Hattori Junko, Okumura Naoya, Yamazaki Yumiko, Uchiyama Masataka, Hamaguchi Motohiro, Nishiyama Yukihiro, Kaneda Tsuguhiro
Clinical Research Center, National Hospital Organization Nagoya Medical Center (Tokai Area Central Hospital for AIDS Treatment and Research), Nagoya, Aichi, Japan.
Microbiol Immunol. 2007;51(2):193-200. doi: 10.1111/j.1348-0421.2007.tb03901.x.
Several reports have documented a better prognosis for HIV-1-infected patients co-infected with GBV-C, while other reports have contradicted such findings with the result that this issue remains controversial. We attempted to clarify the complicated status of the effect of GBV-C co-infection on HIV-1-infected patients. GBV-C RNA was detected in 37 samples in 182 HIV-1-infected patients (20.3%) using RT/nested PCR. Of these, 3 were determined to be GBV-C genotype 1, 12 were genotype 2, and the remaining 22 were genotype 3. The GBV-C viral load quantified by real-time PCR ranged from 7.8x10(3) to 3.3x10(6) copies/ml. Weakly negative correlation was observed between GBV-C viral load and HIV-1 viral load in 19 HAART-naïve patients, indicating that a higher GBV-C viral load is associated with a greater suppression of HIV-1 replication. A previously published in vitro study suggested that GBV-C infection would induce up-regulation of RANTES, leading to suppression of HIV-1 replication. However, in our present study, the blood RANTES level was significantly lower in the GBV-C co-infected group than in the uninfected group (190-9,959 vs. 264-31,038 pg/ml, P=0.004). Our results suggested that a suppression of HIV-1 replication by GBV-C co-infection is not mediated by up-regulated RANTES, and thus call for another as yet unknown factor.
有几份报告记录了合并感染GBV-C的HIV-1感染患者预后较好，而其他报告则与这些发现相矛盾，因此这个问题仍然存在争议。我们试图阐明GBV-C合并感染对HIV-1感染患者影响的复杂情况。使用RT/巢式PCR在182例HIV-1感染患者的37份样本中检测到GBV-C RNA（20.3%）。其中，3份被确定为GBV-C基因型1，12份为基因型2，其余22份为基因型3。通过实时PCR定量的GBV-C病毒载量范围为7.8x10(3)至3.3x10(6)拷贝/毫升。在19例未接受高效抗逆转录病毒治疗（HAART）的患者中，观察到GBV-C病毒载量与HIV-1病毒载量之间存在弱负相关，这表明较高的GBV-C病毒载量与对HIV-1复制的更大抑制相关。先前发表的一项体外研究表明，GBV-C感染会诱导调节激活正常T细胞表达和分泌的趋化因子（RANTES）上调，从而导致HIV-1复制受到抑制。然而，在我们目前的研究中，GBV-C合并感染组的血液RANTES水平显著低于未感染组（190 - 9959对264 - 31038 pg/ml，P = 0.004）。我们的结果表明，GBV-C合并感染对HIV-1复制的抑制不是由RANTES上调介导的，因此需要另一个未知因素。
