Abstract
Human cytomegalovirus (HCMV) is a ubiquitous double-stranded DNA virus belonging to the β-subgroup of the herpesvirus family. After the initial infection, the virus establishes latency in poorly differentiated myeloid precursors from where it can reactivate at later times to cause recurrences. In immunocompetent subjects, primary HCMV infection is usually asymptomatic, while in immunocompromised patients, HCMV infection can lead to severe, life-threatening diseases, whose clinical severity parallels the degree of immunosuppression. The existence of a strict interplay between HCMV and the immune system has led many to hypothesize that HCMV could also be involved in autoimmune diseases (ADs). Indeed, signs of active viral infection were later found in a variety of different ADs, such as rheumatological, neurological, enteric disorders, and metabolic diseases. In addition, HCMV infection has been frequently linked to increased production of autoantibodies, which play a driving role in AD progression, as observed in systemic lupus erythematosus (SLE) patients. Documented mechanisms of HCMV-associated autoimmunity include molecular mimicry, inflammation, and nonspecific B-cell activation. In this review, we summarize the available literature on the various ADs arising from or exacerbating upon HCMV infection, focusing on the potential role of HCMV-mediated immune activation at disease onset.
Highlights
The adaptive immune response recognizes external pathogens as non-self antigens as opposed to the antigens from one’s own body, known as self-antigens
The tremendous research effort undertaken to understand the mechanisms of Human cytomegalovirus (HCMV) pathogenesis and develop new diagnostic techniques and antiviral drugs has led to the discovery of novel functions of this virus in other pathophysiological processes such as autoimmunity
We have summarized past and current literature on the emerging role of HCMV in several autoimmune diseases (ADs), elucidating mechanisms (Figure 2) and related clinical manifestations (Table 1)
Summary
The adaptive immune response recognizes external pathogens as non-self antigens as opposed to the antigens from one’s own body, known as self-antigens. A large body of evidence has shown how HCMV can use several of its genes to manipulate the innate and adaptive immune system of the infected subject [14,15,16,17,18,19] This feature alongside many others, such as its wide tropism [20,21,22,23], its ability to persist in the host during phases of latency and reactivation, and, as already mentioned, its global distribution [24], makes HCMV a candidate etiological agent of ADs. A causative link between. Hypergammaglobulinemia, cryoglobulinemia, and autoantibody production are common features of HCMV-driven mononucleosis [31,32] This unspecific hyperactivation of humoral immunity is thought to represent a mechanism of viral immune evasion, because it curbs host B-cell responses. This review aims to provide an updated overview on the role of HCMV in the etiopathogenesis of ADs, focusing on the underlying mechanism that has been proposed for each specific disorder
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