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Strain-specific differences in LFA-1 induction on measles virus-infected monocytes and adhesion and viral
K B Hummel1, W J Bellini, M K Offermann
1Respiratory and Enteric Viruses Branch, Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA. kbh2@cdc.gov
Abstract:
Measles virus (MV) infection of monocytes induces leukocyte function-associated antigen-1 (LFA-1), an integrin that mediates intercellular adhesion to the endothelium. Thus, an increase in LFA-1 expression could lead to enhanced monocyte adherence and virus dissemination to endothelial cells (ECs) and potentially be an important means of distinction between MV strains. We identified both vaccine and wild-type strains that induced LFA-1 and others that failed to induce. Although adhesion of MV-infected monocytes and viral transmission to ECs was demonstrated, strain-specific differences were not correlated with LFA-1 induction. MV infection of ECs was dramatically reduced in the absence of cell contact, suggesting virus dissemination by cell-cell transmission.
Insights
Measles virus (MV) infection can increase leukocyte function-associated antigen-1 (LFA-1) on monocytes, potentially aiding virus spread. However, strain differences in LFA-1 induction did not correlate with enhanced monocyte adhesion or transmission to endothelial cells.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Measles virus (MV) infects monocytes, potentially altering their adhesion properties.
- Leukocyte function-associated antigen-1 (LFA-1) is an integrin crucial for cell adhesion to endothelium.
- LFA-1 induction by MV could influence monocyte adherence and virus dissemination.
Purpose of the Study:
- To investigate whether MV infection induces LFA-1 expression in monocytes.
- To determine if LFA-1 induction correlates with enhanced monocyte adherence and transmission to endothelial cells (ECs).
- To explore potential strain-specific differences in LFA-1 induction and their impact on MV dissemination.
Main Methods:
- Infection of monocytes with vaccine and wild-type MV strains.
- Assessment of LFA-1 expression on infected monocytes.
- Evaluation of monocyte adhesion to ECs and viral transmission.
- Comparison of LFA-1 induction and transmission across different MV strains.
Main Results:
- Both vaccine and wild-type MV strains were identified that either induced or failed to induce LFA-1.
- Adhesion of MV-infected monocytes and viral transmission to ECs were observed.
- No correlation was found between LFA-1 induction and strain-specific differences in monocyte adhesion or viral transmission.
- MV infection of ECs was significantly reduced without cell contact, indicating cell-cell transmission.
Conclusions:
- MV infection can induce LFA-1 on monocytes, but this does not consistently enhance monocyte adherence or transmission to ECs.
- Virus dissemination appears to occur primarily through cell-cell transmission, rather than solely via LFA-1 mediated adhesion.
- The role of LFA-1 in MV pathogenesis may be complex and not directly linked to strain-specific dissemination efficiency.