J. Exp. Med., Volume 187, Number 7, April 6, 1998 1139-1144

BRIEF DEFINITIVE REPORT:
Productive Infection of Neonatal CD8⁺ T Lymphocytes by HIV-1

By Liang Peng Yang,^* James L. Riley,^§ Richard G. Carroll, Carl H. June, James Hoxie, Bruce K. Patterson,^** Yusei Ohshima,^* Richard J. Hodes,^¶ and Guy Delespesse^*

From the ^* University of Montreal, Centre de Recherche Louis-Charles Simard, Hôpital Notre-Dame, Montreal, Quebec H2L 4M1, Canada; the  Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, Maryland 20889; the ^§ Division of Retrovirology, Walter Reed Army Institute for Research, Rockville, Maryland 20850; the  Experimental Immunology Branch, National Institutes of Health, Bethesda, Maryland 20892; the ^¶ National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892; the ^** Department of Obstetrics/Gynecology and Medicine, Division of Infectious Diseases, Northwestern University Medical School, Chicago, Illinois 60611; and the  Hematology-Oncology Division, University of Pennsylvania, Philadelphia, Pennsylvania 19104

CD8⁺ T lymphocytes confer significant but ultimately insufficient protection against HIV infection. Here we report that activated neonatal CD8⁺ T cells can be productively infected in vitro by macrophage-tropic (M-tropic) HIV-1 isolates, which are responsible for disease transmission, whereas they are resistant to T cell-tropic (T-tropic) HIV strains. Physiological activation of CD8-/⁺ CD4 T cell receptor-/⁺ neonatal T cells, including activation by allogeneic dendritic cells, induces the accumulation of CD4 messenger RNA and the expression of CD4 Ag on the cell surface. The large majority of anti-CD3/B7.1-activated cord blood CD8⁺ T cells coexpress CD4, the primary HIV receptor, as well as CCR5 and CXCR4, the coreceptors used by M- and T-tropic HIV-1 strains, respectively, to enter target cells. These findings are relevant to the rapid progression of neonatal HIV infection. Infection of primary HIV-specific CD8⁺ T cells may compromise their survival and thus significantly contribute to the failure of the immune system to control the infection. Furthermore, these results indicate a previously unsuspected level of plasticity in the neonatal immune system in the regulation of CD4 expression by costimulation.

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