HIV infection disrupts the sympatric host-pathogen relationship in human tuberculosis.
HIV infection disrupts the sympatric host-pathogen relationship in human tuberculosis.
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艾滋病毒感染破坏了人结核中的同胞宿主 - 病原体关系。
DOI：
10.1371/journal.pgen.1003318
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发表时间：
2013
期刊：
影响因子：
4.5
通讯作者：
Swiss HIV Cohort and Molecular Epidemiology of Tuberculosis Study Groups
中科院分区：
文献类型：
--
作者：
Fenner L;Egger M;Bodmer T;Furrer H;Ballif M;Battegay M;Helbling P;Fehr J;Gsponer T;Rieder HL;Zwahlen M;Hoffmann M;Bernasconi E;Cavassini M;Calmy A;Dolina M;Frei R;Janssens JP;Borrell S;Stucki D;Schrenzel J;Böttger EC;Gagneux S;Swiss HIV Cohort and Molecular Epidemiology of Tuberculosis Study Groups
结核分枝杆菌的系统发育地理学种群结构表明其对同域人类种群的局部适应。我们假设，导致免疫缺陷的艾滋病毒感染将改变结核分枝杆菌与其人类宿主之间的同域关系。为了检验这一假设，我们于 2000 年至 2008 年间在瑞士对 HIV 感染者和 HIV 阴性结核病 (TB) 患者进行了一项为期九年的全国性分子流行病学研究。我们分析了 518 名结核病患者，其中 112 名 (21.6%) 感染了 HIV，233 名 (45.0%) 出生在欧洲。我们发现，在欧洲出生的结核病患者中，与异域宿主-病原体组合相比，近期传播更有可能发生在同域传播（调整后的比值比 [OR] 7.5，95% 置信区间 [95% CI] 1.21–无穷大，p = 0.03）。 HIV 感染与异域（而非同域）结核分枝杆菌谱系引起的结核病显着相关（OR 7.0，95% CI 2.5–19.1，p<0.0001）。在调整频繁旅行、与外国人接触、年龄、性别和出生国家后，这种关联仍然存在（调整后 OR 5.6，95% CI 1.5–20.8，p = 0.01）。此外，随着 CD4 T 细胞耗竭所定义的免疫抑制程度的增加，它变得更强，而不是 HIV 感染者社会融合增加的结果。我们的观察结果在 1991 年至 2011 年间在伯尔尼州进行的一项基于人群的研究中收集的 440 株结核分枝杆菌菌株的第二个独立小组中得到了重复。总而言之，这些发现支持了一种结核病模型，其中人类宿主与其本地适应的结核分枝杆菌之间的稳定关系被 HIV 感染破坏。由结核分枝杆菌引起的人类结核病 (TB) 每年导致 150 万人死亡。结核分枝杆菌已经影响人类数千年，这表明不同的菌株谱系可能适应特定的人群。特定菌株谱系及其相应患者群体的组合可分为同域谱系（例如欧洲人中的欧美谱系）或异域谱系（例如欧洲人中的东亚谱系）。我们假设，人类免疫缺陷病毒（HIV）感染会损害人类免疫系统，从而干扰这种宿主与病原体的关系。 2000 年至 2008 年间，我们在瑞士对 HIV 感染者和 HIV 阴性结核病患者进行了一项全国范围的分子流行病学研究。我们发现，在欧洲出生的患者中，艾滋病毒感染与适应性较差的异域血统有关，而这不能用社会或其他患者因素（例如艾滋病毒感染者的社会融合程度增加）来解释。引人注目的是，在免疫缺陷更明显的患者中，HIV 感染与适应性较差的结核分枝杆菌谱系之间的关联性更强。我们的观察结果在伯尔尼州一项基于人群的研究中收集的第二个独立的结核分枝杆菌菌株组中得到了重复。总之，我们的研究提供了证据，表明艾滋病毒感染破坏了结核病中的同域宿主-病原体关系。
The phylogeographic population structure of Mycobacterium tuberculosis suggests local adaptation to sympatric human populations. We hypothesized that HIV infection, which induces immunodeficiency, will alter the sympatric relationship between M. tuberculosis and its human host. To test this hypothesis, we performed a nine-year nation-wide molecular-epidemiological study of HIV–infected and HIV–negative patients with tuberculosis (TB) between 2000 and 2008 in Switzerland. We analyzed 518 TB patients of whom 112 (21.6%) were HIV–infected and 233 (45.0%) were born in Europe. We found that among European-born TB patients, recent transmission was more likely to occur in sympatric compared to allopatric host–pathogen combinations (adjusted odds ratio [OR] 7.5, 95% confidence interval [95% CI] 1.21–infinity, p = 0.03). HIV infection was significantly associated with TB caused by an allopatric (as opposed to sympatric) M. tuberculosis lineage (OR 7.0, 95% CI 2.5–19.1, p<0.0001). This association remained when adjusting for frequent travelling, contact with foreigners, age, sex, and country of birth (adjusted OR 5.6, 95% CI 1.5–20.8, p = 0.01). Moreover, it became stronger with greater immunosuppression as defined by CD4 T-cell depletion and was not the result of increased social mixing in HIV–infected patients. Our observation was replicated in a second independent panel of 440 M. tuberculosis strains collected during a population-based study in the Canton of Bern between 1991 and 2011. In summary, these findings support a model for TB in which the stable relationship between the human host and its locally adapted M. tuberculosis is disrupted by HIV infection. Human tuberculosis (TB) caused by Mycobacterium tuberculosis kills 1.5 million people each year. M. tuberculosis has been affecting humans for millennia, suggesting that different strain lineages may be adapted to specific human populations. The combination of a particular strain lineage and its corresponding patient population can be classified as sympatric (e.g. Euro-American lineage in Europeans) or allopatric (e.g. East-Asian lineage in Europeans). We hypothesized that infection with the human immunodeficiency virus (HIV), which impairs the human immune system, will interfere with this host–pathogen relationship. We performed a nation-wide molecular-epidemiological study of HIV–infected and HIV–negative TB patients between 2000 and 2008 in Switzerland. We found that HIV infection was associated with the less adapted allopatric lineages among patients born in Europe, and this was not explained by social or other patient factors such as increased social mixing in HIV–infected individuals. Strikingly, the association between HIV infection and less adapted M. tuberculosis lineages was stronger in patients with more pronounced immunodeficiency. Our observation was replicated in a second independent panel of M. tuberculosis strains collected during a population-based study in the Canton of Bern. In summary, our study provides evidence that the sympatric host–pathogen relationship in TB is disrupted by HIV infection.
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低发病率国家艾滋病毒阴性和艾滋病毒感染者的结核病：临床特征和治疗结果。
影响因子：
3.7
作者：
Fenner L;Gagneux S;Janssens JP;Fehr J;Cavassini M;Hoffmann M;Bernasconi E;Schrenzel J;Bodmer T;Böttger EC;Helbling P;Egger M;Swiss HIV Cohort and Molecular Epidemiology of Tuberculosis Study Groups
通讯作者：
Swiss HIV Cohort and Molecular Epidemiology of Tuberculosis Study Groups
影响因子：
56.9
作者：
Falush, D;Wirth, T;Suerbaum, S
通讯作者：
Suerbaum, S
结核分枝杆菌复杂的遗传多样性：挖掘第四个国际螺旋型数据库（SpoldB4），用于分类，种群遗传学和流行病学。
影响因子：
4.2
作者：
Brudey K;Driscoll JR;Rigouts L;Prodinger WM;Gori A;Al-Hajoj SA;Allix C;Aristimuño L;Arora J;Baumanis V;Binder L;Cafrune P;Cataldi A;Cheong S;Diel R;Ellermeier C;Evans JT;Fauville-Dufaux M;Ferdinand S;Garcia de Viedma D;Garzelli C;Gazzola L;Gomes HM;Guttierez MC;Hawkey PM;van Helden PD;Kadival GV;Kreiswirth BN;Kremer K;Kubin M;Kulkarni SP;Liens B;Lillebaek T;Ho ML;Martin C;Martin C;Mokrousov I;Narvskaïa O;Ngeow YF;Naumann L;Niemann S;Parwati I;Rahim Z;Rasolofo-Razanamparany V;Rasolonavalona T;Rossetti ML;Rüsch-Gerdes S;Sajduda A;Samper S;Shemyakin IG;Singh UB;Somoskovi A;Skuce RA;van Soolingen D;Streicher EM;Suffys PN;Tortoli E;Tracevska T;Vincent V;Victor TC;Warren RM;Yap SF;Zaman K;Portaels F;Rastogi N;Sola C
通讯作者：
Sola C
影响因子：
6.7
作者：
Caws M;Thwaites G;Dunstan S;Hawn TR;Lan NT;Thuong NT;Stepniewska K;Huyen MN;Bang ND;Loc TH;Gagneux S;van Soolingen D;Kremer K;van der Sande M;Small P;Anh PT;Chinh NT;Quy HT;Duyen NT;Tho DQ;Hieu NT;Torok E;Hien TT;Dung NH;Nhu NT;Duy PM;van Vinh Chau N;Farrar J
通讯作者：
Farrar J
影响因子：
11.8
作者：
Baker L;Brown T;Maiden MC;Drobniewski F
通讯作者：
Drobniewski F