human immunodeficiency virus type-1 (HIV-1);
reverse transcriptase;
host factor;
D O I:
10.1248/bpb.28.893
中图分类号:
R9 [药学];
学科分类号:
1007 ;
摘要:
Infection of human cell with human immunodeficiency virus type-1 (HIV-1) was suppressed by cellular genetic factor(s) at reverse transcription step. Although same amount of virus adsorbed on both cells, small amount of HIV-1 (11113 strain) infected HeLa (MAGI/CCR5) cell, while large amount of RIV-1 infected HOS (GHOST/CXCR4) cell. Regulation of virus replication at postentry level by cellular factor(s) had an important role for low efficiency of RIV-1 infection to MAGI/CCR5 cell. Provirus DNA formation in MAGI/CCR5 cell was less efficient than in GHOST/CXCR4 cell. Once GHOST/CXCR4 cell was fused with MAGI/CCR5 cell, susceptibility against HIV-1 decreased. Further, HIV-1 reverse transcriptase (RT) activity was strongly inhibited by cytosolic protein, derived from MAGI/CCR5 cell, in vitro. This research cleared a certain human cell genetically carries some factor(s) which inhibits the activity of HIV-1 RT.
机构:
VANDERBILT UNIV, MED CTR, SCH MED, MED CTR N, DEPT PATHOL, C-3321, NASHVILLE, TN 37232 USAVANDERBILT UNIV, MED CTR, SCH MED, MED CTR N, DEPT PATHOL, C-3321, NASHVILLE, TN 37232 USA
ROBINSON, WE
MONTEFIORI, DC
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机构:
VANDERBILT UNIV, MED CTR, SCH MED, MED CTR N, DEPT PATHOL, C-3321, NASHVILLE, TN 37232 USAVANDERBILT UNIV, MED CTR, SCH MED, MED CTR N, DEPT PATHOL, C-3321, NASHVILLE, TN 37232 USA
MONTEFIORI, DC
MITCHELL, WM
论文数: 0引用数: 0
h-index: 0
机构:
VANDERBILT UNIV, MED CTR, SCH MED, MED CTR N, DEPT PATHOL, C-3321, NASHVILLE, TN 37232 USAVANDERBILT UNIV, MED CTR, SCH MED, MED CTR N, DEPT PATHOL, C-3321, NASHVILLE, TN 37232 USA