Contribution of inflammation to fat redistribution and metabolic disturbances in HIV-1 infected patients.
Antiretroviral therapy (ART) has significantly reduced the morbidity and mortality of patients infected with the human immunodeficiency virus 1 (HIV-1). In a significant number of patients, ART is associated with fat redistribution and metabolic alterations such as dyslipidemia, insulin resistance (IR) and type 2 diabetes, summarized under the term HIV-associated lipodystrophy syndrome (HIV-LS). The pathogenesis of HIV-LS is complex and involves a number of factors including ART, HIV-1, abnormal fat redistribution, metabolic abnormalities and chronic inflammation. In view of a novel understanding on how chronic inflammation contributes to the pathogenesis of HIV-1 infection, this review focuses on the interaction of the immune system and metabolic pathways and the potential consequences for the HIV-LS. Based on the current literature, we suggest a central role of systemic inflammation in triggering and deteriorating various components of the HIV-LS.
Stankov
Metodi V
MV
Clinic for Immunology and Rheumatology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany.
Behrens
Georg M N
GM
D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D019380:Anti-HIV Agents / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D050171:Dyslipidemias / Q000209:etiology; D015658:HIV Infections / Q000188:drug therapy; D039682:HIV-Associated Lipodystrophy Syndrome / Q000209:etiology* / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000473:pathology; D007333:Insulin Resistance
D019380:Anti-HIV Agents