminivirus lacking a functional L2 gene. Consistent with its ability to interact with multiple cellular kinases, we also demonstrate that AL2 is present in both the nucleus and the cytoplasm of infected plant cells. These data indicate that ADK is targeted by viral pathogens and provide evidence that this "housekeeping" enzyme might be a part of host defense responses. In previous work, we showed that AL2 and L2 also interact with and inactivate SNF1 kinase, a global regulator of metabolism that is activated by 5'-AMP. Together, these observations suggest that metabolic alterations mediated by SNF1 are an important component of innate antiviral defenses and that the inactivation of ADK and SNF1 by the geminivirus proteins represents a dual strategy to counter this defense. AL2 proteins also have been shown to act as suppressors of RNA silencing, an adaptive host defense response. A possible relationship between ADK inactivation and silencing suppression is discussed.

Adenosine Kinase↗