Treating young children co-infected with tuberculosis and HIV

Treating young children co-infected with tuberculosis and HIV
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治疗同时感染结核病和艾滋病毒的幼儿

DOI:
10.1016/s2352-3018(18)30326-6
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发表时间:
2019
期刊:
The Lancet HIV
影响因子:
--
通讯作者:
Turkova A
Turkova A
中科院分区:
--
文献类型:
--
作者:
Turkova A

文献摘要

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这些发现并不完全与之前的报告相反。Esbjörnsson及其同事的研究也表明,几内亚比绍的队列数据支持艾滋病毒-2相关的高死亡率4,艾滋病毒-1感染的死亡率是艾滋病毒-2感染的三倍。2来自西非队列协作的最新数据也显示,艾滋病毒-2感染者的高死亡率为每100人年观察5.2人。5然而,以前没有艾滋病发展时间的数据,因此Esbjörnsson和他的同事的研究2增加了对艾滋病毒-2疾病发展的理解。有趣的是,他们发现,与HIV-1感染者相比,HIV-2感染者临床艾滋病的CD4细胞计数似乎更高。这一发现表明,免疫缺陷对于HIV-2感染是不同的,值得进一步研究,以表征特定的HIV类型在免疫表型和功能上的差异。自然疾病的进展是可以观察到的,因为在抗逆转录病毒疗法(ART)可用之前,该队列被跟踪了数十年。2006年,抗逆转录病毒治疗成为可能,但真正接受抗逆转录病毒治疗的人寥寥无几,这也解释了相当高的死亡率。个体在开始抗逆转录病毒治疗时受到审查,但这实际上对艾滋病的进展和死亡率的影响相当小,可能是因为在比绍,治疗的保留率和治疗的依从性都非常低。HIV-2的治疗选择不同,因为非核苷逆转录酶抑制剂无效,9并且只有几个临床试验支持其治疗指南。1感染艾滋病毒-2的人中有很大一部分人的艾滋病毒RNA浓度检测不到,10这些人以前被认为可能没有进展。尽管Esbjörnsson和他的同事的报告受到缺乏HIV RNA测量的限制,但结论是HIV-2感染者遵循与HIV-1感染者相似的生存曲线,但速度较慢。因此,还应向艾滋病毒-2检测呈阳性的所有个人提供抗逆转录病毒治疗。HIV-2是研究HIV减毒形式的一个有趣的模型。有人提出,HIV-2可能诱导对HIV-1感染的交叉反应免疫反应,从而减缓HIV-1和HIV-2双重感染者的疾病进展。11研究人员对艾滋病毒宿主和治疗尝试的兴趣也在增加,12但艾滋病毒-2感染流行率的下降1为研究这种疾病留下了一个很小的机会之窗。
The findings are not completely in opposition to previous reports. There are cohort data from Guinea Bissau that support a high HIV-2-associated mortality4 with a three-times increased mortality for HIV-1 infection versus HIV-2 infection, also shown by Esbjörnsson and colleagues’ study. 2 Recent data from a west African cohort collaboration also showed a high mortality at 5· 2 per 100 person-years of observation for HIV-2-infected individuals. 5 However, data for the time to development of AIDS have not been available before, and Esbjörnsson and colleagues’ study2 therefore adds to the understanding of disease progression in HIV-2. Interestingly, they found that clinical AIDS seems to occur at higher CD4 cell counts for HIV-2-infected individuals than for HIV-1-infected individuals. This finding suggests that immunodeficiency is different for HIV-2 infection and warrants further research into characterising specific HIV-type differences in immunophenotype and functionality. Natural disease progression was possible to observe because the cohort was followed-up for decades before antiretroviral therapy (ART) was available. In 2006, ART became available, but few individuals actually received ART, 6 which also explains the considerable mortality. Individuals were censored when commencing ART, but this actually had quite a low impact on progression to AIDS and mortality, maybe because retention on treatment and adherence if on treatment are both very low in Bissau. 7, 8 Treatment options are different for HIV-2 as nonnucleoside reverse transcriptase inhibitors are not effective, 9 and there are only a few clinical trials to support guidelines for its treatment. 1 A large proportion of people infected with HIV-2 have undetectable HIV RNA concentrations, 10 and these individuals have previously been thought of as possible non-progressors. Although the report by Esbjörnsson and colleagues is limited by the lack of HIV RNA measurements, the conclusion stands that HIV-2-infected individuals follow survival curves similar to that of HIV-1-infected individuals, but at a slower rate. Hence, ART should also be offered to all individuals testing positive for HIV-2. HIV-2 is an interesting model for studying an attenuated form of HIV. It has been suggested that HIV-2 might induce a cross-reactive immune response against HIV-1 infection thereby slowing the disease progression among those dually infected with HIV-1 and HIV-2. 11 Interest in the HIV reservoir and cure attempts have also been growing among researchers, 12 but the declining prevalence of HIV-2 infection1 leaves a small window of opportunity for research on the disease.