Mani Indu, Gilbert Peter, Sankalé Jean-Louis, Eisen Geoffrey, Mboup Souleymane, Kanki Phyllis J
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
J Virol. 2002 Nov;76(21):10745-55. doi: 10.1128/jvi.76.21.10745-10755.2002.
The human immunodeficiency virus type 1 (HIV-1) viral setpoint during the disease-free interval has been strongly associated with future risk of disease progression. An awareness of the correlation between viral setpoint and HIV-1 genetic evolution over time is important in the understanding of viral dynamics and infection. We examined genetic diversity in HIV-1 CRF02_A/G-IbNG-infected seroincident women in Dakar, Senegal; determined whether a viral setpoint kinetic pattern existed for CRF02_A/G-IbNG during the disease-free interval; and correlated viral load level and diversity. Samples were drawn during the disease-free interval from consenting CRF02_A/G-IbNG-infected, antiretroviral therapy-naïve female commercial sex workers in Dakar, Senegal. Based on sequential plasma RNA values, low and high viral setpoint groups were established. Intrapatient diversity and divergence over time was determined from earlier and later time point DNA samples from each person. Most individuals followed the viral setpoint paradigm. For each 1/-/log(10) copy/ml of plasma increase in viral load, intrapatient diversity increased by 1.4% (P = 0.028). A greater diversification rate was observed in the high viral setpoint group than in the low viral setpoint group (P = 0.01). Greater nucleotide (P = 0.015) and amino acid (P = 0.048) divergences and a greater nucleotide divergence rate (P = 0.03) were found in the high viral setpoint group. There was no difference between the groups in the ratio of the number of nonsynonymous substitutions per nonsynonymous site to the number of synonymous substitutions per synonymous site. The greater intrapatient diversity, divergence, and diversification rates observed in the high viral setpoint group supports the notion that diversity is driven by cycles of viral replication resulting in accumulated mutations. Recognizing diversity potential based on viral load levels in individuals may inform the design of vaccines and therapies.
在无病期,人类免疫缺陷病毒1型(HIV-1)的病毒载量设定点与未来疾病进展风险密切相关。了解病毒载量设定点与HIV-1随时间的基因进化之间的相关性,对于理解病毒动力学和感染至关重要。我们研究了塞内加尔达喀尔感染HIV-1 CRF02_A/G-IbNG的血清学初发女性的基因多样性;确定在无病期CRF02_A/G-IbNG是否存在病毒载量设定点动力学模式;并关联病毒载量水平和多样性。在无病期,从塞内加尔达喀尔同意参与研究的、感染CRF02_A/G-IbNG且未接受抗逆转录病毒治疗的女性商业性工作者中采集样本。根据连续的血浆RNA值,建立了低病毒载量设定点组和高病毒载量设定点组。从每个人早期和晚期的DNA样本中确定患者体内随时间的多样性和差异。大多数个体遵循病毒载量设定点模式。血浆病毒载量每增加1/ - /log(10)拷贝/毫升,患者体内多样性增加1.4%(P = 0.028)。高病毒载量设定点组比低病毒载量设定点组观察到更高的多样化率(P = 0.01)。高病毒载量设定点组中发现更大的核苷酸(P = 0.015)和氨基酸(P = 0.048)差异以及更高的核苷酸差异率(P = 0.03)。两组之间每个非同义位点的非同义替换数与每个同义位点的同义替换数之比没有差异。在高病毒载量设定点组中观察到的更大的患者体内多样性、差异和多样化率支持了这样一种观点,即多样性是由病毒复制循环导致积累突变所驱动的。基于个体病毒载量水平认识多样性潜力可能为疫苗和治疗方法的设计提供信息。