![]() ![]() Currently, it is thought that one in a million B cells carry the EBV genome in an individual after recovery from acute infection ( 27). EBV persists mostly in the memory B-cell compartment and possibly also in epithelial cells ( 201) (Fig. Latency is the state of persistent viral infection without active viral production. The number of infected B cells decreases over time after the onset of symptoms of primary infection ( 72), but these cells are never eliminated entirely. (Fig.1), 1), resulting in detectable levels of virus in the blood, as discussed below. Infected memory B cells are released into the peripheral circulation (Fig. ![]() An important consequence of EBV infection in B cells is that they are induced to activate their growth program and trigger differentiation into memory B cells via the germinal center reaction. The early products (e.g., BNLF2a) have a wide array of functions, including replication, metabolism, and blockade of antigen processing, while late products tend to code for structural proteins such as the viral capsid antigens (VCA) and gene products used for immune evasion (e.g., BCRF1). Activation of lytic replication or reactivation from latency is key to transmission. BZLF1 and BRLF1 are some of the IE products that further act as transactivators of the viral lytic program ( 204). Briefly, there are three temporal classes of viral lytic gene products (immediate-early, early, and late ). ( 204) have published a complete review of lytic and latent replication. Viral DNA polymerase accomplishes linear viral replication, which occurs during the lytic phase of the viral life cycle. Once the viral nucleocapsid is dissolved, the genome is transported to the nucleus, where it is replicated by DNA polymerases. Endocytosis of the virus into vesicles and fusion of the virus with the vesicle membrane release the nucleocapsid into the cytoplasm. In epithelial cells, which lack CD21, the EBV BMRF-2 protein interacts with β1 integrins ( 205, 219, 220), and the EBV gH/gL envelope protein triggers fusion via interaction with αvβ6/8 integrins ( 35). EBV gp42 then interacts with B-cell HLA class II molecules and triggers fusion with the host membrane. EBV attaches to B cells via binding of the viral gp350 protein to CD21 on B cells ( 188). The host cells of EBV are mainly lymphocytes and epithelial cells ( 113). Initial infection is thought to occur in the oral (tonsillar) compartment (Fig. These isolates are distinguished by their restriction endonuclease digestion patterns and exhibit different transforming capabilities ( 1, 170, 199) and the ability to spontaneously enter the lytic cycle ( 31). Type 1 is dominant in the Western hemisphere and Southeast Asia, whereas types 1 and 2 are equally prevalent in Africa ( 169, 224). There are two subtypes of EBV, which differ from each other at the EBV nuclear antigen (EBNA) loci for EBNA2, -3A, -3B, and -3C ( 175). The EBV genome of approximately 100 genes has been described in detail ( 57). Mature virions are approximately 120 to 180 nm in diameter ( 51, 111). A protein tegument lies between the capsid and the envelope, which is embedded with glycoproteins that are important for cell tropism, host range, and receptor recognition ( 113). Like those of other herpesviruses, EBV virions have a double-stranded, linear DNA genome surrounded by a protein capsid. Virus Structure, Genome, and Strain VariabilityĮBV, formally designated human herpesvirus 4 (HHV-4), is one of the eight known human herpesviruses. Understanding the pathogenesis of EBV infection and applying that knowledge to patient care are of great interest to basic and translational scientists and also to clinicians, especially those in family practice, pediatrics, and internal medicine. We discuss the spectrum of clinical illness due to primary EBV infection, risk factors for acquisition and severity of infectious mononucleosis, treatment options for EBV infections, and prospects for a vaccine. ![]() This review describes advances in the clinical, virologic, and immunologic aspects of primary EBV infection, which have been the focus of our research for the past decade. The unifying and perplexing characteristic of human herpesviruses, including EBV, is that acquisition results in lifelong infection after the initial viral replication has been contained ( 172). Four years later, EBV was linked conclusively to infectious mononucleosis, which is its most common clinical manifestation ( 78). Epstein-Barr virus (EBV) was discovered in 1964 by electron microscopy of suspension cultures of African Burkitt lymphoma cells ( 51). ![]()
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