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病毒因素对感染猿猴免疫缺陷病毒SIVagm的非洲绿猴体内极早期复制谱的影响。

Impact of viral factors on very early in vivo replication profiles in simian immunodeficiency virus SIVagm-infected African green monkeys.

作者信息

Pandrea Ivona, Kornfeld Christopher, Ploquin Mickael J-Y, Apetrei Cristian, Faye Abdourahmane, Rouquet Pierre, Roques Pierre, Simon François, Barré-Sinoussi Françoise, Müller-Trutwin Michaela C, Diop Ousmane M

机构信息

Division of Comparative Pathology, Tulane National Primate Research Center, 18703 Three Rivers Road, Covington, LA 70433, USA.

出版信息

J Virol. 2005 May;79(10):6249-59. doi: 10.1128/JVI.79.10.6249-6259.2005.

Abstract

To better understand which factors govern the levels of viral loads in early lentiviral infections of primates, we developed a model that allows distinguishing between the influences of host and viral factors on viremia. Herein we report that two species of African green monkeys (Chlorocebus sabaeus and C. pygerythrus) infected with their respective wild-type simian immunodeficiency virus SIVagm viruses (SIVagm.sab92018 and SIVagm.ver644) consistently showed reproducible differences in viremia during primary infection but not at later stages of infection. Cross-infections of SIVagm.sab92018 and SIVagm.ver644 into, respectively, C. pygerythrus and C. sabaeus revealed that the dynamics of viral replication during primary infection were dependent on the viral strain used for the infection but not on the host. Hence, the kinetics of SIVagm.sab92018 and SIVagm.ver644 were similar in both sabaeus and vervet animals, indicating that the difference in viremia levels between the two groups during the early phase of infection was not associated with the host. Coreceptor usage for these two strains showed a larger coreceptor repertoire for SIVagm.sab92018, which is able to efficiently use CXCR4 in addition to CCR5, than for SIVagm.ver644, which showed a classical CCR5 coreceptor usage pattern. These differences could not be explained by different charges of the V3 loop for SIVagm.sab92018 and for SIVagm.ver644. In conclusion, our study showed that the extent of virus replication during the primary infection is primarily dependent on viral determinants.

摘要

为了更好地理解哪些因素决定灵长类动物早期慢病毒感染中的病毒载量水平,我们开发了一个模型,该模型能够区分宿主因素和病毒因素对病毒血症的影响。在此我们报告,两种感染了各自野生型猴免疫缺陷病毒SIVagm病毒(SIVagm.sab92018和SIVagm.ver644)的非洲绿猴(赤猴和绿猴)在初次感染期间病毒血症始终呈现可重复的差异,但在感染后期则没有。将SIVagm.sab92018和SIVagm.ver644分别交叉感染到绿猴和赤猴中,结果显示初次感染期间病毒复制的动态取决于用于感染的病毒株,而非宿主。因此,SIVagm.sab92018和SIVagm.ver644在赤猴和绿猴中的动力学相似,这表明两组在感染早期病毒血症水平的差异与宿主无关。这两种毒株的共受体使用情况表明,SIVagm.sab92018除了能有效利用CCR5外,还能利用CXCR4,其共受体谱比SIVagm.ver644更大,后者呈现典型的CCR5共受体使用模式。SIVagm.sab92018和SIVagm.ver644的V3环电荷不同无法解释这些差异。总之,我们的研究表明,初次感染期间病毒复制的程度主要取决于病毒决定因素。

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