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Actions of complement on Junin virus.

R H Kenyon¹, C J Peters

¹Disease Assessment Division, United States Army Medical Research Institute of Infectious Diseases, Frederick, Maryland 21701-5011.

Reviews of Infectious Diseases

|May 1, 1989

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Normal animal sera inactivated attenuated Junin virus (JV) via complement. Complement plays a dual role in host resistance to Argentine hemorrhagic fever, impacting both virus attenuation and immune neutralization.

Area of Science:

Virology
Immunology
Complement System

Background:

Junin virus (JV) causes Argentine hemorrhagic fever.
The role of complement in JV infectivity and neutralization is not fully understood.

Purpose of the Study:

To investigate the role of complement in the inactivation of Junin virus by normal sera.
To explore complement's function in neutralizing both attenuated and virulent JV strains.

Main Methods:

Inactivation assays using fresh sera from various animal species.
Selective depletion studies to identify the complement pathway involved.
Virus adsorption experiments to assess antibody involvement.
Comparison of virus passaged in different cell lines.

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Main Results:

Normal sera inactivated 90%-99% of attenuated JV strains through the classical complement pathway.
Complement had minimal effect on virulent JV strains.
Virus propagation method influenced susceptibility to complement-mediated inactivation.
Complement was crucial for neutralizing virulent JV strains with immune sera but not attenuated strains.

Conclusions:

Complement activation contributes to the attenuated phenotype of some Junin virus strains.
Complement is essential for efficient in vitro neutralization of virulent JV strains by immune sera.
Complement plays a significant role in host resistance against Argentine hemorrhagic fever.