To measure the virus load in patients with symptomatic Epstein-Barr virus (EBV) infections, we used a real-time PCR assay to quantify the amount of EBV DNA in blood. The real-time PCR assay could detect from 2 to over 107 copies of EBV DNA with a wide linear range. We estimated the virus load in peripheral blood mononuclear cells (PBMNC) from patients with symptomatic EBV infections. The mean EBV-DNA copy number in the PBMNC was 103.7 copies/μg of DNA in patients with EBV-related lymphoproliferative disorders, 104.1 copies/μg of DNA in patients with chronic active EBV infections, and 102.2copies/μg of DNA in patients with infectious mononucleosis. These numbers were significantly larger than those in either posttransplant patients or immunocompetent control patients without EBV-related diseases. In a patient with infectious mononucleosis, the virus load decreased as the symptoms resolved. The copy number of EBV DNA in PBMNC from symptomatic EBV infections was correlated with the EBV-positive cell number determined by the in situ hybridization assay (r = 0.842; P < 0.0001). These results indicate that the real-time PCR assay is useful for diagnosing symptomatic EBV infection and for monitoring the virus load.

Herpes simplex encephalitis (HSE) in children sometimes exacerbates after successful treatment; yet the frequency, etiology, and clinical features of exacerbation remain unclear. We report data for 27 children with HSE confirmed by polymerase chain reaction (PCR) analysis; all were successfully treated with acyclovir, but 7 (26%) had a relapse of encephalitic illness. In 2 of those 7, serial examination with a PCR assay showed that herpes simplex virus (HSV) DNA reappeared temporarily in the cerebrospinal fluid (CSF). For 5 of the 7 patients, a second course of acyclovir therapy was effective. Coxsackievirus A9 was isolated from CSF of 1 case patient during subsequent exacerbation. The total dose during initial acyclovir therapy was significantly lower in the relapse group than in the control group (P=.027). In conclusion, exacerbation of HSE in children may be more common than previously recognized. It is suggested that the replication of HSV or another viral pathogen caused a second encephalitic illness (HSE) in some cases.

Neonatal herpes simplex virus (HSV) infection is a severe disease with high mortality and morbidity in spite of the development of effective anti-viral therapies. The viral load in neonatal herpes simplex virus (HSV) infection was measured retrospectively in 37 patients. HSV DNA copy numbers in serum and cerebrospinal fluid (CSF) were quantified using a real-time PCR assay. Patients with disseminated infection had a higher viral load in their sera. whereas patients with central nervous system (CNS) infection exhibited a higher viral load in the CSF. The viral load was significantly higher in the serum of patients who died later. Interestingly, patients with HSV type-2 infection exhibited more CNS involvement and neurological impairment, together with a high viral load in the CSF, than did HSV type-1 patients. These results suggest that quantitation of HSV viral load may be useful for assessing the prognosis, and may provide additional information for the management of neonatal HSV infection.

Background: Expression level of chondroitin sulfate (CS) is important in embryonic development. However, its involvement in skeletal myogenesis is unknown. Results: The CS level is temporally decreased during skeletal muscle development, and its forced reduction enhances myogenic differentiation/regeneration. Conclusion: Temporal decline in CS levels is required for skeletal muscle differentiation/regeneration. Significance: Lowering CS abundance is a promising approach for skeletal muscle regenerative therapy.

Abstract:The