A potential explanation for the relationship is that the inflammatory and autoimmune processes accompanying the infections contracted during early childhood are less intense, compared to those seen in adults having a fully mature immune system. before the initial manifestations of MS, and the extremely rare event of MS in individuals seronegative for EBV. However, the data within the mechanism MSH4 underlying the relationship between EBV and MS are controversial. Moreover, many observations indicate that EBV contributes also to the pathomechanism of SLE. However, this contribution differs from the relationship between EBV and MS, as demonstrated by the lack of any increase in the risk of SLE after IM. In SLE, EBV serology is definitely quantitatively and qualitatively different from the normal response C that is, EBV viral weight is definitely higher and a strong cross-reaction can be recognized between particular EBV antigens and autoantigens of pathological importance. These observations, along with the findings pointing to a possible part of EBV in rheumatoid arthritis and myasthenia gravis show that illness by EBV may be one of the environmental factors, which can facilitate the development of some autoimmune disorders in genetically vulnerable individuals. and the subfamily of HTS01037 gamma herpesviruses HTS01037 C it is also referred to as the human being herpesvirus type 4 (HHV-4). The structure of EBV is similar to that of additional herpesviruses: the linear, double-stranded DNA spiral is definitely enclosed by a nucleocapsid of 100C120-nm diameter and icosahedral structure, consisting of very many tiny parts. The nucleocapsid is definitely engulfed by an amorphous compound (the tegument); the outer coating of the disease consists of the envelope transporting several viral proteins necessary for binding of the EBV to its receptor. The most important of these is definitely GP350, a glycoprotein of 350 kD molecular excess weight. The genome of the disease encodes several proteins of antigenic nature that are indicated on the surface of infected cells only during specific phases of the illness (see later on). These comprise nuclear antigens (EBNA-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, EBNA-LP), transmembrane proteins (LMP-1, LMP-2A, LMP-2B), and early antigens (EBV-EA) produced exclusively during the lytic cycle (see later on), membrane antigens (EBV-MA), the viral capsid antigen (EBV-VCA). Additionally, cells infected by EBV are characterized by the manifestation of small-molecular-weight RNA (EBER1 and EBER2), BHRF, and many viral micro-RNAs processed from transcripts of BHRF1 and BART genes. The life cycle of EBV in the body EBV can infect and activate B lymphocytes, as well as it is capable of persisting lifelong in these cells It also infects the epithelial cells in the oropharynx. The life cycle of EBV within the organism is rather complicated. In the tonsils C the subjects of the initial illness C the epithelial cells pass on the disease to B lymphocytes. The virus-specific receptor of B lymphocytes is the type 2 match receptor (CR2, CD21); HTS01037 however, MHC II antigens will also be necessary for viral penetration. This receptor is present on resting B lymphocytes and therefore, EBV infects these cells, mainly. According to the most widely approved, current scenario, EBV activates resting lymphocytes, which transform into lymphoblasts. Then C similar to the normal, antigen-triggered differentiation processes of B lymphocytes C these blasts develop into B memory space cells with latent EBV illness. In the meantime, the disease can launch several latency programs in infected B cells: HTS01037 Table 1. The most important properties of the EpsteinCBarr disease ??It belongs to the family of herpesviruses and to the subfamily of gamma-herpesviruses (HHV-4)??Structure: globular, diameter 150C200 nm, capsid membrane, membrane proteins??Genome: double-stranded, circular DNA??Main target cells: B lymphocytes, epithelial cells??Receptor on B-1 lymphocytes: CD21, latent illness, episome formation??Multiple forms (III, II, I) of disease latency, lytic cycle, replication cycle in B lymphocytes and in epithelial cells??Immortalization.