Lymphoid fibrosis occurs in long-term nonprogressors and persists with antiretroviral therapy but may be reversible with curative interventions
| Autor: | Timothy W. Schacker, Alexander Khoruts, Jodi Anderson, Ma Somsouk, Jake S. Jasurda, Cavan S. Reilly, Ann Thorkelson, Samuel Russ, Peter W. Hunt, Hiroyu Hatano, Steven G. Deeks, Joyce L. Sanchez, Gregory J. Beilman |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
CD4-Positive T-Lymphocytes
Male Biopsy HIV Infections Virus Replication Medical and Health Sciences Cohort Studies Fibrosis Immunology and Allergy 2.1 Biological and endogenous factors Longitudinal Studies Aetiology Lung Interleukin virus diseases Middle Aged Biological Sciences Lymphatic system Infectious Diseases Anti-Retroviral Agents Disease Progression HIV/AIDS Female medicine.symptom Infection Adult Lymphoid Tissue Inflammation Biology Microbiology Virus HIV Long-Term Survivors Major Articles and Brief Reports Clinical Research medicine Humans fibrosis Rectum HIV HIV controllers medicine.disease Virology CD4 Lymphocyte Count Good Health and Well Being Viral replication Immunology HIV-1 CD8 |
| Zdroj: | The Journal of infectious diseases, vol 211, iss 7 |
| Popis: | The hallmark of human immunodeficiency virus (HIV) infection is progressive loss of CD4+ T cells in peripheral blood (PB) and lymphoid tissues (LTs) that is not fully restored with antiretroviral therapy (ART) [1–4]. HIV infection is also associated with chronic inflammation that is only partially normalized with ART [5, 6]. This chronic inflammatory state is maintained by several factors, including the direct effects of HIV replication [7], coinfections such as cytomegalovirus (and other herpes viruses) [8], and chronic damage to the gut mucosa that causes microbial translocation [9–11]. Acute and chronic inflammation associated with HIV infection leads to upregulation of transforming growth factor β in the LT, where HIV replicates and stimulates local production of collagen [12–14]. Collagen deposition into LT dramatically alters the architecture and function of the LT and ultimately causes progressive loss of naive T cells. This happens because the fibroblastic reticular network that produces interleukin 7 (important for naive T-cell homing and survival) is replaced by collagen [13, 15–17]. Potent and sustained suppression of HIV replication with ART reduces immune activation, but the degree to which LT pathologies are reversed and tissue architecture is restored is unknown. A subset of HIV-infected individuals called elite controllers have durable control of HIV in the absence of therapy, in that their plasma viral load is maintained at |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|