Rheumatological Diseases in HIV Infection

Abstract

Abstract:: We performed a review of the available literature in order to summarize the pathogenic and clinical connections between HIV infection and rheumatological syndromes. The increasing life expectancy during human immunodeficiency virus (HIV) infection has led to the observation of many rheumatological manifestations over the years in this type of patients. Although the pathological mechanisms are still not fully understood, several rheumatological diseases have been more commonly observed than in the general population especially after the advent of highly active antiretroviral therapy (HAART) and sometimes clinical and serological findings are influenced by the underlying condition which define a characteristic onset or development of the disease. Autoimmune diseases occur during specific stages of the HIV infection, depending on the underlying pathogenic mechanism being mainly influenced by the CD4+ cells count. Several rheumatological diseases show peculiar clinical manifestations influenced by the underlying HIV infection leading to specific features less commonly observed in healthy population. Conversely to pathological findings, broadly HIV-1-neutralizing antibodies (BnAb) observed in several autoimmune diseases such as SLE, could exert a protective part against HIV infection. It is important to evaluate the onset of autoimmune diseases in HIV patients, in order to start the appropriate treatment to avoid harmful events. More studies are needed to enlighten the trend of autoimmune diseases during HIV infection. Pathogenic mechanisms and clinical manifestations of rheumatological diseases during HIV infection will be discussed in this review.

Epstein‒Barr virus and human herpesvirus 6 infection in patients with systemic lupus erythematosus

“…The potential mechanisms of infectious agents in the pathogenesis of SLE involve induction of aberrant innate and adaptive immunity, leading to a loss of tolerance to autoantigens. Some predominant pathogens have been reported to be associated with SLE [ 6 ], such as Epstein‒Barr virus (EBV) [ 7 ], human T-lymphotropic virus type 1 (HTLV-1) [ 8 ], and human immunodeficiency virus (HIV) [ 9 ].…”

“…The potential mechanisms of infectious agents in the pathogenesis of SLE involve induction of aberrant innate and adaptive immunity, leading to a loss of tolerance to autoantigens. Some predominant pathogens have been reported to be associated with SLE [6], such as Epstein-Barr virus (EBV) [7], human T-lymphotropic virus type 1 (HTLV-1) [8], and human immunodeficiency virus (HIV) [9]. Some immunochemical evidence suggests that molecular mimicry by infectious agents can active autoreactive T cells via exogenous antigens when these two antigens are sufficiently similar to one another to imitate or be a mimic.…”