This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Neal, Z. C. Articles by Splitter, G. A. Search for Related Content PubMed PubMed Citation Articles by Neal, Z. C. Articles by Splitter, G. A.

 Previous Article  |  Next Article 

J. Virol., 08 1995, 4914-4923, Vol 69, No. 8
Copyright © 1995, American Society for Microbiology

Picornavirus-specific CD4+ T lymphocytes possessing cytolytic activity confer protection in the absence of prophylactic antibodies

ZC Neal and GA Splitter
Department of Animal Health and Biomedical Sciences, University of Wisconsin-Madison 53706, USA.

Picornaviruses are a family of positive-strand RNA viruses that are responsible for a variety of devastating human and animal diseases. An attenuated strain of mengovirus (vMC24) is serologically indistinguishable from the lethal murine wild-type mengovirus and encephalomyocarditis virus (EMCV). Immunogen-specific stimulation of vMC24-immune splenocytes in vitro demonstrates preferential activation of CD4+ lymphocytes. vMC24-immune splenocytes adoptively transferred to naive recipients conferred protection against lethal EMCV challenge. Immune splenocytes, expanded in vitro, were > 92% CD4+ T lymphocytes. Interestingly, adoptive transfer of these expanded cells engendered protection against lethal challenge. In vivo depletion of CD4+ T lymphocytes prior to lethal challenge abrogated survival of transfer recipients, confirming that CD4+ T lymphocytes were essential for protection. Subsequent rechallenge of vMC24-immune splenocyte recipients with a greater EMCV dose elicited serum neutralizing antibody titers paralleling the high titers observed in vMC24-immunized mice. Unexpectedly, an augmented humoral response was absent in vMC24- specific CD4+ T-cell recipients after the secondary challenge. Moreover, comparably low serum neutralizing antibody titers failed to protect passive transfer recipients when correspondingly challenged. vMC24-immune splenocytes expanded in vitro (> 94% CD4+) lysed vMC24- infected A20.J target cells. The ability to transfer protection with primed CD4+ T cells, in the absence of primed B lymphocytes or immune sera, is novel for picornaviral infections. Consequently, mechanisms such as CD4+ cytolytic T-lymphocyte activity are implicated in mediating protection.

This article has been cited by other articles:

• Li, J., Zhang, C., Jostock, T., Dubel, S. (2007). Analysis of IgG heavy chain to light chain ratio with mutant Encephalomyocarditis virus internal ribosome entry site. Protein Eng Des Sel 0: gzm038v1-6 [Abstract] [Full Text]  
• Smiley, K. L., McNeal, M. M., Basu, M., Choi, A. H.-C., Clements, J. D., Ward, R. L. (2007). Association of Gamma Interferon and Interleukin-17 Production in Intestinal CD4+ T Cells with Protection against Rotavirus Shedding in Mice Intranasally Immunized with VP6 and the Adjuvant LT(R192G). J. Virol. 81: 3740-3748 [Abstract] [Full Text]  
• Ilyinskii, P. O., Wang, R., Balk, S. P., Exley, M. A. (2006). CD1d Mediates T-Cell-Dependent Resistance to Secondary Infection with Encephalomyocarditis Virus (EMCV) In Vitro and Immune Response to EMCV Infection In Vivo. J. Virol. 80: 7146-7158 [Abstract] [Full Text]  
• VanCott, J. L., Prada, A. E., McNeal, M. M., Stone, S. C., Basu, M., Huffer, B. Jr., Smiley, K. L., Shao, M., Bean, J. A., Clements, J. D., Choi, A. H.-C., Ward, R. L. (2006). Mice Develop Effective but Delayed Protective Immune Responses When Immunized as Neonates either Intranasally with Nonliving VP6/LT(R192G) or Orally with Live Rhesus Rotavirus Vaccine Candidates.. J. Virol. 80: 4949-4961 [Abstract] [Full Text]  
• LaRue, R., Myers, S., Brewer, L., Shaw, D. P., Brown, C., Seal, B. S., Njenga, M. K. (2003). A Wild-Type Porcine Encephalomyocarditis Virus Containing a Short Poly(C) Tract Is Pathogenic to Mice, Pigs, and Cynomolgus Macaques. J. Virol. 77: 9136-9146 [Abstract] [Full Text]  
• McNeal, M. M., VanCott, J. L., Choi, A. H. C., Basu, M., Flint, J. A., Stone, S. C., Clements, J. D., Ward, R. L. (2002). CD4 T Cells Are the Only Lymphocytes Needed To Protect Mice against Rotavirus Shedding after Intranasal Immunization with a Chimeric VP6 Protein and the Adjuvant LT(R192G). J. Virol. 76: 560-568 [Abstract] [Full Text]  
• Martin, L. R., Neal, Z. C., McBride, M. S., Palmenberg, A. C. (2000). Mengovirus and Encephalomyocarditis Virus Poly(C) Tract Lengths Can Affect Virus Growth in Murine Cell Culture. J. Virol. 74: 3074-3081 [Abstract] [Full Text]  
• Gagnon, S. J., Ennis, F. A., Rothman, A. L. (1999). Bystander Target Cell Lysis and Cytokine Production by Dengue Virus-Specific Human CD4+ Cytotoxic T-Lymphocyte Clones. J. Virol. 73: 3623-3629 [Abstract] [Full Text]  
• Neal, Z. C., Splitter, G. A. (1998). Protection against Lethal Encephalomyocarditis Virus Infection in the Absence of Serum-Neutralizing Antibodies. J. Virol. 72: 8052-8060 [Abstract] [Full Text]