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Simian immunodeficiency virus infection in neonatal macaques
Ronald S Veazey1, Jeffrey D Lifson, Ivona Pandrea
1Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana 70433, USA. veazey@tpc.tulane.edu
Journal of Virology
|July 30, 2003
Summary
Neonatal macaques infected with simian immunodeficiency virus (SIV) experienced rapid CD4(+) T-cell depletion in the gut. This early intestinal immune damage contributes to higher viral loads and faster disease progression in infants.
Area of Science:
- Immunology
- Virology
- Pediatric Infectious Diseases
Background:
- Human immunodeficiency virus (HIV) infection progresses faster in children than adults.
- The intestinal tract is a key site for early viral replication and CD4(+) T-cell loss in adults.
Purpose of the Study:
- To investigate the impact of simian immunodeficiency virus (SIV) on peripheral and intestinal lymphocytes in neonatal macaques.
- To understand the early dynamics of CD4(+) T-cell depletion in the neonatal gut during SIV infection.
Main Methods:
- Analysis of peripheral and intestinal lymphocytes in 13 SIVmac239-infected neonatal macaques.
- Comparison of lymphocyte populations (CD4(+) and CD8(+) T cells) between neonates and adults.
- Assessment of CD4(+) T-cell activation and memory phenotype in different tissues.
Main Results:
- Neonates possess a higher proportion of activated CD4(+) T cells in the intestinal lamina propria compared to adults.
- SIV infection led to rapid and selective depletion of jejunum lamina propria CD4(+) T cells within 21 days.
- Higher viral loads correlated with less CD4(+) T-cell depletion in tissues, suggesting complex immune responses.
Conclusions:
- Early and severe CD4(+) T-cell depletion in the neonatal gut is a hallmark of SIV infection.
- The intestinal immune environment plays a critical role in the accelerated disease progression observed in infants.
- Factors like increased T-cell turnover or resistance to depletion may influence viral load and disease severity in neonatal hosts.