Wei Xue-Mei, Xu Hua-Feng, Cheng Xue-Di, Bu Nan, Zhou Hai-Zhou
Department of Laboratory Diagnosis, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang, 150001, People's Republic of China.
Department of Laboratory Diagnosis, Heilongjiang Provincial Hospital, Harbin, Heilongjiang, 150081, People's Republic of China.
Arch Virol. 2017 Mar;162(3):637-643. doi: 10.1007/s00705-016-3138-7. Epub 2016 Nov 5.
Human immunodeficiency virus subtype 1B (HIV-1B) binds to the CD4 receptor and co-receptor CCR5 or CXCR4 to enter T lymphocytes. The amino acid sequence of the HIV envelope glycoprotein V3 region determines the co-receptor tropism, thereby influencing the infectivity of the virus. Our research group previously found that the amino acid at position 22 of the V3 region may affect the infectivity of the virus, and in this study, we tested this hypothesis. We constructed pseudoviruses by changing the amino acids at position 22 of the V3 region in CCR5-tropic and CXCR4-tropic viruses and tested their infectivity. When the amino acid at V3 position 22 was altered in the CCR5- and CXCR4-tropic viruses, their ability to infect cells decreased to 20.6% and 17.14%, respectively. Therefore, we propose that residue 22 in the V3 region of subtype HIV-1B significantly influences the infectivity of the virus.
人类免疫缺陷病毒1B型（HIV-1B）与CD4受体及共受体CCR5或CXCR4结合，从而进入T淋巴细胞。HIV包膜糖蛋白V3区的氨基酸序列决定了共受体嗜性，进而影响病毒的感染性。我们的研究小组之前发现V3区第22位的氨基酸可能影响病毒的感染性，在本研究中，我们对这一假设进行了验证。我们通过改变CCR5嗜性和CXCR4嗜性病毒V3区第22位的氨基酸构建了假病毒，并检测了它们的感染性。当CCR5嗜性和CXCR4嗜性病毒V3区第22位的氨基酸发生改变时，它们感染细胞的能力分别降至20.6%和17.14%。因此，我们提出HIV-1B亚型V3区的第22位残基显著影响病毒的感染性。
