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HEREDITAS(Beijing) ›› 2015, Vol. 37 ›› Issue (5): 480-486.doi: 10.16288/j.yczz.15-004

• Research Articles • Previous Articles     Next Articles

Genetic variance in the HIV-1 founder virus Vpr affects its ability to induce cell cycle G2 arrest and cell apoptosis

Jianyuan Zhao1, 2, Jiwei Ding2, Zeyun Mi2, Jinming Zhou2, Tao Wei1, Shan Cen2   

  1. 1. Department of Food Science, College of Arts & Science of Beijing Union University, Beijing 100192, China;
    2. Institute of Medicinal Biotechnology, Chinese Academy of Medical Science and Peking Union Medical School, Beijing 100050, China
  • Received:2015-01-04 Online:2015-05-20 Published:2015-05-20

Abstract: In the event of acute infection, only a few HIV-1 viral variants can establish the initial productive clinical infection, and these viral variants are known as transmitted/founder viruses (T/F viruses). As one of the accessory proteins of HIV-1, viral protein R (Vpr) plays an important role in viral replication. Therefore, the characterization of T/F virus Vpr is beneficial to understand how virus replicates in a new host. In this study, flow cytometry was used to analyze the effect of G2 arrest and cell apoptosis induced by the T/F virus Vpr and the chronic strain MJ4 Vpr. The results showed that the ability of T/F virus ZM246 Vpr and ZM247 Vpr inducing G2 arrest and cell apoptosis are more potent than the MJ4 Vpr. The comparison of protein sequences indicated that the amino acids of 77, 85 and 94 contain high freqency mutations, suggesting that these sites may be involved in inducing G2 arrest and cell apoptosis. Taken together, our work suggests that in acute infections, T/F viruses increase the capacity of G2 arrest and cell apoptosis and promote viral replication and transmission in a new host by Vpr genetic mutation.

Key words: HIV-1, founder virus, Vpr, cell G2 arrest, cell apoptosis