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Journal of Virology, May 2001, p. 4649-4654, Vol. 75, No. 10
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.10.4649-4654.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Passive Transfer of Antibodies Protects Immunocompetent and Immunodeficient Mice against Lethal Ebola Virus Infection without Complete Inhibition of Viral Replication

Manisha Gupta,1,2 Siddhartha Mahanty,1 Mike Bray,3 Rafi Ahmed,2 and Pierre E. Rollin1,*

Special Pathogens Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention,1 and Emory Vaccine Center, Emory University,2 Atlanta, Georgia, and U.S. Army Research Institute for Infectious Diseases, Frederick, Maryland3

Received 10 November 2000/Accepted 20 February 2001

Ebola hemorrhagic fever is a severe, usually fatal illness caused by Ebola virus, a member of the filovirus family. The use of nonhomologous immune serum in animal studies and blood from survivors in two anecdotal reports of Ebola hemorrhagic fever in humans has shown promise, but the efficacy of these treatments has not been demonstrated definitively. We have evaluated the protective efficacy of polyclonal immune serum in a mouse model of Ebola virus infection. Our results demonstrate that mice infected subcutaneously with live Ebola virus survive infection and generate high levels of anti-Ebola virus immunoglobulin G (IgG). Passive transfer of immune serum from these mice before challenge protected upto 100% of naive mice against lethal Ebola virus infection. Protection correlated with the level of anti-Ebola virus IgG titers, and passive treatment with high-titer antiserum was associated with a delay in the peak of viral replication. Transfer of immune serum to SCID mice resulted in 100% survival after lethal challenge with Ebola virus, indicating that antibodies alone can protect from lethal disease. Thus antibodies suppress or delay viral growth, provide protection against lethal Ebola virus infection, and may not require participation of other immune components for protection.

* Corresponding author. Mailing address: Special Pathogens Branch, DVRD, Centers for Disease Control and Prevention, Mailstop G14, 1600 Clifton Rd. N. E., Atlanta, GA 30333. Phone: (404) 639-1124. Fax: (404) 639-1118. E-mail: pyr3{at}cdc.gov.

Journal of Virology, May 2001, p. 4649-4654, Vol. 75, No. 10
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.10.4649-4654.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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