HIV-1感染的创始变异多重性与CD4+下降率之间的协调。

IF 3.7 2区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES
Journal of The Royal Society Interface Pub Date : 2024-10-01 Epub Date: 2024-10-30 DOI:10.1098/rsif.2024.0255
James Baxter, Ch Julián Villabona-Arenas, Robin N Thompson, Stéphane Hué, Roland R Regoes, Roger D Kouyos, Huldrych F Günthard, Jan Albert, Andrew Leigh Brown, Katherine E Atkins
{"title":"HIV-1感染的创始变异多重性与CD4+下降率之间的协调。","authors":"James Baxter, Ch Julián Villabona-Arenas, Robin N Thompson, Stéphane Hué, Roland R Regoes, Roger D Kouyos, Huldrych F Günthard, Jan Albert, Andrew Leigh Brown, Katherine E Atkins","doi":"10.1098/rsif.2024.0255","DOIUrl":null,"url":null,"abstract":"<p><p>HIV-1 transmission precipitates a stringent genetic bottleneck, with 75% of new infections initiated by a single genetic variant. Where multiple variants initiate infection, recipient set point viral load (SpVL) and the rate of CD4<sup>+</sup> T cell decline may be elevated, but these findings remain inconsistent. Here, we summarised the evidence for this phenomenon, then tested whether previous studies possessed sufficient statistical power to reliably identify a true effect of multiple variant infection leading to higher SpVL. Next, we combined models of HIV-1 transmission, heritability and disease progression to understand whether available data suggest a faster CD4<sup>+</sup> T cell decline would be expected to associated with multiple variant infection, without an explicit dependency between the two. First, we found that most studies had insufficient power to identify a true significant difference, prompting an explanation for previous inconsistencies. Next, our model framework revealed we would not expect to observe a positive association between multiple variant infections and faster CD4<sup>+</sup> T cell decline, in the absence of an explicit dependency. Consequently, while empirical evidence may be consistent with a positive association between multiple variant infection and faster CD4<sup>+</sup> T cell decline, further investigation is required to establish a causal basis.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"21 219","pages":"20240255"},"PeriodicalIF":3.7000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11606301/pdf/","citationCount":"0","resultStr":"{\"title\":\"Reconciling founder variant multiplicity of HIV-1 infection with the rate of CD4<sup>+</sup> decline.\",\"authors\":\"James Baxter, Ch Julián Villabona-Arenas, Robin N Thompson, Stéphane Hué, Roland R Regoes, Roger D Kouyos, Huldrych F Günthard, Jan Albert, Andrew Leigh Brown, Katherine E Atkins\",\"doi\":\"10.1098/rsif.2024.0255\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>HIV-1 transmission precipitates a stringent genetic bottleneck, with 75% of new infections initiated by a single genetic variant. Where multiple variants initiate infection, recipient set point viral load (SpVL) and the rate of CD4<sup>+</sup> T cell decline may be elevated, but these findings remain inconsistent. Here, we summarised the evidence for this phenomenon, then tested whether previous studies possessed sufficient statistical power to reliably identify a true effect of multiple variant infection leading to higher SpVL. Next, we combined models of HIV-1 transmission, heritability and disease progression to understand whether available data suggest a faster CD4<sup>+</sup> T cell decline would be expected to associated with multiple variant infection, without an explicit dependency between the two. First, we found that most studies had insufficient power to identify a true significant difference, prompting an explanation for previous inconsistencies. Next, our model framework revealed we would not expect to observe a positive association between multiple variant infections and faster CD4<sup>+</sup> T cell decline, in the absence of an explicit dependency. Consequently, while empirical evidence may be consistent with a positive association between multiple variant infection and faster CD4<sup>+</sup> T cell decline, further investigation is required to establish a causal basis.</p>\",\"PeriodicalId\":17488,\"journal\":{\"name\":\"Journal of The Royal Society Interface\",\"volume\":\"21 219\",\"pages\":\"20240255\"},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11606301/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of The Royal Society Interface\",\"FirstCategoryId\":\"103\",\"ListUrlMain\":\"https://doi.org/10.1098/rsif.2024.0255\",\"RegionNum\":2,\"RegionCategory\":\"综合性期刊\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/30 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MULTIDISCIPLINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of The Royal Society Interface","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1098/rsif.2024.0255","RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/30 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
引用次数: 0

摘要

HIV-1 的传播会造成严格的基因瓶颈,75% 的新感染由单一基因变异引发。在多个变异体引发感染的情况下,受体的设定点病毒载量(SpVL)和 CD4+ T 细胞下降率可能会升高,但这些研究结果仍不一致。在此,我们总结了这一现象的证据,然后检验了之前的研究是否具有足够的统计能力,以可靠地识别多重变异感染导致更高的 SpVL 的真实效应。接下来,我们结合了 HIV-1 传播、遗传性和疾病进展模型,以了解现有数据是否表明 CD4+ T 细胞下降速度加快与多重变异感染有关,而两者之间并不存在明确的依赖关系。首先,我们发现大多数研究没有足够的力量来确定真正的显著差异,这促使我们对之前的不一致性做出解释。其次,我们的模型框架显示,在没有明确依赖关系的情况下,我们不会期望观察到多重变异感染与 CD4+ T 细胞下降速度加快之间的正相关。因此,虽然经验证据表明多重变异感染与 CD4+ T 细胞下降速度之间存在正相关,但要确定其因果关系还需要进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reconciling founder variant multiplicity of HIV-1 infection with the rate of CD4+ decline.

HIV-1 transmission precipitates a stringent genetic bottleneck, with 75% of new infections initiated by a single genetic variant. Where multiple variants initiate infection, recipient set point viral load (SpVL) and the rate of CD4+ T cell decline may be elevated, but these findings remain inconsistent. Here, we summarised the evidence for this phenomenon, then tested whether previous studies possessed sufficient statistical power to reliably identify a true effect of multiple variant infection leading to higher SpVL. Next, we combined models of HIV-1 transmission, heritability and disease progression to understand whether available data suggest a faster CD4+ T cell decline would be expected to associated with multiple variant infection, without an explicit dependency between the two. First, we found that most studies had insufficient power to identify a true significant difference, prompting an explanation for previous inconsistencies. Next, our model framework revealed we would not expect to observe a positive association between multiple variant infections and faster CD4+ T cell decline, in the absence of an explicit dependency. Consequently, while empirical evidence may be consistent with a positive association between multiple variant infection and faster CD4+ T cell decline, further investigation is required to establish a causal basis.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Journal of The Royal Society Interface
Journal of The Royal Society Interface 综合性期刊-综合性期刊
CiteScore
7.10
自引率
2.60%
发文量
234
审稿时长
2.5 months
期刊介绍: J. R. Soc. Interface welcomes articles of high quality research at the interface of the physical and life sciences. It provides a high-quality forum to publish rapidly and interact across this boundary in two main ways: J. R. Soc. Interface publishes research applying chemistry, engineering, materials science, mathematics and physics to the biological and medical sciences; it also highlights discoveries in the life sciences of relevance to the physical sciences. Both sides of the interface are considered equally and it is one of the only journals to cover this exciting new territory. J. R. Soc. Interface welcomes contributions on a diverse range of topics, including but not limited to; biocomplexity, bioengineering, bioinformatics, biomaterials, biomechanics, bionanoscience, biophysics, chemical biology, computer science (as applied to the life sciences), medical physics, synthetic biology, systems biology, theoretical biology and tissue engineering.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信