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Journal of Virology, March 2006, p. 2369-2379, Vol. 80, No. 5
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.5.2369-2379.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Selective Lymphocyte Depletion during the Early Stage of the Immune Response to Foot-and-Mouth Disease Virus Infection in Swine

Fayna Díaz-San Segundo,1,{dagger} Francisco J. Salguero,1,2,{dagger} Ana de Avila,1 M. Mar Fernández de Marco,2 Miguel A. Sánchez-Martín,1 and Noemí Sevilla1,3*

Centro de Investigación en Sanidad Animal, INIA, 28130 Valdeolmos, Madrid, Spain,1 Departamento de Anatomía y A. Patológica Comparadas, Universidad de Córdoba, Campus de Rabanales, 14014 Córdoba, Spain,2 Centro de Biología Molecular Severo Ochoa, Universidad Autónoma de Madrid, Cantoblanco, Madrid 28049, Spain3

Received 31 July 2005/ Accepted 28 November 2005

Foot-and-mouth disease virus (FMDV) is the causative agent of a highly contagious vesicular disease of cloven-hoofed animals. In the present study we use FMDV serotype C infection of swine to determine, by analytical techniques, the direct ex vivo visualization of virus-infected immune cells during the first 17 days of infection. We report, for the first time, that FMDV C-S8c1 can infect T and B cells at short periods of time postinoculation, corresponding with the peak of the viremia. There is a significant lymphopenia that involves CD3+ CD4– CD8+/–, CD3+ CD4– CD8+Tc, and CD3+ CD4+ CD8+ memory Th but not CD3+ CD4+ CD8– naïve Th lymphocytes. In addition, a profound depletion of the vast majority of peripheral T cells in lymph nodes and spleen is observed. This selective depletion of T cells is not due mainly to in situ death via apoptosis as visualized by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique. Thus, early infection of T cells by FMDV may be the main cause of the observed T-cell depletion. Importantly, this lack of T cells is reflected in a reduced response to mitogen activation, which in many cases is totally eliminated. These data suggest a mechanism by which the virus causes a transient immunosuppression, subvert the immune systems, and spreads. These results have important implications for our understanding of early events in the development of a robust immune response against FMDV.

* Corresponding author. Mailing address: Centro de Biología Molecular Severo Ochoa, Universidad Autónoma de Madrid, Cantoblanco, Madrid 28049, Spain. Phone: 34 91 497 8477. Fax: 34 91 497 4799. E-mail: nsevilla{at}cbm.uam.es.

{dagger} These authors have contributed equally to this work.

Journal of Virology, March 2006, p. 2369-2379, Vol. 80, No. 5
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.5.2369-2379.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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