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非细胞病变性HIV分离株导致人外周血淋巴细胞-严重联合免疫缺陷小鼠中CD4+ T细胞迅速丧失。

Rapid loss of CD4+ T cells in human-PBL-SCID mice by noncytopathic HIV isolates.

作者信息

Mosier D E, Gulizia R J, MacIsaac P D, Torbett B E, Levy J A

机构信息

Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.

出版信息

Science. 1993 Apr 30;260(5108):689-92. doi: 10.1126/science.8097595.

DOI:10.1126/science.8097595
PMID:8097595
Abstract

Human immunodeficiency virus (HIV) isolates differ in cell tropism, replication, pathogenicity, and syncytial induction in vitro. CD4+ T cells were enumerated in severe combined immunodeficient mice transplanted with human peripheral blood leukocytes (hu-PBL-SCID mice) and infected with HIV isolates with different in vitro cytopathicity. Two noncytopathic, macrophage-tropic strains, HIV-1SF162 and HIV-2UC1, induced extensive CD4+ T cell depletion, whereas HIV-1SF33, which is highly cytopathic for T cells in vitro, caused little CD4+ T cell depletion at equivalent virus burden. In vitro cytopathicity assays therefore do not predict CD4 depletion in the hu-PBL-SCID model.

摘要

人类免疫缺陷病毒(HIV)分离株在细胞嗜性、复制、致病性以及体外合胞体诱导方面存在差异。在移植了人外周血白细胞的严重联合免疫缺陷小鼠(hu-PBL-SCID小鼠)中计数CD4+ T细胞,并使其感染具有不同体外细胞病变效应的HIV分离株。两种无细胞病变效应、巨噬细胞嗜性的毒株HIV-1SF162和HIV-2UC1,可导致广泛的CD4+ T细胞耗竭,而在体外对T细胞具有高度细胞病变效应的HIV-1SF33,在同等病毒载量下引起的CD4+ T细胞耗竭却很少。因此,体外细胞病变效应测定无法预测hu-PBL-SCID模型中的CD4耗竭情况。

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