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The entry into host cells of Sindbis virus, vesicular stomatitis virus and Sendai virus
Abstract:
We have compared the mechanisms of entry into host cells of three enveloped viruses: Sendai virus, vesicular stomatitis virus (VSV) and Sindbis virus. Virus entry by membrane fusion should antigenically modify the surface of a newly infected cell in such a way that it will be killed by anti-viral antibody and complement. On the other hand, virus entry by a mechanism involving uptake by the cell of the whole virion should not make cells sensitive to antibody and complement. As expected, cells newly infected with Sendai virus were readily and completely lysed by anti-Sendai antibody and complement. In marked contrast, however, cells newly infected with either Sindbis virus or VSV were killed by anti-viral antibody and complement only when infected at an extremely high multiplicity of infection, in excess of 1000 plaque-forming units per cell. We favor the following explanation for these results with Sindbis virus and VSV: a very large majority of the Sindbis and VSV virions entered the infected cells by some means other than membrane fusion, presumably engulfment of the whole particle. Efficient entry by way of membrane fusion may therefore not be a general characteristic of enveloped viruses.
Insights
Sendai virus enters host cells via membrane fusion, making them susceptible to antibody and complement. Sindbis virus and vesicular stomatitis virus (VSV) primarily use engulfment, evading this immune response.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Enveloped viruses utilize diverse mechanisms to enter host cells.
- Host cell entry is a critical step in viral replication and pathogenesis.
- Understanding viral entry mechanisms informs antiviral strategies.
Purpose of the Study:
- To compare host cell entry mechanisms of three enveloped viruses: Sendai virus, vesicular stomatitis virus (VSV), and Sindbis virus.
- To determine if membrane fusion is a general characteristic of enveloped virus entry.
- To investigate the immunological consequences of different viral entry pathways.
Main Methods:
- Infection of host cells with Sendai virus, VSV, and Sindbis virus at varying multiplicities of infection.
- Assessment of host cell susceptibility to lysis by antiviral antibody and complement following infection.
- Analysis of viral entry pathways based on observed immunological responses.
Main Results:
- Cells infected with Sendai virus were readily lysed by antibody and complement, consistent with membrane fusion entry.
- Cells infected with Sindbis virus or VSV showed significant resistance to antibody and complement-mediated lysis.
- Resistance to lysis in Sindbis virus and VSV infected cells was overcome only at very high infection multiplicities, suggesting alternative entry mechanisms.
Conclusions:
- Sendai virus entry involves membrane fusion, leading to cell surface antigen modification and immune-mediated lysis.
- Sindbis virus and VSV predominantly enter host cells via a non-fusion mechanism, likely engulfment.
- Efficient membrane fusion entry is not a universal characteristic of all enveloped viruses.
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