Knockdown of ERM family member moesin in host cells increases HIV type 1 replication.

Abstract

Moesin is a member of the ERM (ezrin, radixin, moesin) family of cytoskeleton/membrane structure organizing and signal transduction proteins. Previously, we found an increased expression of moesin during HIV-1 infection. Moesin was also reported to be incorporated into HIV-1 virions. To analyze whether moesin is a host factor affecting the replication cycle of human immunodeficiency virus type 1 (HIV-1), we used small interfering RNAs (siRNAs) to evaluate the effect of moesin knockdown on HIV-1 replication in P4-CCR5 cells. Moesin's knockdown did not affect the cell viability or cell phenotype. Interestingly, we observed a marked increase in viral replication, as demonstrated by enhanced HIV-1 RNA, p24 antigen, and ß-galactosidase reporter expression. Moesin-dependent enhancement of HIV-1 replication was confirmed in lymphocytic host cells (Jurkat). These results suggest an overall rather restrictive role of moesin for HIV-1 replication in host cells in vitro.

• Authors: Gianni Capalbo, Thea Mueller-Kuller, Sandra Markovic, Stefan A Klein, Ursula Dietrich, Dieter Hoelzer, Oliver G Ottmann, Urban J Scheuring
• Journal: AIDS research and human retroviruses (AIDS Res Hum Retroviruses) Vol. 27 Issue 12 Pg. 1317-22 (Dec 2011) ISSN: 1931-8405 [Electronic] United States
• PMID: 21486194 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Microfilament Proteins
• RNA, Small Interfering
• moesin
• Interferon-beta

Topics

• HIV Long Terminal Repeat
• HIV-1 (physiology)
• HeLa Cells
• Humans
• Interferon-beta (pharmacology)
• Microfilament Proteins (physiology)
• RNA, Small Interfering (genetics)
• Virus Replication