NDLI: A primary production deficit in the thrombocytopenia of equine infectious anemia.

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Mutational analysis of ICP0R, a transrepressor protein created by alternative splicing of the ICP0 gene of herpes simplex virus type 1.

Identification of amino acids controlling the low-pH-induced conformational change of rabies virus glycoprotein.

Disulfide bonds of herpes simplex virus type 2 glycoprotein gB.

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Evidence that the UL84 gene product of human cytomegalovirus is essential for promoting oriLyt-dependent DNA replication and formation of replication compartments in cotransfection assays.

Retroviral insertional activation of the c-myb proto-oncogene in a Marek's disease T-lymphoma cell line.

The herpes simplex virus type 1 latency-associated transcript promoter is activated through Ras and Raf by nerve growth factor and sodium butyrate in PC12 cells.

Identification of cis-acting sequences in the promoter of the herpes simplex virus type 1 latency-associated transcripts required for activation by nerve growth factor and sodium butyrate in PC12 cells.

The RGG box motif of the herpes simplex virus ICP27 protein mediates an RNA-binding activity and determines in vivo methylation.

Cytomegalovirus "missing" capsid protein identified as heat-aggregable product of human cytomegalovirus UL46.

Infectivities of human and other primate lentiviruses are activated by desialylation of the virion surface.

Attenuation of DNA-dependent protein kinase activity and its catalytic subunit by the herpes simplex virus type 1 transactivator ICP0.

The oncoprotein Tax of the human T-cell leukemia virus type 1 activates transcription via interaction with cellular ATF-1/CREB factors in Saccharomyces cerevisiae.

Identification of the major membrane and core proteins of vaccinia virus by two-dimensional electrophoresis.

Evaluation of the concentration and bioactivity of adenovirus vectors for gene therapy.

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DNA encapsidation by viruslike particles assembled in insect cells from the major capsid protein VP1 of B-lymphotropic papovavirus.

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Enhanced transcriptional activation by E2 proteins from the oncogenic human papillomaviruses.

Feline immunodeficiency virus vaccination: characterization of the immune correlates of protection.

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Retroviral mutation rates and A-to-G hypermutations during different stages of retroviral replication.

Dynamics and modulation of human immunodeficiency virus type 1 transcripts in vitro and in vivo.

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A primary production deficit in the thrombocytopenia of equine infectious anemia.

Content Provider	PubMed Central
Author	Crawford, T. B. Wardrop, K. J. Tornquist, S. J. Reilich, E. Meyers, K. M. Mcguire, T. C.
Abstract	The purpose of this study was to identify the mechanisms responsible for the thrombocytopenia that develops following infection of horses by the lentivirus equine infectious anemia virus (EIAV). Immunocompetent Arabian foals and Arabian foals with severe combined immunodeficiency (SCID), which lack functional B and T lymphocytes, were experimentally infected with EIAV. Levels of viremia and a number of clinical and hematologic parameters were examined prior to and following infection. Thrombocytopenia was not dependent on the immune response: SCID foals were affected as severely as immunocompetent foals. Production of platelets, measured by metabolic incorporation of radioactive label, was significantly reduced. The decrease ranged from 35 to 89% in three SCID and two immunocompetent foals examined. Platelet survival, measured by 51Cr labeling, also declined following infection in both SCID and immunocompetent foals: 51 and 68%, respectively, relative to the preinfection life spans. The difference between immunocompetent and immunodeficient foals was not statistically significant. The number of megakaryocytes (MK) per square millimeter of bone marrow, determined by digitizing morphometry, was not significantly altered in either SCID or immunocompetent thrombocytopenic foals. Numbers of denuded MK nuclei per unit area increased, but the elevation was not statistically significant. No evidence for viral replication in MK was found. Three different parameters of intravascular coagulation (activated prothombin time, fibrin degradation products, and one-step prothombin time) remained normal until after platelet numbers had declined significantly, arguing against an important role for disseminated intravascular coagulation. The findings indicate that EIAV induces thrombocytopenia principally through an indirect, noncytocidal suppressive effect on platelet production, the mechanism of which is unknown. A shortening of platelet life span apparently contributes moderately to the platelet deficit as well. The shortening of platelet life span is multifactorial in origin, including both mechanisms that depend on an active immune response and those that do not.
Starting Page	7842
File Format	PDF
ISSN	10985514
e-ISSN	10985514
Journal	Journal of Virology
Issue Number	11
Volume Number	70
Language	English
Publisher Date	1996-11-01
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Virology Immunology Microbiology Insect Science

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