Koot M, van 't Wout A B, Kootstra N A, de Goede R E, Tersmette M, Schuitemaker H
Department of Clinical Viro-Immunology, Netherlands Red Cross Blood Transfusion Service, University of Amsterdam, Netherlands.
J Infect Dis. 1996 Feb;173(2):349-54. doi: 10.1093/infdis/173.2.349.
The relationship between the evolution of human immunodeficiency virus type 1 (HIV-1) biologic phenotype, changes in the proportion of infected peripheral blood mononuclear cells, and the relative contribution of non-syncytium-inducing (NSI) and syncytium-inducing (SI) HIV-1 variants to virus load was studied during the course of HIV-1 infection. In 65 HIV-1-infected subjects, the proportion of infected CD4 T cells was higher in persons who carried SI variants. Longitudinal studies revealed that the emergence of SI HIV-1 variants can occur at relatively low numbers of HIV-1-infected cells. Emergence of SI variants frequently coincided with an increase of virus load due to an expansion of both NSI and SI variants, although the contribution of SI viruses to the total virus population significantly increased with time after SI phenotype conversion. These data indicate that NSI to SI phenotype conversion, rather than resulting from high virus load, is part of the sequence of events that leads to increased virus load and CD4 cell depletion.
在人类免疫缺陷病毒1型（HIV-1）感染过程中，研究了HIV-1生物学表型的演变、感染外周血单核细胞比例的变化以及非合胞体诱导（NSI）和合胞体诱导（SI）HIV-1变异体对病毒载量的相对贡献。在65名HIV-1感染受试者中，携带SI变异体的人感染的CD4 T细胞比例更高。纵向研究表明，SI HIV-1变异体可在相对少量的HIV-1感染细胞中出现。SI变异体的出现通常与病毒载量增加同时发生，这是由于NSI和SI变异体均增多所致，尽管SI病毒在SI表型转换后对总病毒群体的贡献随时间显著增加。这些数据表明，NSI向SI表型的转换并非由高病毒载量导致，而是导致病毒载量增加和CD4细胞耗竭的一系列事件的一部分。
