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| Content Provider | Springer Nature Link |
|---|---|
| Author | Liu, Feng Liang Zhu, Jia Wu Mu, Dan Zheng, Yong Tang |
| Copyright Year | 2016 |
| Abstract | 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. |
| Starting Page | 3019 |
| Ending Page | 3027 |
| Page Count | 9 |
| File Format | |
| ISSN | 03048608 |
| Journal | Archives of Virology |
| Volume Number | 161 |
| Issue Number | 11 |
| e-ISSN | 14328798 |
| Language | English |
| Publisher | Springer Vienna |
| Publisher Date | 2016-08-04 |
| Publisher Place | Vienna |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Virology Medical Microbiology Infectious Diseases |
| Content Type | Text |
| Resource Type | Article |
| Subject | Virology Medicine |
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