Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Analysis of the replication of HIV-1 forced to use tRNAMet(i) supports a link between primer selection, translation and encapsidation. | Retrovirology BioMed Central Open Access Analysis of the replication of HIV-1 forced to use tRNAMet i supports a link between primer selection translation and encapsidation Uros V Djekic and Casey D Morrow Address Department of Cell Biology University of Alabama at Birmingham Birmingham Alabama 35294 USA Email Uros V Djekic - uros@ Casey D Morrow - caseym@ Corresponding author Published 2 February 2007 Received I December 2006 Retrovirology 2007 4 10 doi 1742-4690-4-10 Accepted 2 February 2007 This article is available from http content 4 1 10 2007 Djekic and Morrow licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Previous studies have suggested that the process of HIV-1 tRNA primer selection and encapsidation of genomic RNA might be coupled with viral translation. In order to further investigate this relationship proviruses were constructed in which the primer-binding site PBS was altered to be complementary to elongator tRNAMet tRNAMet e HXB2-Met e or initiator tRNAMet tRNAMet i HXB2-Met i . These tRNAMet not only differ with respect to the 3 terminal 18-nucleotides but also with respect to interaction with host cell proteins during protein synthesis. Results Consistent with previous studies HXB2-Met e were infectious and maintained this PBS following short-term in vitro culture in SupT1 cells. In contrast transfection of HBX2-Met i produced reduced amounts of virus as determined by p24 and did not establish a productive infection in SupT1 cells. The low infectivity of the virus with the PBS complementary to tRNAMet i was not due to differences in endogenous levels of cellular tRNAMet i compared to tRNAMet e tRNAMet i was also capable of being selected as the
