Fundação Oswaldo Cruz; Campo Grande, Mato Grosso do Sul, Brazil.
Laboratório de Diagnóstico de Doenças Infecciosas por Técnicas de Biologia Molecular, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, São Paulo, Brazil.
PLoS Negl Trop Dis. 2022 Mar 30;16(3):e0010317. doi: 10.1371/journal.pntd.0010317. eCollection 2022 Mar.
Chagas disease also known as American trypanosomiasis, is caused by Trypanosoma cruzi and transmitted by triatominae-contaminated feces. It is considered a neglected tropical disease that affects 6 to 7 million people worldwide. The reactivation of Chagas disease occurs when the chronically infected hosts are not able to control T. cruzi infection, generating recurrence of the acute phase. HIV is the main immunosuppressive infection that can lead to the reactivation of chronic Chagas disease in AIDS conditions. In co-infected patients, the reactivation of Chagas disease is related to their high parasite load, high HIV viral load, and CD4 T-cell counting less than 200/mm3, which may evolve to meningoencephalitis and myocarditis. Eight T. cruzi/HIV co-infected patients under antiretroviral therapy (ART) and ten Chagas disease patients without HIV infection that attended at Study Group of Chagas Disease, Hospital de Clínicas, University of Campinas (GEdoCh/HC/UNICAMP-SP) and Pontifical Catholic University of Campinas SP (PUCC/SP) were evaluated. Tests for Chagas disease were performed, such as qPCR and T. cruzi blood culture. The patient's medical records were analyzed to verify clinical and epidemiological data, viral load, and CD4 T-cell counting since the outset of ART. For both groups, we found no statically significant differences between parasite load via blood culture and qPCR. In T. cruzi/HIV co-infected subjects, we observed a significant increase of CD4 T-cells counting and viral load decrease, which became undetectable over the years after ART. Parasites isolated from the patient's blood culture were genotyped, being the majority of them infected with TcII and one case of mixed infection (TcII and TcV/TcVI). These results were expected according to the region of origin of the patients. We suggest that the parasite load be monitored through qPCR in T.cruzi/HIV co-infected patients. We conclude that ART in people living with HIV improves infection and immunosuppression control, enabling the natural evolution of the American trypanosomiasis.
恰加斯病，又称美洲锥虫病，由克氏锥虫引起，通过受污染的粪便传播。它被认为是一种被忽视的热带病，影响全球 600 至 700 万人。当慢性感染的宿主无法控制克氏锥虫感染时，恰加斯病会复发。HIV 是主要的免疫抑制性感染，可导致艾滋病条件下慢性恰加斯病的再激活。在合并感染的患者中，恰加斯病的再激活与寄生虫负荷高、HIV 病毒载量高、CD4 T 细胞计数低于 200/mm3 有关，可能发展为脑膜脑炎和心肌炎。8 名接受抗逆转录病毒治疗（ART）的克氏锥虫/HIV 合并感染患者和 10 名未感染 HIV 的恰加斯病患者在坎皮纳斯大学临床医院恰加斯病研究组（GEdoCh/HC/UNICAMP-SP）和坎皮纳斯天主教大学（PUCC/SP）接受了评估。进行了恰加斯病检测，如 qPCR 和克氏锥虫血液培养。分析了患者的病历，以验证自开始接受 ART 以来的临床和流行病学数据、病毒载量和 CD4 T 细胞计数。对于两组患者，我们发现血液培养和 qPCR 的寄生虫负荷之间没有统计学上的显著差异。在克氏锥虫/HIV 合并感染的患者中，我们观察到 CD4 T 细胞计数显著增加，病毒载量下降，在接受 ART 多年后检测不到。从患者血液培养中分离的寄生虫进行了基因分型，其中大多数感染了 TcII，一例混合感染（TcII 和 TcV/TcVI）。根据患者的来源地区，我们预计会出现这些结果。我们建议在克氏锥虫/HIV 合并感染患者中通过 qPCR 监测寄生虫负荷。我们得出结论，接受 HIV 感染者的 ART 改善了感染和免疫抑制控制，使美洲锥虫病的自然演变成为可能。
