Transmission is an essential part of the survival strategy of plant viruses. The most common insect vectors for virus transmission are aphids, leafhoppers, and whitefly. Little is known about the molecular process of vector transmission for many viruses, or how the virus isolate variation affects transmission efficacy.Here we examined the effect of the 5`end genes from different isolates of Citrus tristeza virus (CTV) for aphid vector transmission. CTV, which consists of at least 6 different strains, exhibits a variety of different phenotypic characteristics. These strains are VT, T30, T68, T36, T3 and RB, the nucleotide identities change between 80.5-92.4%. The 5`half of the CTV genome is more diverse than 3`end of the genome. To make matters more complex, in addition to these different strains, the rates of aphid transmission are different for different isolates of the strains. CTV encapsidation into long flexuous virions occurs via a complex mechanism involving at least four genes: CPm, CP, Hsp70 homologue and p61.The involvement of the Hsp70h and p61 proteins in aphid transmission has been reported. However, no work has been done to determine if there are replication-associated proteins involved in aphid transmission. We cloned the different 5`end genes from VT, T68, and T30 isolates of CTV into our T36-based infectious clone, which is very poorly transmitted by the aphid vector. Interestingly, interchanging entire 5`half of the genome produced a substantial increase in transmission by the aphid vector, from 0% transmission efficacy to 23.84% with the T68 substitution.