Lipopolysaccharide suppresses human immunodeficiency virus 1 reverse transcription in macrophages
Autor: | Feng-Liang Liu, Dan Mu, Jia-Wu Zhu, Yong-Tang Zheng |
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Rok vydání: | 2016 |
Předmět: |
Lipopolysaccharides
0301 basic medicine Lipopolysaccharide Human immunodeficiency virus (HIV) Biology medicine.disease_cause Antiviral Agents Virus Cell Line 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation Virology medicine Humans Immunologic Factors Macrophage Macrophages virus diseases Reverse Transcription Vesiculovirus General Medicine Reverse transcriptase 030104 developmental biology chemistry Cell culture HIV-1 030215 immunology |
Zdroj: | Archives of Virology. 161:3019-3027 |
ISSN: | 1432-8798 0304-8608 |
DOI: | 10.1007/s00705-016-3000-y |
Popis: | HIV-1-infected macrophages are long-lived and act as human immunodeficiency virus 1 (HIV-1) virus reservoirs. Lipopolysaccharide (LPS) has been demonstrated to suppress HIV-1 replication in macrophages, but the mechanism is not clear. Previous research suggested that downregulation of CD4 and CCR5 as well as blockage of the interaction of HIV-1 with cells are major causes of inhibition of HIV-1 replication in macrophages by LPS. In order to study whether LPS blocks the post-entry event of HIV-1 replication, we developed a macrophage HIV-1 infection model by using VSV-G pseudotyped HIV-1-luciferase virus to infect THP-1 differentiated macrophage-like cells. We found that LPS can suppress HIV-1 replication at post-entry steps. Further study suggested that HIV-1 reverse transcription was blocked by LPS, but addition of exogenous deoxyribonucleosides led to only partial recovery of HIV-1 replication. However, the inhibition of pro-inflammatory pathway completely rescued HIV-1 replication. Thus, our study shows that LPS can suppress the events of HIV-1 replication post-entry, including reverse transcription, and this restriction is mediated by more than one mechanism. |
Databáze: | OpenAIRE |
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