As a member of the tumor necrosis factor receptor (TNFR) protein superfamily, equine lentivirus receptor 1 (ELR1) has been shown to be expressed in various equine cells that are permissive for equine infectious anemia virus (EIAV) replication. The EIAV Tat protein (eTat) activates transcription initiated at the viral long terminal repeat (LTR) promoter through a unique mechanism that requires the recruitment of the equine cyclin T1 (eCT1) cofactor into the viral TAR RNA target element. 

According to the explanation of Dr. Wang Xiaojun, the head of the research team of equine infectious diseases and lentivirus infection, in vitro studies have demonstrated that mouse fibroblast cell lines (e.g., NIH 3T3 cells) that express the EIAV receptor ELR1 and eCT1 support the productive replication of EIAV, but it was unclear whether the introduction of these two genes into the mice may result in a permissive environment for EIAV infection and replication in vivo.

For answering this question, Dr. Wang Xiaojun’s team constructed mice transgenic for ELR1 and eCT1, and the results of the related experiments have showed that the transgenic mice are susceptible to EIAV infection and replication. Further, EIAV infection can cause lesions on the spleen and lymph nodes, similar to those frequently observed in horses, the natural hosts. Therefore, ELR1 and eCT1 are essential in vivo for EIAV invasion and replication.

In addition, because it is more expensive to use horses in animal experiments and horse-related antibodies and reagents are not easily obtained, ELR1/eCT1 mice may provide an alternative in vivo infection model for evaluating the effectiveness of candidate EIAV vaccines and for studying the pathobiology of EIAV infection.

(http://www.retrovirology.com/content/12/1/36)

 

（By Cheng Du）