Li Xi, Guo Yaolin, Li Hanping, Huang Xiaofeng, Pei Zhichao, Wang Xiaolin, Liu Yongjian, Jia Lei, Li Tianyi, Bao Zuoyi, Wang Xiaorui, Han Leilei, Han Jingwan, Li Jingyun, Li Lin
State Key Laboratory of Pathogen and Biosecurity, Department of AIDS Research, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
The Second Medical Center, National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China.
Front Microbiol. 2021 May 17;12:662573. doi: 10.3389/fmicb.2021.662573. eCollection 2021.
Human endogenous retroviruses (HERVs) make up ~8% of the human genome, and for millions of years, they have been subject to strict biological regulation. Many HERVs do not participate in normal physiological activities in the body. However, in some pathological conditions, they can be abnormally activated. For example, HIV infection can cause abnormal activation of HERVs, and under different infection conditions, HERV expression may be different. We observed significant differences in HERV-K transcription levels among HIV-1 subtype-infected individuals. The transcriptional levels in the HERV-K region were significantly increased in HIV-1 B subtype-infected patients, while the transcriptional levels in the HERV-K region were significantly increased in CRF01_AE and CRF07_BC subtype-infected patients. , the transcriptional levels of HEVR-K were increased 5-fold and 15-fold in MT2 cells transfected with two different HIV-1 strains (B and CRF01_AE, respectively). However, there was no significant difference in transcriptional levels among regions of HERV-K. When MT2 cells were infected with different subtypes of HIV-1 Tat proteins (B, CRF01_AE), which is constructed by lentiviruses, and the transcription levels of HERV-K were increased 4-fold and 2-fold, respectively. Thus, different subtypes of HIV-1 have different effects on HERV-K transcription levels, which may be caused by many factors, not only Tat protein.
人类内源性逆转录病毒（HERVs）占人类基因组的约8%，数百万年来，它们一直受到严格的生物学调控。许多HERVs不参与体内正常的生理活动。然而，在某些病理情况下，它们可能会被异常激活。例如，HIV感染可导致HERVs的异常激活，并且在不同的感染条件下，HERV的表达可能会有所不同。我们观察到HIV-1亚型感染个体之间HERV-K转录水平存在显著差异。在HIV-1 B亚型感染患者中，HERV-K区域的转录水平显著升高，而在CRF01_AE和CRF07_BC亚型感染患者中，HERV-K区域的转录水平也显著升高。在用两种不同的HIV-1毒株（分别为B和CRF01_AE）转染的MT2细胞中，HEVR-K的转录水平分别增加了5倍和15倍。然而，HERV-K各区域之间的转录水平没有显著差异。当MT2细胞用慢病毒构建的不同亚型的HIV-1 Tat蛋白（B、CRF01_AE）感染时，HERV-K的转录水平分别增加了4倍和2倍。因此，HIV-1的不同亚型对HERV-K转录水平有不同影响，这可能由多种因素引起，而不仅仅是Tat蛋白。
