Format

Send to

Choose Destination
Sci Rep. 2017 Sep 13;7(1):11474. doi: 10.1038/s41598-017-10965-z.

Evolution of T Cell Responses during Measles Virus Infection and RNA Clearance.

Author information

1
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
2
Vanderbilt University School of Medicine, Nashville, TN, 37232, USA.
3
Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
4
University of North Carolina School of Medicine, Chapel Hill, NC, USA.
5
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. dgriffi6@jhu.edu.

Abstract

Measles is an acute viral disease associated both with immune suppression and development of life-long immunity. Clearance of measles virus (MeV) involves rapid elimination of infectious virus during the rash followed by slow elimination of viral RNA. To characterize cellular immune responses during recovery, we analyzed the appearance, specificity and function of MeV-specific T cells for 6 months after respiratory infection of rhesus macaques with wild type MeV. IFN-γ and IL-17-producing cells specific for the hemagglutinin and nucleocapsid proteins appeared in circulation in multiple waves approximately 2-3, 8 and 18-24 weeks after infection. IFN-γ-secreting cells were most abundant early and IL-17-secreting cells late. Both CD4+ and CD8+ T cells were sources of IFN-γ and IL-17, and IL-17-producing cells expressed RORγt. Therefore, the cellular immune response evolves during MeV clearance to produce functionally distinct subsets of MeV-specific CD4+ and CD8+ T cells at different times after infection.

PMID:
28904342
PMCID:
PMC5597584
DOI:
10.1038/s41598-017-10965-z
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center