Mice Transgenic For ELR1and Equine Cyclin T1Are Susceptible To EIAV Infection

The biological factor other than receptors specifically used by viruses is a major determinant of viral tropism, and provides an important target for antibodies and drugs to block virus infection. Although ELR1was identified initially as the receptor for EIAV, transduced NIH3T3(ELR1) cells supported the early steps of EIAV replication, from infection to provirus integration, but not for productive virus replication. Further studies suggesting that NIH3T3cells expressing the EIAV receptor ELR1and equine cyclin T1(e-cycT1) supported replication of EIAV and produced infectious virions at levels similar to those found in a reference permissive equine cell line.Here, we ascertain whether expression of ELR1and e-cycT1is sufficient to make mice support productive replication of EIAV and there are other restrictions for EIAV replication in vivo, and represent a new model for understanding lentivirus tropism and pathogenesis.Using pronuclear microinjection, we established the mice transgenic for ELR1and equine cyclin T1. PCR, Real time quantitative PCR, Fisher hybridization in situ, Western blotting, Immunohistochemical method was used to direct the expression of ELR1and equine cyclin T1intransgenic mice and the replication of EIAV after inoculation. As results, ELR1and equine cyclinT1mRNA and protein were detected in intestine, spleen and lymph nodes of transgenic mice. Moreover, EIAV mRNA and protein could detect in these organs. The quantitation of EIAV RNA in the plasma of transgenic mice grew time-dependently after in vivo inoculation, indicating the production of virus particles.In a word, ELR1/e-cycT1mice were established by pronuclear microinjection. ELR1and e-cycT1were expressed in cells of transgenic mice, and EIAV replicated in mice. In addition to providing in vivo verification for the important role of e-cycT1in EIAV infection, ELR1/e-cycT1mice should also prove useful for developing a system in which HIV-1could replicate in mice.