Kiyingi Herbert Samuel, Egwang Thomas Gordon, Nannyonga Maria
Homecare Department, St. Raphael of St. Francis Nsambya Hospital/Elizabeth Glaser Pediatric AIDS Foundation Collaboration, Centers for Disease Control and Prevention, Uganda.
Pan Afr Med J. 2010;7:11. Epub 2010 Nov 9.
Malaria and HIV-1 infection cause significant morbidity and mortality in children in sub-Saharan Africa. Recurrent malaria infection increases HIV-1 viral load in adults and increases the rate of progression of HIV-1 infection to AIDS. The effect of malaria on viral loads in children living with AIDS (CLWA) is not clearly known.
One hundred thirty five afebrile HIV-1 positive children having negative blood slides for malaria were recruited at Apac Hospital and followed up for one year. They were monitored for development of Plasmodium falciparum malaria, which was treated with chloroquine (CQ) + sulfadoxine-pyrimethamine (SP) and the children followed up for 28 days. HIV-1 viral loads were measured over three time-points: at enrolment (no malaria), during an episode of malaria, and at a visit about 8 weeks (range 6-19 weeks) after the malaria visit when the child had neither parasites nor any intervening malaria episodes (post-malaria). Primary analyses were restricted to children who on follow up had HIV-1 viral loads measured at the three relevant time-points.
Malaria increased HIV-1 viral load significantly in CLWA. Low parasitemia (200-4000/Cl) transiently increased viral load by 0.42 log (95% CI 0.29-0.78, p = 0.0002), higher than that reported in adults. These patients' viral loads returned to levels similar to those at baseline after treatment. In 13 patients with high parasitemia (>4000/Cl), the mean increase in viral load was 0.53 log (95% CI 0.14 to 0.51), p<0.0001, remaining significantly higher than at baseline after treatment i.e. mean difference (signed-rank test) in viral load "before" and "after" malaria was significant.
Plasmodium falciparum malaria is associated with increasing HIV-1 viral loads in children, with some viral loads remaining significantly elevated several weeks after antimalarial treatment. Prolonged post-treatment elevation has important implications for the clinical course in pre-ART HIV-1 positive children and the potential for transmission in sexually active adults.
疟疾和HIV-1感染在撒哈拉以南非洲地区的儿童中导致了严重的发病和死亡。反复的疟疾感染会增加成人的HIV-1病毒载量,并加快HIV-1感染向艾滋病的进展速度。疟疾对艾滋病患儿(CLWA)病毒载量的影响尚不清楚。
在阿帕克医院招募了135名无发热、HIV-1阳性且疟原虫血涂片检查呈阴性的儿童,并对其进行了为期一年的随访。监测他们是否感染恶性疟原虫,若感染则用氯喹(CQ)+磺胺多辛-乙胺嘧啶(SP)进行治疗,并对儿童进行28天的随访。在三个时间点测量HIV-1病毒载量:入组时(无疟疾)、疟疾发作期间以及疟疾就诊后约8周(6-19周)的一次就诊时,此时儿童既无寄生虫也无任何间歇性疟疾发作(疟疾后)。主要分析仅限于在随访中在三个相关时间点测量了HIV-1病毒载量的儿童。
疟疾显著增加了艾滋病患儿的HIV-1病毒载量。低寄生虫血症(200-4000/Cl)使病毒载量短暂增加0.42对数(95%可信区间0.29-0.78,p = 0.0002),高于成人报告的增幅。这些患者的病毒载量在治疗后恢复到与基线水平相似。在13名高寄生虫血症(>4000/Cl)患者中,病毒载量的平均增加为0.53对数(95%可信区间0.14至0.51),p<0.0001,治疗后仍显著高于基线水平,即疟疾“之前”和“之后”病毒载量的平均差异(符号秩检验)显著。
恶性疟原虫疟疾与艾滋病患儿HIV-1病毒载量增加有关,一些病毒载量在抗疟治疗数周后仍显著升高。治疗后病毒载量长期升高对接受抗逆转录病毒治疗前的HIV-1阳性儿童的临床病程以及性活跃成年人的传播可能性具有重要意义。