When looking for a cure for HIV, scientists are turning to our closest genetic relative: monkeys. Monkeys can be infected with HIV, but there is one key difference when compared with their human counterparts: HIV doesn’t often replicate in monkeys. There are several restriction factors that prevent replication of HIV-1 in primates, namely TRIMCyp, a fusion protein. This protein developed independently in Old World monkeys and in owl monkeys. However, TRIMCyp in Old World monkeys differs from that in owl monkeys in that the former lacks exon7. Interestingly, in Old World monkeys TRIMCyps is unable to restrict HIV-1 activity. Therefore, LIU Feng Liang and researchers surmised that exon7 might play a role in restricting HIV-1 activity.

LIU Feng Liang, under the supervision of ZHENG Yong Tang, discovered that exon7 affected multimer assembly and the formation of cytoplasmic bodies, and therefore the function of TRIMCyp. They used rhesus macaques as a model to study the effects of removing exon7 from Old World monkey TRIMCyps. They results showed that the cytoplasmic bodies and multimers of owl monkey TRIMCyp (omTRIMCyp) were significantly different from those of northern pig-tailed macaque TRIMCyp (npmTRIMCyp), and that exon7 deletion affected the development of the cytoplasmic bodies and multimerization. However, further research demonstrated that these changes did not contribute to the ability of TRIMCyp to restrict HIV-1. However, they did find that monomeric TRIMCyp can play a role in restricting HIV-1 when it can bind to HIV-1.

The article “The Effect of Exon 7 Deletion during the Evolution of TRIMCyp Fusion Proteins on Viral Restriction, Cytoplasmic Body Formation and Multimerization” was recently published in PLoS One. The full-text is available online at: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0121666