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Marked Enteropathy in an Accelerated Macaque Model of AIDS
Joshua D Croteau1, Elizabeth L Engle1, Suzanne E Queen1
1Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
The American Journal of Pathology
|January 6, 2017
Summary
Combination antiretroviral therapy prevents intestinal disease in SIV-infected macaques. A robust cytotoxic T-lymphocyte response may protect against SIV-induced intestinal damage, independent of microbial translocation.
Area of Science:
- Immunology
- Gastroenterology
- Virology
Background:
- Enteropathy persists in HIV infection despite combination antiretroviral therapy (cART).
- Microbial translocation is a potential driver of HIV-related enteropathy.
- The SIV/pigtailed macaque model offers insights into HIV pathogenesis.
Purpose of the Study:
- To investigate the relationship between enteropathy, microbial translocation, and antiretroviral therapy in an SIV macaque model.
- To identify factors conferring resilience to SIV-induced intestinal damage.
Main Methods:
- Histological examination of intestinal tissue from SIV-infected macaques.
- Assessment of enteropathy markers (caspase-3, CD3+ T cells, SIV-infected cells, claudin-3).
- Measurement of microbial translocation markers (soluble CD14, CD163, LBP, 16S rDNA) and cytotoxic T-lymphocyte response.
Main Results:
- cART initiated during acute infection prevented intestinal disease.
- Enteropathy was associated with increased caspase-3, decreased CD3+ T cells, and more SIV-infected cells.
- Microbial translocation markers were unexpectedly low and did not correlate with intestinal disease or claudin-3 loss.
- Resilience to intestinal damage correlated with increased cytotoxic T-lymphocyte response.
Conclusions:
- SIV-induced enteropathy is not solely driven by microbial translocation.
- Early cART effectively prevents intestinal pathology in this model.
- Cytotoxic T-lymphocyte responses play a crucial role in protecting the gut from SIV-induced damage.
