Divergent CD4+ T memory stem cell dynamics in pathogenic and nonpathogenic simian immunodeficiency virus infections

Recent studies have identified a subset of memory T cells with stem cell-like properties (T(SCM)) that include increased longevity and proliferative potential. In this study, we examined the dynamics of CD4(+) T(SCM) during pathogenic SIV infection of rhesus macaques (RM) and nonpathogenic SIV infec...

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Published in:	The Journal of immunology (1950) Vol. 192; no. 10; p. 4666
Main Authors:	Cartwright, Emily K, McGary, Colleen S, Cervasi, Barbara, Micci, Luca, Lawson, Benton, Elliott, Sarah T C, Collman, Ronald G, Bosinger, Steven E, Paiardini, Mirko, Vanderford, Thomas H, Chahroudi, Ann, Silvestri, Guido
Format:	Journal Article
Language:	English
Published:	United States 15.05.2014
Subjects:	Animals CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - pathology Cercocebus atys Immunologic Memory Macaca mulatta Simian Acquired Immunodeficiency Syndrome - immunology Simian Acquired Immunodeficiency Syndrome - pathology Simian Immunodeficiency Virus - immunology Time Factors
ISSN:	1550-6606, 1550-6606
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Summary:	Recent studies have identified a subset of memory T cells with stem cell-like properties (T(SCM)) that include increased longevity and proliferative potential. In this study, we examined the dynamics of CD4(+) T(SCM) during pathogenic SIV infection of rhesus macaques (RM) and nonpathogenic SIV infection of sooty mangabeys (SM). Whereas SIV-infected RM show selective numeric preservation of CD4(+) T(SCM), SIV infection induced a complex perturbation of these cells defined by depletion of CD4(+)CCR5(+) T(SCM), increased rates of CD4(+) T(SCM) proliferation, and high levels of direct virus infection. The increased rates of CD4(+) T(SCM) proliferation in SIV-infected RM correlated inversely with the levels of central memory CD4(+) T cells. In contrast, nonpathogenic SIV infection of SM evidenced preservation of both CD4(+) T(SCM) and CD4(+) central memory T cells, with normal levels of CD4(+) T(SCM) proliferation, and lack of selective depletion of CD4(+)CCR5(+) T(SCM). Importantly, SIV DNA was below the detectable limit in CD4(+) T(SCM) from 8 of 10 SIV-infected SM. We propose that increased proliferation and infection of CD4(+) T(SCM) may contribute to the pathogenesis of SIV infection in RM.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1550-6606 1550-6606
DOI:	10.4049/jimmunol.1303193